Epidemic: the obesity gene in women is being eradicated more and more often. The obesity gene does not outgrow weight loss. The obesity gene
Very often at the core development of obesity lie down slump official. True, it is not the fatness itself that is transmitted to the fat, but the subtlety of the fat. Many children are either born with normal weight or they are deficient (in cases of prematurity). And then, in the world, older and older people develop excess body mass.
The main stages of lipid (fat) metabolism include:- Motivation for taking steps to increase appetite
- Soaking grub fats in the intestines
- Synthesis of fats from carbohydrates, which are created during the breakdown of glycogen
- Transport of fats in tissue by specific carriers – lipoproteins
- Penetration of fats into cells from blood plasma
- Adding fat to the so-called fat depots, in the subcutaneous tissue
- Fat breakdown – lipolysis
- Synthesis of glucose from fatty tissues - glyconeogenesis
- Removal of lipid metabolism products from food through the intestines.
All these stages are ensured by numerous biologically active substances (BAS)-enzymes and hormones. The most common ones are insulin, leptin, glucagon, lipase, and many others. The synthesis of biologically active substances is, in its own way, controlled by genes.
The skin gene is a part of a chromosome (a double strand of DNA) with a given sequence of nucleic acids. Humans have 46 chromosomes or 23 pairs (1 pair - state chromosomes, 22 - non-state chromosomes or autosomes). Moreover, one autosome in the couple was passed on to us from the mother, the other from the father. Such autosomes that are in the same pair are called homologous. It’s the same with genes - in one autosome the genes are the father’s, in the other the genes are the mother’s. One and the same sign can be represented by decal variations. Apparently, the genes that encode this sign can be subject to modification or alleles.
Moreover, some types of alleles prevent obesity, while others actually protect against it. Excess body weight is a polygenic pathology. This means that there is no specific gene for obesity - it is represented by a whole complex of gene changes and mutations. Moreover, in some cases, for the manifestation of obesity, one changed allele is sufficient. In these cases we talk about an autosomal dominant type of inheritance. In some situations, obesity manifests itself only if the gene is changed in both parents - this is an autosomal recessive type of decline.
Obesity patients often suffer from other illnesses: hypertensive disease, atherosclerosis, recessionary hypercholesterolemia (elevated level of cholesterol in the blood plasma), Alzheimer's disease (aging incompetence).
Types of gene mutations in obesity
ApoE gene . This gene is located in the 19th autosome and contains several alleles - E2, E3 and E4. The remaining allele is responsible for changing the structure of nasal fat, apolipoproteins, and for the formation of hypercholesterolemia and obesity.
ApoC3 gene. This gene activates the synthesis of lipoprotein lipase, an enzyme responsible for the breakdown of fats. When a gene mutates, this process is disrupted.
Gen Arov 1000. This mutation leads to increased binding of low-density lipoproteins, which are deposited on the walls of blood vessels in the form of atherosclerotic plaques.
LPL gene. This gene, like ApoC3, controls the synthesis of lipoprotein lipase, an enzyme that significantly ensures fat metabolism. Deficiency of this enzyme due to LPL mutation leads to the central type of obesity
PON1 gene. It synthesizes another enzyme, paraoxanase, the deficiency of which promotes the risk of hypertensive disease and myocardial infarction in obesity.
GNB3 gene. This mutation is a common cause of obesity in women during pregnancy and after menopause.
PAI gene – 1. Several alleles of this gene are consistent with age-old obesity in men and women.
Apparently, only a small part of gene mutations are the causes of obesity. With the development of genetics, the number of genes responsible for obesity increases. It has long been established that low genetic factors lead to insulin resistance, in which adipose tissue receptors do not respond to insulin. Insulin in this case vibrates at high rates. Indeed, exercise is one of the causes of obesity. Other treatments lead to changes in the structure of leptin. This hormone, which is excreted by adipose tissue, flows into the saturation center in the hypothalamus and stimulates lipolysis.
Diagnosis of these and many other mutations is carried out during molecular genetic studies. The positive results of these studies indicate the need for correction of the child’s diet and way of life.
Apparently, those carrying the FTO gene, which is associated with obesity, are on average 3 kg more likely to suffer from obesity and are 70% more likely to suffer from obesity.
