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Is telomerase the Holy Grail of molecular biology?

By: Lionel Perez Valenzuela

At the heart of most human cancers is present an enzyme, this enzyme called telomerase is so important. Almost 95% of cancer cells show active telomerase.

Telomerase expression shows a particular pattern and is active only in embryonic stem cells, stem cells adult, germ cells and tumor cells. While in somatic cells are those that are most differentiated tissues is inactive.

recently discovered the structure of a key catalytic component of the enzyme, opening the way for better anti-cancer drugs and perhaps some kind of anti-aging therapy.


What happens in somatic cells with the telomerase?

somatic cells carried the cell cycle. First G1 phase of high metabolic activity, then the S phase where DNA is replicated, and finally the G2 stage, last stage before perform mitotic division.

The telomerase gene is not expressed in somatic cells and each time the cell divides, because of the mechanism of DNA replication, telomeres shorten. Thus, with each ensuing mitotic division telomeres becoming shorter, it somehow affect the stability of chromosomes prevents the cells can divide indefinitely.

When the cell can no longer divide more due to shortened telomeres, die. Some researchers believe this limit to the number of cell divisions that a cell can make is a form of protection against cancer.

As stated above, telomerase is inactive in most tissues and is active only in stem cells (especially in embryonic stem cells) in germline cells and tumor cells.

tumor cell lines grown "in vitro" is said to be "immortal." Ie the cell itself is not immortal, but can be divided indefinitely, unlike the somatic tissue cells that have a defined number of divisions.

What is replicative senescence?

The senescence comes from the Greek word senex (old) and refers to biological aging.

When eukaryotic cells extracted from tissues are placed in a cell culture medium, begin to divide but do not indefinitely. Initially divide very rapidly, but slowly began to make less mitosis and finally did not fall over and die. Cells can not move beyond the stage G1 to S. This process is called replicative senescence. For example, human cells can replicate a young adult between 60-80 times, but an elderly person may not exceed 20 divisions.

Consider that for decades scientists believed that both plant and animal cells, could be replicated indefinitely in cell culture. But in 1961 U.S. researcher Leonard Hayflick showed that this was a misconception. Fibroblasts showed lung and skin cells cultured in vitro initially multiply vigorously but then decline and eventually die. The limit of cell divisions that can make normal cells is called "Hayflick Limit." Cancer cells can be grown "in vitro" indefinitely.




How can they be related cancer and cell aging?

Telomerase is responsible for adding a repetitive sequence at the ends of chromosomes, called telomeres. Telomeres protect the chromosomes, preventing their breakdown, degradation and other problems. If telomeres become too short, start occurring chromosomal abnormalities. Recall that one of the hallmarks of cancer are these abnormalities. If the cell could somehow detect this condition so risky (the shortening of telomeres) would be divided. Thus, the shortening of telomeres is one way to prevent the disappearance of tumor cells and the cost would replicative senescence.

remember that there are two key genes that can halt the cell cycle before the accumulation of mutations, these genes are p53 and p16. The result of stopping the cell cycle, Antel accumulation of mutations or the inability to repair damaged DNA is replicative senescence.

This would explain several of the syndromes that affect humans, related to premature aging or accelerated. The common denominator that appears in these diseases is the mutation of genes related to DNA repair or maintain the integrity of the genome.

For example, Werner syndrome, affected people have gray hair at age 20 and most die before age 50. Suffer from several enfrmedades associated with aging such as osteoporosis, cataracts and arteriosclerosis. Even at a young age their cells undergo replicative senescence luegode make only 20 cell divisions, normal is 70 or 80 divisions. This syndrome is caused by a mutation in the gene WRN , which encodes a helicase required for the repair and maintenance of DNA and telomeres. The accumulation of mutations, the problems at telomeres activate the mechanisms of p53 and p16 to arrest the cell cycle and cause replicative senescence.



Another syndrome of premature aging is the Progeria (Aging) or Hutchinson-Gilford Syndrome (HGPS). Children born with this rare disease already showing signs of premature aging by two years and usually die before the age of ten. have mutated the gene LMNA, which encodes intermediate filament to the nuclear lamina. The machinery of DNA repair, transcription and replication are intensive in the face of the nuclear envelope. These children show high rates of DNA damage and other defects in gene expression.




Why, if the stem cells have active telomerase, age? Apparently

embryonic stem cells are the only ones that have a completely telomerase active since shortly after birth, and telomeres are shortened sample of stem cells even in newborns. Ie shortly after our birth, including stem cells show a less active telomerase. This would be progressive as we age thus losing the ability to regenerate our tissues because stem cells and their daughter cells gradually lose the ability to replicate.

Based on these findings it has been postulated anti-aging therapy based on activating telomerase in different tissues. There are already numerous lines of research in this direction, showing that it is possible to activate telomerase in a given tissue and that retain their functional characteristics and tissue does not become cancerous.

What about telomerase in tumor cells?

When telomerase is expressed in tissues that should not and is more active than usual, telomeres are not shortened and the cells continue to divide beyond their limit and can become cancer cells.

The fact that telomerase is active in most tumors, has become a prime target for anticancer therapies.

When determining the three dimensional structure of an enzyme can save lives ...

Telomerase is a ribonucleoprotein.

has a small RNA of nucleolar origin (not to be confused with small nuclear RNA) and a catalytic subunit protein.

small RNA molecule provides a mold 3 `-AAUCCC-5 'in maíferos TERC and is referred to by its acronym in English (the RNA Component of Telomerase).

subunit protein is called TERT (Telomerase Reverse Transcriptase).

determine the three dimensional structure of telomerase, has been a very difficult task. As we said telomerase is a ribonucleoprotein with transcriptase activity reverse (ie an enzyme that synthesizes DNA using a template strand of RNA).

Skordalakes researcher Emanuel and his team at the Wistar Institute telomerase finally managed to produce in large quantities and crystallize, a necessary step to determine their three dimensional structure by x-ray crystallography. But producing massive amounts of telomerase was a real problem until they found they could manipulate the gene for telomerase flour beetle to produce the required amounts of protein,


structure analysis has determined that TERT (Telomerase Reverse Transcriptase Protein) is a complex structure with three domains creating a ring structure. This ring structure has a central hole that when telomeres are being synthesized can be occupied by a molecule of ribonucleic acid template.

