If your waist circumference is greater than or equal to 88 cm in women and greater than or equal to 102 cm in men, then we recognize abdominal obesity that is a serious risk of developing diabetes.
The simplest measurement allowing to determine the health-threatening type of abdominal obesity is to measure the waist circumference. If the waist circumference is greater than or equal to 88 cm in women and greater than or equal to 102 cm in men, then we recognize abdominal (visceral) obesity, characterized by a high content of visceral dysfunction that is toxic to health.
Insulin - the key to supplying energy to cells
The insulin hormone is indispensable for humans to obtain energy from food carbohydrates. Let's remind - glucose - simple sugar obtained during digestion from food carbohydrates is the basic source of energy for physiological functions of tissues and organs of the body. And insulin is the chemical key that "opens" the cell to penetrate this basic fuel, which is sugar glucose. Inside the cell, energy from glucose becomes a "drive" for the so-called cellular respiration. As part of these processes, high-efficiency energy substances are indispensable for the system, including adenosine triphosphate (ATP) - a high-energy phosphorus compound; as well as amino acids needed for growth and regeneration of the body.
Hormones produced by adipose tissue may disturb the production of insulin [9,20] In response to the variable level of glucose and insulin in the blood - adipocytes secrete actively biological substances with the role of hormones called adipokines - such as: adiponectin, apelin, leptin, visfatin, resistive, etc. These substances are characterized in that, depending on their concentration in blood may stimulate or block the production and secretion of insulin from the pancreas. It is believed that apelin and visfatin are the most dependent on pancreatic secretion and effective insulin action. In total, the hormones secreted by adipose tissue, depending on their concentration in the blood, may contribute to insulin sensitivity or vice versa to insulin resistance of tissues.
Pathomechanism of insulin resistance [5,6,9,20]
Resistance of cells and tissues to insulin is a special health condition in which the pancreas still produces the right amount of insulin, but the body does not seem to notice it and reacts as if the hormone was missing. Periodically, it helps the patient to stimulate the pancreas to increase insulin production, which is especially true for type 2 diabetes. However, for the effective introduction of glucose into the cells - the body is demanding ever larger doses of insulin. Under the influence of such a regression mechanism - the next pathology appears - the loss of sensitivity of the receptors and membranes of target cells to the insulin key that opens them to absorb glucose. This is particularly true for fat cells, muscle cells, including cardiac muscle, liver hepatocytes. All these cells intensely absorb and process glucose, which is why first their cell membranes lose sensitivity to insulin and thus they gradually become more and more "closed" for glucose supplies, i.e. insulin-resistant! In other words, glucose from the blood is getting worse and worse, although the level of glucose and insulin in the blood is getting higher. As a result, the body is running out of energy! Therefore, in diabetic patients not requiring insulin injections, after years of increasing the state characterized by excess insulin in the blood (hyperinsulinaemia!) And increasing resistance of cells to insulin, finally the secretory power of the pancreas is exhausted. This negative feedback usually has its own final illness.A person suffering from insulin resistance eventually becomes a person suffering from diabetes!
Abdominal obesity promotes muscle insulin resistance [4,5, 9, 11,20]
Abdominal (visceral) overgrown fat tissue intensifies pancreatic production of the insulin hormone. As a result, it saturates the blood with the hormone causing the so-called hyperinsulinemia. A special threat is the abundance of so-called mesenteric adipose tissue. Let us recall that the mesentery is a structural element of the abdominal cavity and is made of peritoneal membrane laminae. It serves a strong and at the same time elastic fixation of abdominal organs to the abdominal wall, in particular the fixing of the liver and kidneys; as well as fixing vessels and nerves leading to these organs. Unfortunately, it can also be a support for the excessive growth of abnormal fatty tissue in the abdominal cavity. An additional pathomechanism generated by the abundance of this line adipose tissue is the reduction in the number and impairment of the so-called glucose transporters. The presence of a sufficient number of these transporters is essential for proper penetration of glucose into the interior of fat cells (for further production and storage of triglycerides), inside muscle cells (glycogen production), as well as for penetration into liver hepatocytes and inside nerve cells or erythrocytes using only from energy derived from the breakdown of this sugar.