Do you blame your genius for the fact that you can’t seem to lose weight? However, have mercy: the obesity gene does not outgrow weight loss. 09.21.2016 r. Apparently, those carrying the FTO gene, which is associated with obesity, are on average 3 kg more likely to suffer from obesity and are 70% more likely to suffer from obesity. Today, having carried out an examination of 8 studies on the participation of over 9,000 people, they concluded that this gene does not overcome the process of weight loss.
They made the following statement: “You can no longer recognize your genes. More children and physical activity will help you lose weight, regardless of your genetic make-up.
Obesity is a serious health problem. In Great Britain, over 25% of the adult population is obese. In some people, carrying the FTO gene increases the risk of developing obesity. It has been shown that the very presence of the FTO gene is the most important risk factor for the development of obesity.
The obesity-associated gene FTO does not prevent weight loss
In a large-scale systematic review and meta-analysis, the international team collected data from 9563 adults who were insured before randomized controls to track the waste of food throughout the world. The research was aimed at understanding whether the FTO gene has anything to do with how much money people spend.
It has recently been discovered that the FTO gene does not prevent weight loss. It turned out that people with the FTO version of the risk react to the weight loss system in the same way as they do. This is an important news for people who are trying to lose weight. This means that diet, physical activity, or the use of weight loss medications in particular with the FTO gene will work as well as in the part of the population that has lost it. Unfavorable effects of the FTO genotype on increased vaginal weight are a hindrance for effective weight loss.
Carrying the obesity-associated FTO gene
It is important to note that the evidence for effective weight loss methods for people carrying the FTO gene variant was the same for men and women of different ages and different nationalities. Dr Alison Tedstone, England's top nutritionist, says the causes of the obesity epidemic are numerous and complex. However, there is evidence that the smell may have little connection with the profiles of the genes.
If we want to turn back obesity, we must not talk about personalized approaches based on the human genome. It is important to rebalance research across whole systemic approaches (including environmental factors) which can be of great benefit to the population in the long term.
It is clear that obesity is associated with illness due to sluggishness. And although the likelihood of the development of obesity and its stage will be largely due to the way of life and the nature of food, studies conducted on twins have shown that genetic factors play an important role in the etiology ї obesity. Over 430 genes, markers and chromosomal divisions associated with obesity in humans, have been described in recent publications.
Among rare forms of obesity, two groups can be seen - syndromes associated with the development of obesity, and monogenic forms of obesity.
Syndromic forms include obesity, which is avoided in Albright osteodystrophy, Prader-Willi, Down, Cohen, Lawrence-Moon-Bardet-Biedl syndrome (Table 1). These forms of obesity vary by wide clinical polymorphism. Peculiarities of syndromic forms of obesity include the early onset of obesity - from the first months of life to the period of late childhood, the different stages of its diversity - from morbid to morbid, the presence of specific phenotypes them characteristics. As a rule, all these patients suffer from neurological disorders, a marked delay in psychomotor development and a decrease in intelligence.
Regardless of the fact that most syndromes have genetic defects and markers, their function becomes unknown. Therefore, the pathogenesis and causes of the development of obesity syndromic forms have also not been established.
For Prader-Willi syndrome (photo 1) characterized by marked hypotonia, which is avoided during pregnancy and is preserved throughout the early stages of a child’s life, inhibition of psychomotor development, hypogonadotropic hypogonadism, cryptorchidism, decreased intelligence, low growth, impaired sleep and thermoregulation. Phenotypic features include: apparently small hands and feet (acromicria), dolichocephaly, almond-shaped eyes, low-set ears, wide mouth, small mouth with a thin upper lip.
The frequency of occurrence of this syndrome is not known, but according to the data of the International Partnership of Patients with Prader-Willi Syndrome (www.ipwso.org), there are over 5000 cases in the world. Chromosomal abnormalities in Prader-Willi syndrome include cell deletion or disomy 15 (15 q11-q12) and are found in 70% of these patients.
Children have normal height and height indicators, and may gradually gain weight throughout the first period of life with a further rapid development of morbid obesity, often until the second or third stage of life, and then manifested polyphagy. The development of obesity in Prader-Willi syndrome was associated with a decrease in the level of metabolism in these patients. However, Schoeller D. iz spivat. showed that the low basal metabolic rate in children is primarily due to an excess of healthy fat, rather than a genetically determined low level of metabolism.