Telomerase, a possible key anti-aging treatments and anti-tumor.

The researchers assumed that the telomerase reverse transcriptase of HIV should have a similar structure as both enzymes are reverse transcriptase. Under this assumption developed anti-telomerase drugs.

structural analysis carried out after determining the three dimensional structure of telomerase, confirm these suspicions, but also revealed that the carboxy-terminal of telomerase is unique in its structure and so far unique in its kind.

This unique structural feature of telomerase, could develop drugs that have the sole target molecule, drugs designed on the basis of a high affinity for the carboxy-terminal end.

For example treatments were successful against certain types of tumors combining paclitaxel and AZT. Paclitaxel is a cytostatic drug that stops cells divide by mitosis, and which promotes microtubule polymerization leading to interfere with normal cellular mechanisms in both interphase and during mitosis. Moreover AZT is known primarily for being the first effective drug against HIV and to inhibit virus reverse transcriptase. The researchers estimated that as telomerase reverse transcriptase also, AZT should be inhibited by preventing telomeres synthesized tumor cells, causing you to senescence. Both drugs were used together better than used in isolation. Stephen Neidle


researcher at the School of Pharmacy, University of London estimated that drugs can be designed that can bind to telomerase for its carboxy-terminal and inhibit their activity to anticancer treatments. But they could also develop drugs that stimulate the opposite effect of telomerase activity for anti-aging treatments.



In the near future therapies could be used currently in clinical trial stages, such as certain types of anti-telomerase vaccines, drugs with future anti-telomerase design.

Aubrey de Gray Methuselah Foundation, believes that if we had a really strong anti-cancer therapy against all types of tumors, a therapy could also be used, for example based on a drug to prevent aging by activating telomerase. However

many difficulties, but both animal studies and in cell cultures and in human cancers, opening new perspectives in understanding complex issues such as aging and cancer.

Sources:

Kimball's Biology Pages

Newscientist

Methuselah Foundation

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tardigrades indestructible animals

By: Lionel Perez Valenzuela

The tardigrades are very little known, but they are the toughest animals on the planet and a lot of difference. Able to withstand extreme temperatures, as high as 180 degrees Celsius for a few minutes, or tempearture near absolute zero (-272 degrees Celsius or -200 degrees minutes for days). With regard to radiation tolerance is equally extreme, can withstand 5,700 grays (1 gray = 100 Rad). One gray is equivalent to 5,000 x-rays, 10-20 grays easily kill humans and most animals. Japanese scientists have been exposed to these small animals less than 1 mm in length that live on mosses and ferns, at pressures of more than 6,000 atmospheres, and still refused to die. However

not end there skills as tardigrades can withstand almost complete dehydration of the body (go to have a 85% water to 3%), and are able to survive in this state decades. This state of dehydration and metabolic almost completely suspended is called cryptobiosis . In this way the tarígrados adverse environmental conditions can become dehydrated and suspend their metabolism, for very long periods, decades or perhaps hundreds of years.

Recently, these "little water bears" (so called after its discoverer, Johann August Ephraim Goeze in 1773), made his latest stunt, to survive in the vacuum of space for more than a week, and then be able to reproduce.

was Tardigrada Spallanzani who called for its slow pace. Perhaps I had not called and knowing that tardigrades can travel on dust particles carried by storm, from Africa to America. On these trips in the stratosphere of "water bears" can withstand temperatures of -100 degrees Celsius (a temperature spring for them.) The Russians have also reported that on the roofs of their rockets are tardigrades, once they have reentered the space. Recent research

tardigrades to dehydration due to the disaccharide trehalose . The disaccharide trehalose is a very particular and the two glucoses are joined by a link involving the two anomeric carbon.



Apparently when the tardigrades will stop your metabolism, they begin to produce trehalose to protect cell membranes. Trehalose protects membranes and allows rehydration when amientales adverse conditions change. Trehalose may fulfill this protective function with the same function that the water in the membranes. Water is crucial for maintaining membrane fluidity as being polar is placed between the polar heads of phospholipids, keeping them separate. If we take the water space between the phospholipid polar head disappears, making the Membrana in a gel useless for biological functions.

Trehalose may serve the same function as the water and allows tardigrades to survive for long periods without water. It is noteworthy that this technique of trehalose and is used to preserve organs for transplantation for longer periods.

The amazing capabilities of survival, tardigrades can help with issues related to metabolism, tissue and organ preservation, hibernation or suspended animation. Worth knowing a little more, maybe one day, use your same techniques to travel through space in suspended animation.

Some videos on the tardigrades:

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best for learning and memory ... mitosis and neuronal differentiation!

By: Lionel Perez Valenzuela

tissues repair themselves

Whenever we get hurt or suffer an injury, we observed that in the course of days the wound is closed and tissue repair. These mechanisms repair and generation of new cells to replace damaged or aged stem cells are essential.

undifferentiated stem cells, versatile and almost limitless ability to multiply are similar to embryonic cells. Not only can generate copies of themselves by mitosis, but by mitosis and differentiation can generate other cell types. While

tissues have some ability to repair itself, the brain seemed very limited in this regard. The adult brain can sometimes compensate for injuries suffered by establishing new connections between surviving neurons. But if the damage is too extensive this may not be enough. We must also differentiate

neuronal regeneration of neuronal replacement. When a neuron is cut the axon is regenerated, ie the cell tries to return to their previous structure. Neuronal replacement (neurogenesis) is a different concept is to produce new neurons.

But what thought is that neurons born only during the embryonic period and perhaps during the first two years of life a human being. From that moment, if you lost them, we could not replace them.

Why can not generate new neurons in the adult brain?

Neurobiology until recently argued that it was not possible because the adult brain was devoid of stem cells.

A dogma which falls ...