It has recently been shown that patients with simple (constitutional-exogenous) obesity have high levels of ghrelin in patients with Prader-Willi syndrome. Ghrelin is an orexigenic hormone that is secreted into the vulva and has a wide range of actions: stimulates the secretion of growth hormone, prolactin and adrenocorticotropic hormone (ACTH); induces sleep behavior, promotes appetite, and increases the level of glucose in the blood. Ghrelin activates the neurons of the hypothalamus and arcuate nuclei, which leads to a positive energy balance by stimulating the body and reducing fat utilization. In a healthy person, rhubarb ghrelin rises anteriorly and decreases postprandially. It is possible that hypergrelinemia leads to the development of polyphagia in patients with Prader-Willi syndrome. The reasons for the high level of ghrelin in Prader-Willi syndrome are unknown. The segment of chromosome 15q11-13, which is responsible for this syndrome, does not explain these symptoms, since neither ghrelin nor its receptor is located in this segment. Perhaps, further learning from this phenomenon will help explain the pathogenesis of obesity for this syndrome.
Patients with Lawrence-Moon-Bardet-Biedl syndrome Often with people there is tingling of the accessory fingers of the hands and feet (polydactyly), muscle hypotonia. Obesity develops from another fate of life, characteristic hypogonadism. Other developmental anomalies are often accompanied by low-grade polycystic, retinitis pigmentosa. Intelligence of declines. It is believed that the progressive increase in vaga in these children leads to dysfunction of the saturation center in the hypothalamus, which leads to polyphagia.
For pseudohypoparathyroidism
(photo 2) characteristically obese with short stature, brachydactyly (bilateral shortening of the 4th and 5th metacarpals and metatarsals (photo 3, 4), short neck, month-like appearance, multiple subcutaneous ossificates, hypocalcemia; hormone Characteristics hypothyroidism and hypogonadism, and sometimes - blood diabetes Decreased intelligence Today, there are several types of pseudohypoparathyroidism, most of them in familial forms, with all types of thyroiditis There is resistance of target tissues to parathyroid hormone. The most common pathogenesis is caused by mutation of the gene that encodes the a-subunit G -protein (GNAS1), as a result of any defective G-proteins do not activate adenylate cyclase, or its activity is reduced.
The clearest example of the role of genetics in the control of vaginal energy and energy homeostasis is mutations in single genes that lead to the development of persistent morbid obesity. These are called monogenic forms of obesity.
To ensure that your energy levels are maintained, it is important to comply with your expenditures. Harch behavior is controlled by the hypothalamus through a variety of signaling molecules and receptor systems. Two groups of peptides were detected: stimulating (orexigenic) and important (anorexigenic) appetite (Table 2).
In the remaining cases, the anatomical relationships between different centers of the brain and the neuropeptides they synthesize have been studied in greater detail. It has been shown that when leptin interacts with the cells of the arcuate nucleus of the hypothalamus, two groups of neurons are activated: the neuropeptide Y and/or the endogenous inhibitor of the melanocortin mechanism of agout-binding peptide (AGBP) and Revenge pro-opiomelanocortin (POMC). These cells transmit signals to the paraventricular nucleus and the lateral lobe of the hypothalamus, where their axons interact with other effector cells to act as orexins. Changing the level of leptin stimulates or suppresses the activity of these centers in the brain and thus increases or changes the functioning of the brain.
Leptin is the first of the hormones that specifically play a role in the regulation of body weight in humans. Of the monogenic forms of obesity known today, most obesity is associated with disruption of the leptin-melanocortin pathway regulating body mass.