Argentine biologist Fernando Nottebohm of Rockefeller University, discovered that adult canaries can generate new neurons to replace other brain cells when you have to learn new songs or new sources of food recall or recognize new social companions.

words, when the brain needs to store new information and situations neurogenesis occurs, thus completing a dogma of neuroscience, arguing that generate new neurons in adult brains was impossible. It also established that brain stem cells (stem cells), were responsible for this process.

These investigations Fernando Nottebohm, then were extended and confirmed in different mammals, mice, monkeys and then humans. Therefore, our adult brains produce new neurons also fully functional. This fact, opens a whole new range of possibilities, and that wherever possible therapeutic replacement of neurons in human brains affected by injuries or neurodegenerative diseases, could repair the damaged brains of patients.

also means a whole change in the conception of the brain. It turns out that the brain is so different from other organs and tissues, where cells are constantly renewed from stem cells undifferentiated. The brain also undergoes this process of constant change and treble.

The hippocampus and memory

The hippocampus is a brain region, located in the medial temporal lobe. This curved structure reminiscent of a hippocampus. The hippocampus and adjacent structures perceptions become long-term memories.

While this region of the brain memory is stored, is essential for the formation of memories. In the hippocampus integrates information from other brain regions of alli'su importance and people with brain injuries in the temporal lobes can not form new memories but can remember events before the injury.






Basically the formation of new neurons in rats, monkeys and humans occurs in the hippocampus and the lateral ventricle. Specifically in the hippocampus in a layer of neurons called granule cells or granule neurons (see the first figure of the article). Undifferentiated stem cells do mitosis (proliferation), some die and others survive. Then some surviving cells migrate to the granule cell layer and differentiate to generate new functional neurons.






demonstrates how the proliferation of stem cells in the brain?

In 1965, Joseph Altman and Gopal D. Das of MIT (Massachusetts Institute of Technology) described the development of neurons in the hippocampus of adult rats, specifically in the dentate gyrus (gyrus dentatus). But the methods then available did not allow to estimate the number of neurons that formed, or to demonstrate that these new cells were neurons.

also was unknown concept of brain stem cells and mainstream science at that time required the replication of mature cells (already differentiated). These facts, together with lack of evidence of neurogenesis in monkeys were made Altman studies were underestimated.

This situation continued until the mid-eighties when the spectacular discoveries of Fernando Nottebohm, already mentioned, renewed interest in neurogenesis in the adult brain. The results in canaries were later confirmed in primates by teams of Elizabeth Gould, Bruce McEwen and Eberhard Fuchs. Techniques used

in primates based on DNA replication that occurs in the period S of the cell cycle. Before mitosis, cells replicate (duplicate) the amount of DNA they have to ensure that daughter cells receive a complete chromosome.

In these experiments animals are injected with a material (a nucleoside analogue of thymidine, bromodeoxyuridine the - BrdU - which is used as a marker, replacing thymidine), which integrates into the DNA, but only in cells that replicate their DNA in preparation for cell division. After BrdU antibody can be used to detect cells that incorporated it. As the marker material is integrated newly synthesized DNA, then goes on to be part of the DNA in the resulting daughter cells, which in turn can transmit it to the next cell progeny.

Some of the cells that incorporated BrdU differentiate into neurons or glial cells. The time necessary to differentiate the brain is removed, cut into sections, cuts and stained cells are identified by their anatomical and biochemical characteristics. They can identify cells with the marker (test cells from recent cell division) and which in turn have all the features of differentiated neurons. As the neurons differential can not enter the marker as it is not divide, cells must necessarily be differentiated into neurons after incorporating the marker.

Obviously this technique can not be performed in humans, which seemed an insurmountable obstacle until Peter Eriksson gave the Salk Institute with the solution. Eriksson found the same substance used as a marker BrdU also administered to some patients with cancer of the tongue or larynx terminals. These patients were encuadrdos in an experimental study and were injected with BrdU to control tumor growth. If the hippocampus could be obtained when patients died, could be identified if there neurogenesis in adult patients, analogous to studies in primates. Eriksson won the consent of patients and with their help were able to confirm neurogenesis in all cases.

The new neurons are also essential for learning.

Then the brain is constantly remodeling, there is not only synaptic plasticity (the ability to establish new connections), but a continuous generation of new neurons. The brain is permanently reshaped. Why

Why take the hard work of generating new neurons constantly?
Well apparently, as experiments in mice demonstrate this process is essential for learning and memory.

The crucial experiment, by Ryoichiro Kageyama of Kyoto University, consists of genetically modified mice subjected to an experiment in learning and memory.

These mice can not generate new neurons, so if your memory and learning depend on them, will have difficulties in memorizing and learning when compared with normal mice.

modified mice produce new neurons but by supplying a drug, new neurons produce a protein that kills. This ensures Kagemaya team that mice have no new neurons.

The researchers proceeded to measure how well the mice memorized the position of a concealed hole (a standard test to measure memory in mice). Mice usually takes a couple of days to remember the position of the hole and are able to remember more than a week.

Mice that new neurons can not take five or six days to learn where the hole and forget it completely within a week.

remains to be done

At some point, studies on the control of neurogenesis achieve a degree depth and maturity and should be replaced by Roederer studies in monkeys and then must expand research in humans. The protocols must be highly refined to show that the treatments did not affect normal brain capacity.

"The brain circuits are not written in stone," says Pankaj Sah of the Queensland Brain Institute. The brain is malleable and growing even in adults, and these studies in mice are the first to try the neurogenesis produces functional neurons essential for memory and learning.

Many older people, as they get older they lose this ability to produce new neurons in the hippocampus, perhaps that suffer memory loss. With the discovery of the potential of brain neurons to replace their own opens a whole new field of research in neurobiology and medicine, perhaps in the future may bring relief to people suffering from neurodegenerative diseases or serious injuries.

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Virus ... at the bottom of the Sea

By Lionel Perez Valenzuela

is not the title of a horror novel or science fiction, but the result of a Research conducted by the Polytechnic University of Marche in Italy and published in the journal Nature.

has always struck the seabed rich in organic matter, so keep a few animals. It was known that such an abundance of carbon and nutrients, could have a huge amount of heterotrophic bacteria, which in turn could be the food of other organisms such as protozoan, worms, filter and other animals.