Melanocortins are a group of hormones that include agouti protein (the name “agouti” is given after the color outside, for example), melanocyte-stimulating hormone (MSH) and AGSP. Better for other treatments a-MSH; This is a fragment of a large POMC molecule that vibrates at the anterior part of the pituitary gland. ACTH is also established with ROMS. ACTH regulates the function of the epithelium, and MSH regulates a number of processes, including skin pigmentation. MSH acts through melanocortin receptors, such as MC3R and MC4R, to regulate body weight. The importance of MC4R for the regulation of body weight was shown in studies on transgenic mice in which the receptor is not synthesized. Obesity and insulin resistance develop. MSH and other ligands that stimulate MC4R suppress the life of hedgehogs. The importance of endogenous α-MSH for the regulation of body weight has been demonstrated in mice with a gene mutation that ensures the synthesis of POMC. This is accompanied by a lack of α-MSH, overeating, and obesity. Thus, it can be assumed that endogenous -MSH is an MC4R agonist and the disruption of its synthesis is associated with obesity. MSH receptors have been identified in the bark of the supernatant; They are implemented by ACTH.
Apparently, gene mutations that disrupt the synthesis of any of the components of the leptin-melanocortin pathway can lead to the development of persistent morbid obesity in aphids and polyphagy. In humans, mutations in the genes for leptin (LEP, 7q31.3), leptin receptor (LEPR, 1p31-p32), proopiomelanocortin (POMC, 2p23.3), melanocortin receptors 3 and 4 (MC3R and M4) have been described Morbid obesity , what progresses from early childhood - the most common feature of all monogenic forms, which confirms the central role of these genes in the regulation of body weight.
Born in 1997 Montague C. from spivat. described two children with severe obesity and insignificant levels of leptin in their blood. The children had a closely related mutation from Pakistan and a small homozygous mutation (ΔG133) of the leptin gene (LEP), which disrupted protein synthesis. To date, data have been published on 12 patients with congenital leptin deficiency due to a mutation in the LEP gene, of which 3 patients are adults.
Children with born with leptin deficiency They may smell normal during pregnancy, but even during the first months of life, the stench indicates an increase in appetite, which leads to a catastrophically rapid gain of excess fat. They are characterized by polyphagia with manifestations of aggression when trying to feed themselves and early hyperinsulinemia, which is accompanied by the development of type 2 diabetes, often in the 3rd-4th decade of life. Clinically obese people are uniformly, with an important development of subcutaneous fat cells, the pink development of children is not damaged. Congenital leptin deficiency is associated with hypogonadotropic hypogonadism and secondary hypothyroidism, which occurs in some patients on levothyroxine replacement therapy. Experimental studies suggest an important role for leptin in the synthesis and secretion of thyroid-stimulating hormone.
Children with leptin deficiency have normal levels of linear growth and insulin-like growth factor 1 (IGF-1). However, the presence of hypogonadotropic hypogonadism is accompanied by a pubertal acceleration in growth, which ultimately results in a lower growth rate for these patients than the population. Another feature of congenital leptin deficiency is the presence of severe T-cell immunodeficiency, which is clinically manifested by partial infectious diseases with a high mortality rate.
The uniqueness of this genetic defect is the possibility of effective treatment: rapid administration of recombinant human leptin leads to a pronounced change in polyphagy already on the 3rd day of treatment, normalizing the low level of the main exchange and resolution, be careful about the persistence of a decrease in blood pressure due to significant changes in the volume of healthy fat. After 1 month of treatment, the follow-up showed normalization of thyroid hormones with additional replacement therapy. In addition, treatment with recombinant leptin was accompanied by a self-induction of pubertal development in both adults and adolescents and did not induce pre-pubertal development in children.
Heterozygous mutations in the LEP gene cause low leptin levels in obese patients.
Born in 1998 Clement K. from spivat. described the development of three Algerian sisters with morbid obesity caused by a mutation in the leptin receptor gene (LEPR). This mutation results in disruption of splicing and shortening of the receptor. All sisters had a high level of leptin in their blood serum – 600, 670 and 526 ng/ml (14). In 2007 Farooqi S. iz spivat. published data on 8 patients (from England (2), Turkey (2), Bangladesh (1), Iran (1), Norway (1), Europe (1)) with a known mutation of the LEPR gene. All described mutations are associated with disruption of receptor signaling. The clinical picture of congenital leptin receptor deficiency is very similar to what is expected in patients with leptin deficiency: hyperphagia with the development of morbid obesity over the course of the first fates of life, hyperphagia is characteristic supotropic hypogonadism, parts of infection, low terminal growth. While insulin levels may be normal in patients with a mutation in the LEPR gene, blood diabetes was detected in only two adult patients aged 41 and 55 years. No decrease in the level of thyroid hormones was observed in any of the patients. Three of the adult women (31, 41, 55 years old) have an irregular menstrual cycle without significant development of secondary signs. All patients have small normal rosomal development.
The most important and significant result of this study is that leptin levels in all patients varied (ranging from 14 to 365 ng/ml) and did not vary from those in patients with morbid obesity In those without a mutation of the LEPR gene, then “super high” leptin levels cannot be a marker of the mutation LEPR gene.
Heterozygous carriers of the LEPR gene mutation are more likely to be obese, and their leptin level correlates with their body mass index.
The association of rapidly progressing morbid obesity, increased appetite and hypersensitivity insufficiency with insignificant blood levels of cortisol and ACTH is characteristic of born with ROMS deficiency . In 1998 and 2003 rocks. Krude N. iz spivat. described the development of five patients with homozygous and heterozygous mutations of the POMC gene, in whom obesity and hypocorticism were associated with ore hair and even pale skin. In 2006 Farooqi S. iz spivat. Similar mutations of the POMC gene were detected in six more patients. All children with identified mutations of the POMC gene are characterized by the early development of clinically severe hyperthyroidism deficiency (secondary, associated with ACTH deficiency, the precursor of which is POMC) with characteristic hypoglycemia , sickly fever, prone to severe infections, which in one episode led to death. All symptoms are relieved with the prescribed replacement glucocorticoid therapy, with obesity and polyphagy developing in the first months of life (in one stage before the initiation of replacement therapy). єyu.
The presence of light hair and pale skin, which occurs in most patients, was considered a reliable sign of a deficiency of POMC, which is a precursor of MSH, which is important for the creation of eumelanin by skin melanocytes . However, in 2006 A dark-haired patient from Turecchini was found to have POMC deficiency. It is possible that this is related to ethnic characteristics - all patients with hair color and POMC deficiency were Europeans. On the other hand, it can be assumed that the synthesis of eumieline is not limited to the influx of melanocortins. A trial of treatment of patients with POMC deficiency with intranasal administration of a synthetic analogue of melanocortin, which has an anorexigenic effect, was unsuccessful: against the background of therapy for three months, there was no significant depression of the vagina.
Another example of monogenic obesity is Convertase deficiency type 1 — an enzyme that converts inactive molecules proinsulin, proopiomelanocortin and proglucagon into their active forms. The underlying clinical symptoms of this form, identified in three patients in the world, are early-onset obesity, hypogonadotropic hypogonadism, postprandial hypoglycemia, low blood pressure blood serum ash in patients with malabsorption syndrome.
With known heterozygous mutations reliably associated with the development of obesity, the most widespread are gene mutations melanocortin receptor type 4 (MC4R), which are found in 4% (0.5-6%) of people with a history of early onset obesity. This form is characterized by increased polyphagia, early hyperinsulinemia, a uniform thick increase in the mass of both fat and meat and bone tissue, which is associated with high Linear growth should be brought to the formation of the “people-mountain” phenotype. Whose daily dysfunction of the thyroid gland, suprathyroid gland; All patients have normal state development, fertility is preserved. Rhubarb leptin correlates with body mass index. Specific therapy for this form is available today.
The most important and least important developments for today are: hypothalamic obesity — the bright butt of the swelling was caused by non-genetic reasons. The term “hypothalamic obesity” refers to obesity associated with the treatment of hypothalamic swellings and brain tumors, metabolic therapy for brain swellings and hemoblastoses, skull trauma or stroke.
Hypothalamic obesity and severe deformities, which occurs in 50% of children who have undergone surgery or surgery for swelling of the hypothalamus and cerebrovascular accident, as well as skull trauma. In this form of obesity, both dietary and pharmacological infusions are ineffective, which often lead to concomitant pathologies such as hypertension, obstructive sleep apnea, dyslipidemia and psychosocial disorders alna dysfunction. It is important that the pathogenesis of this form of obesity is supported by studies in animal models that involve the development of the ventromedial hypothalamus. As a result, there will be a stimulating influx of the vagal nerve on the b-clinitis of the subglottic gland, increasing the secretion of insulin in the response to glucose with further accumulation of energy in the appearance of fat and, rash, development of obesity Inya. Trials of caloric intake and pharmacotherapy with adrenergic and serotonergic drugs resulted in a small and short-term effect on the treatment syndrome. The illness is known to be associated with autonomic dysfunction, which is unknown. The life span of patients with hypothalamic obesity is shorter, which is more important than that of persistent obesity.