This organic matter and decomposing-fermenting bacteria could maintain a complete ecosystem, with an abundant flow of matter and energy. However, none of this happens, and nutrients and carbon are trapped on the ocean floor. A real paradox.

Why seabed worldwide there are no agencies greater than a microbe?

The answer may lie in the bacteriophages.

The bacteriophages, viruses bacteria were discovered in 1917 by French-Canadian researcher Felix d'Herelle (inventor of phage therapy and a remarkable life that I recommend to know). D'Herelle

noted that an invisible agent was destroying their crops of dysentery bacilli (bacteria that cause dysentery). The agent passed through filters that retained bacteria and only multiplied in the presence of live bacteria, causing them to swell and lyse.

remember that there are two basic types bacteriophage, lytic viruses (lytic cycle do) and lysogenic viruses or tempered (made lysogenic).




lytic viruses infecting bacteria, viral genes taking control of bacterial metabolism, and quickly produce new viral proteins and new viral genome copies. The viral proteins self-assemble to form capsids with their respective viral genome. Finally there is lysis of the host bacteria (destruction of bacteria).

lysogenic In the temperate phage that infects bacteria and is integrated into the bacterial genome, replicated viral DNA with bacterial DNA. Bacteriophage could also be stable as plasmid, not integrated. Thus the temperate phage-infected bacteria can carry the virus's genetic information over multiple generations, without releasing phage abroad (this cycle was discovered by André Lwoff). The phage is "latent" until it can be reactivated under certain conditions (eg if the bacteria's DNA is damaged, for lack of nutrients, temperature changes, UV rays, chemical mutagens, etc.).. Once reactivated phage, begin to multiply which will lead to bacterial lysis.

bacteriophages in some cases give new properties to bacteria while they remain in the lysogenic state, a phenomenon known as lysogenic conversion . The best known case is that of the cholera vibrio (Vibrio cholerae), responsible for cholera epidemics. Strains of this bacteria can be harmless can become highly pathogenic by lysogenic conversion, ie by the action of a phage.

Only in 1939, Helmut Ruska, bacteriophages observed by electron microscopy. Remembered for the lunar module structure, and how fixing bacteria.





The top micrograph obtained with a microscope e can see a bacterium surrounded by dozens of bacteriophages have already joined.

Virus in the sea and seabed.

relatively recently discovered the INMESA amount of phages that exist in the sea, there may be billions of phage and other viruses per milliliter of sea water, and 70% of marine bacteria to be infected.

This brings us back to the sea, more precisely in the background. Samples collected from different parts of the world Roberto Danovaro of Italy's University of Marche, found that one gram of marine sediment has one billion virus particles. This result remained in sediments obtained from a few hundreds of meters to 6,000 meters deep seabed.

This amount of virus would explain why there is nothing greater than micro-organisms in the seabed. The bacteria use organic matter as an energy source and multiply, but they are inevitably infected by the extraordinary number of bacteriophages, these bacteria are lysed and release immediately the organic matter back to the seabed, but no other body could use it .. . but other bacteria. Restarting the cycle again. Bacteriophages Therefore, interrupt the flow of matter and energy, this is called "viral diversion" (viral shunt in English).

This will solve the paradox that results from considering that the 10 cm of the seabed are the guardians of 30-45% of organic matter (as imvestigaciones above) and yet almost no animals that use these resources.

While this system deprives the animals of the vast deposits of nitroógeno, phosphorus and carbon, keeps a huge mass of bacteria, also makes an important contribution to bacterial metabolism and can cope with the severe restrictions of organic matter that the ecosystems suffer the deep sea.

It is certainly surprising that bacteriophages have this level of impact on the flow of matter and energy, says Jed Fuhrman parent of Marine Virology.

Surely this is not the last surprise of bacteriophages and viruses in general.


Translation and adaptation of an article from New Scientist:

http://www.newscientist.com/article/dn14616-how-viruses-shortcircuit-the-deep-sea-food-chain.html?DCMP = ILC-hmts & nsref = news5_head_dn14616

Biography of Felix d 'Herelle and interesting ideas and methods, perhaps soon we should use phage therapy as an alternative voice in the world for antibiotics: http:/

/ es.wikipedia.org / wiki / F% C3% A9lix_d% 27Herelle

article Original Nature:

http://www.nature.com/nature/journal/v454/n7208/abs/nature07268.html; jsessionid = A1F8E62D740321CE3B173B3360EB8677

orifinal job on the abundance of material on the seabed orana:

Proceedings of the National Academy of Sciences , vol 95, p 6578

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metabolic syndrome, obesity and diabetes.

By: Lionel Perez Valenzuela.

The disease diabetes is increasing:

In the United States 10% of adults suffer from type II diabetes. Diagnosed one and half million new cases each year. For 2010, we expect 200 million cases of this serious disease in the world.

In the Argentina , some sites report that a 10% of the population have diabetes, about 3, 6 million (about 40% of these people know that a diabetic). According to INDEC, the rate for 2005 was 8.4% of the total population.

Diabetes in Mexico is one of the most important health year recorded 40 000 deaths caused by diabetes. In 1995, with 4 million patients, ranked tenth worldwide and it is estimated that by 2025, was seventh with 12 million.

Brief initial idea about insulin and diabetes.

Insulin is a hormone, a messenger molecule, which is carried by the bloodstream. Like many other hormones, insulin is protein in nature, ie consists of amino acids linked by peptide bonds.

Insulin is the hormone "anabolic" par excellence, ie, makes available the necessary input cells of glucose (cellular fuel), then by glycolysis and cellular respiration we provide the chemical energy in the form of ATP (energy currency) needed for cellular functions.

Its action is activated when the glucose level is elevated in the blood, with the insulin released from pancreatic beta cells. Its function is to promote the cellular uptake of glucose, so insulin is a hypoglycemic hormone (causes decreased glucose concentration in the blood).

Insulin also has other important functions, for example, stimulates the synthesis of protein and DNA synthesis. Therefore also acts as a growth factor to cells throughout the body.

Since antiquity physicians from all civilizations have left no record of the disease now called diabetes.