Looking at what has been said, it is obvious that obesity equals polygenic illnesses. The discovery of current science of monogenic forms of obesity allows us to better understand the complex mechanisms of control of grub behavior and energy homeostasis.
For literature, contact the editor.
V. A. Peterkova Doctor of Medical Sciences, Professor
O. V. Vasyukova, Candidate of Medical Sciences
ENC Rosmedtekhnologii, Moscow
The USB company is a laureate of the National Award in Galusa Business 2007 in the special category “Implementation of innovative projects in biopharmaceuticals”
In 2007, in Moscow, the President-Hotel hosted a local ceremony for the naming of laureates of the National Award “Company of Rock”. Based on the results of expert assessments, the decision of the Honorable Jury and the decisions of the Organizing Committee of the Prize, the UCB company (USB) earned the title of laureate of the National Prize in Galusia Business 2007 in the special category “Realization “I of innovative projects in biopharmaceuticals.”
Behind the scenes of 2007 there was a press conference of the Moscow representative office of the UCB company.
The emergence of new effective medicinal methods gives doctors new opportunities for the successful treatment of severe illnesses. The UCB company is a leading light in the field of biopharmaceuticals, specializing in four therapeutic areas - diseases of the central nervous system (including epilepsy), respiratory diseases and allergies, inflammatory processes Immunology, oncology. The main mission of UCB is to improve the health and reduce the quality of life of patients, therefore the company concentrates its activities on the development of innovative drugs. In 2008, UCB launched a new drug on the market, which became the result of innovative developments of the remaining rocks. Newpra is a drug aimed at treating Parkinson's disease and is a transdermal patch. This is a unique form of speech delivery that lasts 24 years.
The company first entered the Russian market in 1994, and during this period a number of the company’s main products gained wide popularity in Russia. Among them:
Keppra is a leader in the treatment of cured epilepsy and is rated No. 1 in the United States.
Xyzal is an antihistamine drug of the last generation. If such a drug is absorbed into the body, it breaks down into molecules, most of which are inactive, and only one interacts with the histamine receptor, causing an allergic reaction. Xysal is an enantiomer - a molecule that is active and no longer breaks down. The significance lies in the fact that instead of empty inactive molecules, the body removes all the nutrients. Xysal blocks the mediators of allergic inflammation as much as possible, and is also practically harmless to the liver.
Zyrtec – is used for the symptomatic treatment of color and seasonal allergic rhinitis and allergic conjunctivitis and is used in more than 100 countries for the treatment of adults and children.
At the development stage, 10 molecules are present that will be frozen in 17 days. At the moment, the first stage of clinical testing of drugs for the treatment of oncology (cancer of the leg) and multiple sclerosis is underway.
Founded by the UCB Institute of Allergy, the main method of activity of which is the thorough prevention and treatment of allergies through the provision of medicines and the population with current scientific information and the promotion of Other allergology programs. Rozblnaya for all signs for the sizyna lіkarіv that likkariv practices, in the Yakiki was submitted the main Vidomosti about izhmunnі Meminizmi Alergi, nadano described by the dial -up rodbox of the diagnostica algorithm. The Institute is unique in that it conducts initial programs among doctors and patients without knowing about the drugs produced by the UCB company.
17 Bereznya 2016Recession obesity will not always lie in the genes
It appears that metabolic disorders, which can lead to obesity and diabetes, often develop through genetic mutations: the enzyme gene no longer properly follows the metabolism of speech, and through this problems begin From absorbed glucose, from insulin, from adipose tissue (one of the most common And the most affected gene here is the FTO (fat mass and obesity-associated protein) gene - some variants of FTO give an average of three kilograms of it to people.
Such a gene, like a wine, can last a long time to pass from generation to generation, so that all members of the clan along any line, maternal or human, will have to respectfully follow the waist and the equal parts of the blood i.