The first reference to diabetes is found in the Ebers papyrus found in 1862 in Thebes (now Luxor). In the papyrus contains a síntomalogia reminiscent of diabetes and the treatment prescribed.

The early literature Hindu Vedas describe the urine sticky, honey-flavored and strongly attracts ants diabetics. Susruta, the father of Hindu medicine described the diabetes mellitus and even managed to differentiate diabetes that occurred in young people that led to death and others that occurred in people of a certain age.

Demetrius of Apamea refined the diagnosis of diabetes mellitus Apollonius of Memphis coined the term diabetes (from dia "through" and Betes "pass") to refer to a disease characterized by removal of large amounts of urine (polyuria), weakness general and intense thirst. Apollonius thought it was a form of dropsy. Later he added the Latin term mellitus (honey, candy) to refer to the sweet taste of urine of patients.

now know that diabetes is a disorder characterized by high blood glucose (hyperglycemia). Our body works better with some level of blood glucose. If glucose levels rise or fall too low, we feel bad. say that a person is consistently diabetic if their blood glucose levels are high. Diabetes is the most common endocrine disorder.

High levels of glucose in the blood damage the small blood vessels, such as kidney, heart and eye. There are two typical forms of diabetes, diabetes type 1 and type 2 diabetes. The two forms of diabetes kill about 250,000 Americans per year and cause more expenses 130,000,000 million dollars.

Diabetes is the leading cause of kidney failure, amputation and loss of vision in adult Americans. Diabetes also doubles the risk of heart disease.

The pandemic of diabetes and its growth largely to the type 2 diabetes (often called adult onset diabetes, but it also affects some children). Type 2 diabetes appears suddenly (as if you can do the type 1), but it seems to be the end of a process that begins with a condition we now call " metabolic syndrome."

In other words, type 2 diabetes is the culmination of a group of related conditions including:

- high blood pressure

- abdominal obesity

- high concentration of certain blood lipids

So people who have these symptoms or signs, we can say that suffer from "metabolic syndrome " and are more likely of developing diabetes.

Under these conditions as the body stops responding to insulin, pancreatic beta cells are forced to release more thyroid hormone (this process is called insulin resistance ).

Type 2 diabetes do not appear until the beta cells the pancreas are exhausted. As Professor of Medicine, Endocrinology and Diabetes Richard Bergmann of the University of Southern California .

"The metabolic syndrome leads to the need for more insulin secretion , but if the beta cells of the pancreas does not fail, you will not suffer diabetes"

us distinguish between type 1 diabetes and type 2

Type 1 Diabetes:

Characterized by insulin deficiency.

not produce enough insulin from the pancreatic beta cells.

Causes: autoimmune, genetic and environmental factors. In general, children and adolescents suffer. The little ones cry frequently and thoroughly wet diapers. Sometimes the diagnosis is through analysis casual showing high glucose in urine or blood.

requires daily insulin . Includes 5-10% of Americans diagnosed with diabetes.

Symptoms: increased thirst, urination and hunger increased, weight loss, blurred vision and extreme fatigue.

Type 2 Diabetes:

Characterized by insulin resistance.

beta cells produce insulin but the body's cells are resistant to its action. Resulting in a high concentration of glucose in the blood (because the glucose is not transported into the cells.) Therefore the cells that need insulin to get glucose suffer "hunger" (insulin-dependent tissues).

risk factors: age, obesity, family history, physical inactivity and certain ethnicities. Approximately 80% are overweight or obese.

Symptoms: fatigue, frequent urine, increased thirst and hunger, weight loss, blurred vision, wounds heal slowly. Some people show no symptoms.

"Obesity and overweight, illness of wealth?

Far from being a "disease of wealth ", obesity also affects greatly to developing countries. Although in Argentina there are no national nutrition data, according to several studies have estimated that some 20 million people are overweight or obese, and the number of deaths attributable to this disease is 30,000 per year.

At the same time, 1% of the obese than 150 kilos, a figure that translates to 200,000 disabled people with poor or no available medical . According to an estimate of the Centre for Research on Child Nutrition (CESNI), about 2,500,000 children and young Argentines are overweight or obese.

Regarding Latin America, according to WHO figures , Chile leads the statistics of obesity. An average of 21.9% of the Chilean population is overweight among people over 15 years. Thus, 19% of the male population is obese, while women reach an alarming 25% (1 / 4 of the female population). These statistics are similar to other Latin American countries like Mexico.

Worldwide WHO estimates that more than 1,000 million adults are overweight and 300 million obese worldwide, while that 2,000 million children and adolescents are overweight or obese (UNICEF).

We consider what are the social and economic causes of obesity and the epidemic of childhood obesity include:

- Increase food availability and reduced cost for those less healthy (fast food and others).

- Reduced demand for energy at work and home

- Less time and income on food preparation and healthy quality

- Less time for physical activity

- Poverty (barrier to access to quality food)

As childhood obesity:

- Both parents work at home for longer hours

- Changes in the school food (dietary changes in general)

- More food away from home (high-fat foods, soft drinks and juices)

- More leisure time watching television and videos

games

point out only some of the risks of childhood obesity:

-Hypertension-Dyslipidemia (changes in lipid metabolism)

- Asthma

- Joint problems

- Early puberty

- fatty liver

- Sleep Apnea

- Discrimination

What factors are involved in type 2 diabetes?

Professor Bergman explains that most of the genes involved in type 2 diabetes are associated with beta cell function, and this fact helps to explain the pattern of disease seen in the U.S. population: Some ethnic groups, particularly Asians, African Americans and Native Americans are not equipped to compensate for some degree of insulin resistance, as they become more obese, have have more visceral fat and increased risk of type 2 diabetes.

Other factors implicated in metabolic syndrome and diabetes include, as already noted, the epidemic of obesity, Fast-food premises that sell very high-fat foods, a sedentary lifestyle and the massive use of high-fructose syrup from corn during the past 30 years (The average U.S. consumption was 28.4 kg . Per person, mostly from soft drinks, juices and soft drinks). Then come back to the issue of high fructose syrup from corn and how it would affect our metabolism.

metabolic syndrome and cardiovascular disease.