However, the genes do not follow the “on/off” principle; they always have a different range of activity. In other words, a gene can be expressed weakly, not at all weakly, moderately strongly, etc. Those, such as gene adjustments, can be stored as a mutation, as well as external and internal factors - then, roughly speaking, to our way of living with ecology and from the activity of other genes. However, if you become obese, it is not always connected with genetic “curses” - improper eating can completely change the metabolism of speech to obesity without any mutations.
Living organisms have a lot of molecular ways of tuning the activity of genes, and many of these mechanisms function inappropriately - having worked every hour in some force majeure circumstances, the gene rotates to its original state. However, it is carried out in such a way that changes in genetic activity are saved throughout life, and are increasingly transmitted in the next generation. In this case, apparently, the gene itself does not change, its DNA does not change, no mutations occur, the regulatory molecules simply do not release their grip.
Such changes are called epigenetic regulation, as shown by the research of Johannes Beckers and his colleagues at the Munich Center. Helmholtz's research shows that health and obesity can be passed on from generation to generation through the use of epigenetics (You Are What Your Parents Ate!). Then the inheritances from the unhealthy way of life of their fathers can pass on to their land, despite the fact that the genes of these and others will be completely original, without mutant changes.
For six years, researchers have trained genetically different male and female mice on three different diets: high-fat, high-fat, and low-fat. As it turned out, animals that had been fat for years lost their obesity and the first signs of another type of diabetes. Then tissues were taken from all mice for extracorporeal plating. The procedure itself was carried out in all possible combinations: a sperm from a “fat” male was bred from an egg from a female who was on a primary diet, then a sperm from the same male was bred from an egg the tissue of a female who was on a low-fat diet, etc. Embryos and then , when the targets were born, they were nine years old as normal hedgehogs, without fatty distortions, and then transferred to fatty hedgehogs.
The fat hedgehog gave vag to everyone, but, as they say in the article in Nature Genetics (Huypens et al., a lot of the vag clearly lay in what the fathers ate). So, for example, the females that were born from “fat” males and females were 20% smaller than normal mice (the same ones that were the same age as hedgehogs). In the end, according to the authors of the work, the neglect of the father’s children was most pronounced in the daughters themselves.
Another important point is the metabolism of glucose: it is clear that one of the predictors of diabetes of another type is the loss of tissues and organs sensitive to insulin and, as a result, the inability to cope with increased blood levels there is no blood glucose. In the experiment, problems with the cervix passed from one generation to the next, most importantly along the maternal line: if only the mother would suffer from the overworldly vagina, then she has problems, both “boys” and “everyone”. chat”, the prevalence of insulin-induced inadequacies was high, but axis in all other types (then only the father had an overweight vagina, and the mother was on a normal or low-fat diet, etc.). Regarding each episode, we remember once again that genetically all the father mice were the same and without mutations to make them “fat,” and the maturity of the young mice was the result of the adjustment of genes that was formed in the previous generation .
This is far from the first work that is about the epigenetic reduction of obesity and the metabolic problems associated with it, both statistical data and experimental data. However, previously in experimental robots they simply bred mice and looked after their offspring, and in this case it is impossible to believe that obesity in the next generation did not occur through epigenetic factors, not through those that the fathers or fat well, I mean, because of the peculiarities of the embryonic development, it is possible For example, it is clear that in females obesity affects the physiology of the uterus, which, in its turn, flows into the embryo. In the case of extracorporeal impregnation and in the case of vicarious birth as a surrogate mother of a normal, healthy female - as in the above descriptions of the robot - such ambiguities tend to disappear.
Now it would be useful to find out in the same way how obesity can be transmitted from one another to the third generation, and how the fathers have lived for a long time on the wrong diet, so that epigenetic mechanisms consolidate the new unhealthy “met.” absolute reality." Well, of course, nutrition is lost, so specific molecules play a role here. There are a number of molecular devices that can permanently change the activity of genes: these enzymes are responsible for the methylation and demethylation of DNA; enzymes that modify histones - chromosomal proteins that control the archiving and rosarchivation of DNA; that complex of regulatory RNAs. We will not go into details of the cutaneous mechanism; let us say that for a long time it was unclear what such mechanisms were at work in the progenitors of state cells in ssavians. However, we already see the evidence of what really works there - so that epigenetic changes can cross the intergenerational line.