Metabolic syndrome plays an important role in cardiovascular disease, comparing the danger to smoke two packs of cigarettes per day.

Although still being debated the significance and exact definition of the metabolic syndrome, Dr. Francisco Lopez-Jimenez of the Mayo Clinic in Rochester, Minnesota, believes that this concept is useful. "It is controversial as a new diagnosis ... because each individual component has a name: hypertension, obesity, abnormal cholesterol levels"

Skeptics, made an obvious question that he admits: "What is the importance of creating a new diagnosis, when all the symptoms and are identified as separate diseases and the treatment I'm still the same? "Lopez-Jimenez replied: "Unifying measures, which may be trivial separately, metabolic syndrome makes a major difference for patients. If blood glucose is a bit high, the circumference of the waist is slightly abnormal, it is very likely diagnose metabolic syndrome, but that term patient left the office without a sense of risk for diabetes or cardiovascular disease may suffer. If the patient only sees his analysis are only slightly abnormal, will not have sufficient motivation to change their behavior "

As a preventive cardiologist Lopez-Jimenez remarked that metabolic syndrome is a risk factor for heart attacks and strokes , not just diabetes. "Each component of metabolic syndrome has been linked to with cardiovascular disease. Although some people without diabetes develop cardiovascular disease, in many cases, diabetes is the midpoint between metabolic syndrome and heart disease "

The strong correlations between metabolic syndrome, cardiovascular disease and diabetes is not completely understood, Lopez-Jimenez said. "The approach to these problems has been that high sugar levels are harmful, but it is likely that beyond this there are other factors involved, because several studies have failed to show significant reductions in cardiovascular events by controlling only blood glucose. People with diabetes have a constellation of abnormalities. Patients with type 2 diabetes have high levels of insulin, which by themselves can affect the cardiovascular system, causing the diabetic to reabsorb more salt, causing blood pressure to rise and changing the metabolism of cholesterol. Elevated insulin itself may be related to various arterial abnormalities such as arteriosclerosis ¨

We summarize the main features of the metabolic syndrome (also called syndrome of insulin resistance, metabolic syndrome X or obesidadiabética )

- abdominal obesity, circumference of the waist above 88.9 cm (35 inches ) in women or 101.6 cm (40 inches ) in man (one inch = 2.54 cm )

- Low levels of high density lipoprotein (HDL, HDL or "good cholesterol")

- Test high fasting glucose (or fasting glucose test)

- Insulin resistance (the body does not respond properly to the hormone )

- High blood pressure (above 130/80).

Does the diet: a strong response to diabetes and metabolic syndrome or a false hope?

Being overweight or obese are two of the most important factors in metabolic syndrome and diabetes Type 2, diet and exercise are two traditional locations on the prevention of diabetes, but losing weight is easier said than done, as presented by Richard Bergman the University of Southern California. "We have heard many times on the approach to a lifestyle leading to weight loss, but only for a short period of time, 97% of people who lose weight by diet and exercise back to recovery in a period three to five years is very difficult to have an improvement in the long term "

Some research has found that weight loss can be maintained with enough effort. As Bergman says: "In Finland, monitoring groups have been formed and studied people for five years, used a long time and many hours of monitoring and advice, and this reduced the risk of diabetes significantly, but this is generally ineffective in a real life situation. Thin people think it is very simple, but it is almost impossible to lose weight for people in this way. An obese person who has lost weight, not like a thin person. Because their rate of energy use are very low, and gain weight again even with a reduced calorie diet "

The doctor, lose weight or

Nevertheless, research on metabolic syndrome continues to show how much difference can a change in lifestyle, for better or worse, in the progression to diabetes.

This has been demonstrated by studies conducted by the Diabetes Prevention Program, which has studied 3,234 overweight and with impaired glucose tolerance (two key elements of the metabolic syndrome). A combination of diet and exercise reduced diabetes risk by 41%, much better than the drug metformin (used in diabetic patients overweight), which only reduced the risk of diabetes by 17%.

The diabetes prevention program was so effective that was completed a year earlier, to allow the control group received appropriate advice on the combination of diet and exercise, to the cardiologist López-Jiménez results were compelling. "Patients lost only 4 pounds (about two kilos), but those who became more physically active and tried to eat better, the chances of developing diabetes decreased. It's hard to find someone with metabolic syndrome is very active, exercise and have a good diet. Anyone with metabolic syndrome needs a change of behavior "

The benefits of exercise, combined with some weight loss, has led some physicians to change their focus of attention so far always focused on the scale. López-Jiménez points "We try to stay away from the point of view that our goal is to reduce weight. Especially not say, get some exercise, right diet and then we will see. We prescribe the quality and quantity of exercise and work with patients to overcome any physical or also in our case with the horrible winter of Minnesota "

Eat less, exercise more.

What recent studies can show the old advice to the mothers to eat well and exercise, and the effects associated with the metabolic syndrome and diabetes?

Weight training can help: In a new study, progressive resistance training, benefit three key points of the metabolic syndrome: insulin resistance, blood triglycerides (Lipids dangerous) and basal glucose testing or fasting glucose.

Exercise helps even without weight loss: a study on 115 adults in the Johns Hopkins Medical Institute, found that exercise improves blood pressure, total cholesterol and insulin sensitivity. The cause of these results was no improvement in fitness and weight loss, but the reduction of total body fat and abdominal fat.

Being active can have their dividends as we age : Studies in Norway, showed that men who perform physical activity in their free time, had a 40% reduction in the development of metabolic syndrome.

targeted programs can help: A Montreal study focused on people who had already developed type 2 diabetes showed that those who had completed the DiabetAction program, which helps select the optimal exercise trends to reduce diabetic showed a significant reduction in body weight, blood pressure, waist circumference, basal heart rate and prevalence of metabolic syndrome after six months. Even

interventions "moderate" may have better results than simple advice family doctor, as shown by a study of 335 people whose characteristics made them susceptible to diabetes who received professional advice which led them to do more exercise and improve most of the markers of metabolic syndrome. This group had a 31% reduction in the risk of developing diabetes, but "the usual treatment of the family doctor was ineffective in modify the progressive metabolic deterioration."