By the way, the most important food: what kind of world can we give to people? Molecular processes on this level are expected to be universal, and as a result of reduced epigenetic regulation, it was found in mice with high homogeneity, and the same can be found in most animals. riv, including people.
The key is to know “the same”: about the problems associated with the transfer of laboratory results to people, we guessed when they wrote about the work, dedicated to the influx of stress on epigenetics. Here it is not possible to invest in experiments; one cannot rely on medical statistics and mass genetic analysis.
Research into the genetics of obesity has been going on for a long time. So it is good for doctors to know which genes and which world are responsible for the cure. Let's take a closer look at these promises and see what the fakivists are saying to this drive.
Oman. “In our family, we all have the fat gene”
It's true. There is no single gene missing. Each of us has about 200 genes that are associated with obesity. The peculiarities of the work of these genes (so-called polymorphism - minor variations, but not a mutation) may be one of the reasons for the disease. But you may or may not even be able to identify the defective gene for yourself.
Eh, even if there were only one gene for regeneration, it would be much simpler to get rid of the vagina...
Oman. “I was relieved in front of my mother and grandmother”
It's true. When geneticists tested obese people, unfavorable slumpiness was found in 62-63% of patients. And what’s wrong is that there is a need for high-calorie food and a lack of roachal activity - in 97%! It turns out that without a careless slump, people are growing again, as if they are moving and not breaking. The same is true: no matter how much a person’s genes are taken away, no matter how much he overeats and collapses, no claim will be made. In fact, it seems to geneticists that the only way to “correct” sluggishness is to change the way of life.
Oman. “I have such genetics that I love everything”
It's true. It is possible for any person to know a way of living that will help to save or turn the string. A different kind of food, for whom the scope of possibilities is wide, but for those who want to worry about following a narrow corridor.
Our skin gene is a matrix for one single protein (hormone, hormone receptor, enzyme). Since this matrix has been changed, it means that the proteins perform their work in the body in a different way, for example, more active or weaker. If gene changes that are repeated occur only in one of the parents, you may not express them in later life. If such a gene is taken from both mother and father, there are much more chances for those who declare themselves.
All robot genes and protein synthesis still obey the laws of chemistry. How many substances are there in the body to activate this gene? What is the “future material” from which proteins will be synthesized? What are the elements that launch, speed up, and support this process? Only if you have a positive outlook on all nutritional factors (and many others, and even the body is even more complex), you will gain moisture. And why give the “sweat” gene everything it needs, so it can only lie in front of you. It is not surprising for everyone who is wise to begin with to recommend not eating sweet, fatty, greased, processed drinks... Not only because there are calories in them, but because the number of these products is probably small, to avenge a bunch of words that I launch the robot's genes "potovsti" !
Oman. “Since the father’s mentality has subsided completely, then, no matter what kind of diets you sit on, you will still be fat”
It's true. Find reliable data about how external factors influence the “behavior” of a particular gene. For example, there is a gene associated with sensitivity to glucose. However, there is no risk of deterioration, even if malt shortbread is added to the fat. In some cases, it appears to be simple carbohydrates, including fruits, and such products increase the risk of gaining weight. On the other hand, it is clear that chromium, vanadium and zinc take part in absorbed glucose. Then, having taken supplements with these minerals, you can paint your weak skin.
Another option is genes that are responsible for fat metabolism, for increasing the level of fats in the blood. Since the smell is more active, the body is more active in storing fat. For such people, geneticists recommend eating less animal fats, eating more (fat from the blood burns well in the dry world), and more green and leafy vegetables (there are a lot of things that lead to fat metabolism in these genes).
In other words, despite obvious genetic differences, we may not allow them to manifest themselves before the disease. You can take the scientific route: do a genetic analysis of the causes of obesity. Why take blood from you and perform a blood test for 10-15 markers (and not just one, as unscrupulous clinics often preach). Ale is expensive to obtain. Another widely available option is to sit down and analyze how your mother, father and grandmother ate? What is the reason for your “slump”? It may soon appear that the time has come to relax in the presence of large portions of buttered, sweet pies and evening feasts.
Special thought
Anetta Orlova:
— Proper food is a way of living. And it is necessary to conduct it steadily. If a person is unable to change his way of living, then he will no longer be able to stay on a diet. I would like to suggest that it would be better to give due respect to what you have today.