Sitting too long can be harmful: A recent look at the role of sedentary behavior in the death, cardiovascular disease, Type 2 diabetes and metabolic syndrome concluded that the growing trend towards inactivity suggests that "people who do not exercise can become even more metabolically ineffective in the coming years if they sit too much"

" combination of ingredients?

No one questions the metabolic benefits of weight loss. But Edward Weiss University in St. Louis, says that exercise confers a number of perks. "Studies show as if a person matching starting an exercise program and not lose weight can still expect a substantial reduction in risk of diabetes "

If exercise alone is beneficial and weight loss alone is beneficial, should not produce weight loss through exercise even more benefits? That's what Edward Weiss expected when I compare two groups, one who lost weight due to caloric restriction and another who lost weight due to an exercise program. However, both groups showed similar improvements in body weight, glucose tolerance and insulin sensitivity. "It's clearly a result surprising because the assumption was that if it was beneficial weight loss and exercise was beneficial, each separately, should be expected in May benefit by combining both, but the results showed that "

Benefits year focus on insulin action. As Weiss says, "The muscle adapts to exercise, so any release of insulin or insulin application, have a greater hypoglycemic effect, bringing more glucose into the cell or intercellular space. Therefore improves glucose clearance , muscle is more sensitive to exercise "

"Caloric restriction seems to work differently, decreasing oxidative stress (metabolic changes) and even inflammatory bowel may be adaptations"

Since exercise and caloric restriction works by mechanisms different, normally should provide greater benefits by combining both treatments, doing so separately. But Weiss thinks that more research is needed and that in certain conditions the combination of exercise and calorie restriction should be more effective against metabolic syndrome.

A conversation with a specialist in metabolism and biochemistry.

In a conversation with Stephen Brietzke endocrinologist and diabetologist in University of Missouri-Columbia, asked about some topics that help us understand the labyrinthine relationship between metabolic syndrome, diabetes and cardiovascular disease .

Some people think that talking about metabolic syndrome is not useful because doctors and addressing each of the components of all forms. What do you think?

From a public health perspective, it is important not to lose sight of the forest for the trees. Metabolic syndrome can bring together people with a family history of disease, who had heart disease, or are slightly overweight, having blood pressure above normal and blood biochemistry slightly abnormal, but not candidates for a drug based therapy, since their analysis taken individually do not justify it. But we know that a healthier lifestyle, with 30 to 60 minutes of physical activity on most days a week and a small reduction in weight, are associated with profound benefits in metabolic syndrome, whether people are sufficiently motivated to make changes

Does the metabolic syndrome concept has helped to understand diabetes and cardiovascular disease?

The concept of a syndrome makes us think about underlying causes. There are two ways of looking at the concept of metabolic syndrome, first as a series of related phenomena: type 2 diabetes, disorders of blood lipids and coronary heart disease, all with a possible common cause, which could explain them all. Another way to look at it as a group of risk factors for multiple diseases, which is unrelated causes. I favor the first analysis. Evidence suggests that insulin resistance is key in metabolic syndrome, and studies treatments that benefit enjoyed by other insulin resistance syndrome components. There is also some evidence that ACE inhibitors (Angiotensin Converting Enzyme), which are used to treat high blood pressure diabetes also have beneficial effects on the effect of insulin and the incidence of diabetes.

For how metabolic syndrome, why people are so concerned with visceral adipose tissue (fat in the abdomen)?

suspect that the metabolic syndrome can result from disease or lack of balance in visceral adipose tissue. usually only think of fat as an energy storage simple, but in reality is much more complex than that. Visceral adipose tissue plays a ying-yang, good-bad. Produces beneficial compounds that increase insulin sensitivity (then delve into that topic), reduce the blood pressure and keep blood vessels healthy. But it also produces components that promote inflammation. When this tissue is "healthy" components occurs predominantly beneficial, when the tissue is "sick" change its production to the inflammatory components.

never heard anyone speak of adipose tissue as "sick" ...

Ten years ago nobody had said that adipose tissue might be sick he looked just like a store was metabolically inert and treatment for diabetes was to lose weight. We believe that some kind of "change" or "switch" occurs in adipose tissue by promoting the production of molecules that stimulate inflammation. There is also a concept that is emerging , people can be fat inside. If we look at type 2 diabetes patients in Japan, many do not appear to modern Western eyes as obese, but if we make a study of images and measure visceral fat, we see that there are a lot of fat inside .

We've always thought Diabetes is a disease related to the high amount of glucose in blood, but in reality we see that is much more complicated than that ...

complications of diabetes usually fall into two groups. The first one is damage to small blood vessels in the retina, kidney and nervous system, due to high blood glucose levels that bind to structural proteins, and gradually alter its function and damaging the blood vessels. A second complication is arteriosclerosis, hardening of the arteries, which probably has a different basis. Atherosclerosis, may be related to inflammatory changes in arterial walls thicken and lose elasticity. It also accelerates plaque formation (buildup of fatty substances and other) in the lining of the artery wall, these processes tend to block blood flow. In diabetes and metabolic syndrome, visceral adipose tissue tends to inflammatory components and the balance in the arterial walls changes from a healthy condition, rich in antioxidants and compounds that cause the relaxation to an inflammatory condition that leads to high blood pressure and plaque formation. Therefore cardiovascular disease and diabetes from the lack of balance in adipose tissue.

delve a little deeper into the relationship between obesity and diabetes, for that we need to know the functions of the hormone called leptin (from Greek leptos intestine), allowing us better understanding the links between these two diseases.

Leptin is a very important hormone, discovered about ten years ago, is encoded by the obese gene (ob). Its protein structure and consists of 167 amino acids including a signal peptide of 21 amino acids. Three-dimensional structure has four alpha helices and a disulfide bridge between cysteines at position 96 and 146, the latter being required for biological activity of the hormone.

Leptin is secreted by adipose tissue that informs the central nervous system of the body energy status. If we have enough stored energy, increased leptin levels and suppress the appetite, leptin also regulates other neuroendocrine functions. Then is well understood that mice with the mutated ob gene (no leptin), suffer from hyperphagia (feed constantly), obesity, endocrine dysfunction and predisposition to diabetes.

Before the discovery of leptin , adipose tissue was seen only as an energy storage tissue, a tissue that most people tried to get rid of. Following the discovery of leptin and other hormones produced by adipose tissue, completely changed the vision we had of it. Currently

adipose tissue, is seen as a major endocrine gland, which secretes a large number of mediators, a peptide hormone (cytokine) called Adipokines whole being secreted by adipose tissue (adipokines in English) with great influence on metabolism and other organs, particularly the brain. Adipose tissue is one that tells the brain about two of the most important vital functions: food and reproduction.

Despite the important role of leptin, many obese people have high serum leptin concentrations, indicating that the organism also can become resistant to leptin (ie, leptin is unable to exercise its action.)

As adipose tissue synthesizes more leptin (because your body becomes resistant), inflammatory levels increase, because high levels of leptin are highly pro-inflammatory. As we have seen a crucial aspect of metabolic syndrome was the change that occurred in adipose tissue from a state of "healthy" antioxidant, protector of the arteries to a "sick" pro-inflammatory, with increased arterial plaque formation, increased blood pressure, cardiovascular disease and diabetes. Another important lipokines

is ADIPONECTIN that raises levels of insulin sensitivity. An interesting relationship is that the hormone decreases with increasing our levels of body fat. Therefore, overweight and obesity contribute to lower levels of circulating adiponectin contribute to the loss of insulin sensitivity.

Adiponectin is one of the most abundant plasma proteins, and their concentrations sexual dimorphism, as women in the circulating levels are higher than those reported in males.

Finally back on the syrup, high fructose corn, which many researchers think it is related to the epidemic of obesity and type 2 diabetes.

high fructosaa syrup is made from corn starch. After the starch is completely hydrolyzed to glucose. Then by an enzyme glucose isomerase (a aldohexose) is isomerized to fructose (a cetohexosa). Syrup, high fructose corn may have a concentration of 55% fructose.

According to some studies fructose does not cause the same effect that glucose, among others, does not cause the same release of insulin and leptin than glucose (ie that these hormones are maintained at relatively low levels despite the intake drinks or foods sweetened with syrup corn), which is counterproductive because it does not produce the same level of satiety.

Another important question is that fructose, not create a feeling of satiety, increases the release of hormone ghrelin (Ghrelin in English), the appetite-stimulating hormone (produced in the stomach and pancreas) . Therefore high levels of fructose would produce a hormonal imbalance, first low insulin and leptin and ghrelin concentrations increased, resulting in increased appetite. This also demonstrated that fructose consumption increases the level of blood triglycerides in a long, contributing to cardiovascular risk.

Conclusions:

certainly can not present the great depth of investigations carried out, and many have yet to confirm or reject deepened, but at least we can draw some conclusions for immediate implementation:

- The fat tissue is not only a reserve of energy, is also an endocrine tissue which releases a large number of important Lipokines, including leptin and adiponectin.

- Lipokines secreted by adipose tissue regulate pro-inflammatory state, largely responsible for vascular complications (atherosclerosis) seen in metabolic syndrome and type 2 diabetes.

- The concept of metabolic syndrome should be of general application to health policy level.

- We are facing a global epidemic of overweight, obesity and type 2 diabetes.

- we get a significant improvement in quality of life, with changes in behavior:

1 - stop feeding high-fat meals (usually fast food and sweets), stop drinking sweetened with corn syrup (soft drinks and juices in general)

2 - Becoming more active, and in our spare time, walking, exercising or playing sports. Even losing weight very slightly benefits are long term and lower risk of diabetes or cardiovascular complications.

- Changes will not happen by themselves, we need health policies, a shift to community and individual level too deep, to improve our quality of life.

Some important links:

This article is a translation and expansion of following article:

http://whyfiles.org/276metabolic_syndrome/index.php?g=1.txt

To learn more about diabetes:

http://www.msd.com.ar/msdar/corporate/press/diabetes/noticia1.html

To learn more about diabetes, with articles and information important nutritional level:

http://www.drcormillot.com/articulos/100277.htm # A279

http://www.drcormillot.com/articulos/articulos.php?id=3

Diabetes in Latin America and the Caribbean:

http:// www.msd.com.ar/msdar/corporate/press/diabetes/noticia2.html

The adipocyte as an endocrine cell (in English):

http://www.scielo.org.co/scielo.php? script = sci_arttext & pid = S0121-52562007000200010 & lng = en & NRM = iso & tlng = en


http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120- 24482005000300004 & lng = en & NRM = iso

Interesting debate on the existence or not of the metabolic syndrome:

http://www.scielo.org.ar/scielo.php?script=sci_arttext&pid=S1850-37482006000700009&lng=en&nrm = iso

Note the daily La Nacion with some statistics of metabolic syndrome in Argentina:

http://www.lanacion.com.ar/nota.asp?nota_id=955435

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Mocosinh style (part 3)

taken me to upload these photos of the "tour de Mocosinh" the land of the Euro. Here just some of their friendly assistance and curiosities. Unfortunately a number of digital photos disappeared misteriorsamente in an internet cafe, heading to the Coliseum, where there was a Moroccan who allegedly had banned smile. Also some just stayed in my mind, because sometimes the memory is finished or when it happened right when not carrying my camera ... as in the sacral area and streets around the Gothic Quarter ... or that time ran after Mocosinh several Italians, wanting to force them to swallow their stikers hahaha. Madrid

Everywhere they boil beans, repeatedly mentioned my companion ... and he is right, despite being supposedly first world, racism is present in various parts ... how sad.

Bruges

Before taking the train to paradise, under bridges, in this city type maquetero Playmobil, we found a rather good graffiti.

Amsterdam

The night before leaving the country of Pepe le Pu, I spoke a few surprises that I knew left for The following guests of that White Tulip.

Paris

condenadota So I wanted to see! haha, the classic story Mocosinh type.


again, but in front of the Louvre, I found this outrageous stiker, I found a clear example of people walking between the cultured, is so uneducated.