Footnote: There are two types of obesity: [5,6,11,16]
In people with normal body mass, the fat mass does not exceed 20% of the weight in women and 10% in men. In obese people, it is often over 50% of body weight! This high excess of adipose tissue may be differently distributed in the body. Therefore, two basic types of obesity are distinguished:
A. Abdominal obesity - which we define as an android type otherwise called visceral or the type of "apple". This type of obesity is characteristic of men's obesity B. gynoidal - otherwise known as femoral glans or the type of "pear", which is conditioned by sexual dimorphism and highly characteristic of women
If your waist circumference is greater than or equal to 88 cm in women and greater than or equal to 102 cm in men, then we recognize abdominal obesity that is a serious risk of developing diabetes.
The simplest measurement allowing to determine the health-threatening type of abdominal obesity is to measure the waist circumference. If the waist circumference is greater than or equal to 88 cm in women and greater than or equal to 102 cm in men, then we recognize abdominal (visceral) obesity, characterized by a high content of visceral dysfunction that is toxic to health.
An excess of TNF alpha factor it blocks the use of energy from glucose [9, 11,20]
Dysfunctional visceral tissue synthesizes and releases into the blood an excess of apodicin, called tumor necrosis factor. Apodicin marked with the symbol - TNF alpha - blocks the physiological functions of insulin receptors. It threatens insulin resistance and the development of diabetes. Through insulin receptors glucose sugar penetrates inside the cells, where it is metabolized to obtain from it chemical energy necessary for physiological activities, including the production of high-energy phosphorus compounds (ATP), etc. In other words, our cells, adipose tissue and many other organs and tissues they can take energy from the basic systemic carrier - glucose - only through these receptors. So what is the insulin receptor and how does it work?
It is made of specific glycoproteins, which pancreatic hormone - insulin - activates for glucose uptake. A special role is played by membrane glucose transporters - mobile proteins with the GLUT4 symbol. In number adequate to the current insulin concentration, they approach the surface of the cell membrane near the receptor. From where they absorb and transport glucose through the cell membrane into the interior. It can be said in a simplified way that the ability to take glucose extracellularly depends not only on the number of receptors appropriate for a given cell type, but mainly on the number of activated GLUT4 glucose protein transporters operating dynamically at each receptor. And in the context of the physiological processes described above, it is possible to add: - dysfunctional visceral fat tissue releasing too many TNF alpha tumor necrosis factor particles blocks many GLUT-4 receptor proteins, which inhibits the penetration of glucose inside the body cells.In addition, TNF alpha inhibits systemic glucose metabolism and blocks specific fat cell receptors (PPAR-γ) in adipocytes and myocytes, which in turn is not always beneficial for the body's needs, limits cellular production of fat (triglycerides).
Excess leptin inhibits the release of insulin from the pancreas [9 20]
Dysfunctional visceral tissue synthesizes and releases too much leptin hormone into the bloodstream. Meanwhile, it has been shown that the excess of leptin in the blood decreases the production of glucose and glycogen in hepatocytes of the liver, and in beta cells the pancreas inhibits the release (secretion) of insulin. In addition, excessive levels of this hormone in the blood have an inhibitory effect on gluconeogenesis. Leptin can also induce so-called insulin resistance and a pre-emptive resistance. Leptin resistance is a particularly troublesome phenomenon for slimming people with simple obesity (i.e. caused by an excess of calories in the diet). Leptin resistance is a condition in which the level of leptin in the serum of a slimming person is already so high that the addition of an additional supplement in the form of exogenous leptin will no longer cause the expected therapeutic effect in the form of due weight loss [9,20].
Dysfunctional visceral tissue disturbs self-control on appetite [3,6,20]
Leptin plays one more important role in the energy-food economy. This hormone is a biochemical signaling link in the mechanism of appetite self-regulation. It has the indexing ability to signal the body size of energy resources in the form of fat. The level of leptin in the blood is proportional to the mass of triglycerides available at the moment for cellular "burning" on calories. Therefore, the concentration of the hormone in the blood is perceived by the brain as an indicator of the need for fat. This is possible thanks to leptin receptors located mainly in the hypothalamus of the brain as well as the concentration of another indicator protein - gastric ghrelin. Thanks to the correlation in the center of hunger and satiety of these two biochemical indicators - appetite called appetite appears. Therefore, disorders of leptin production or insensitivity of receptors to this hormone lead to dysregulation of the center of hunger and satiety, and consequently to loss of control over appetite. In addition, the lack of receptor control over leptin may result in a decrease in insulin production as well as a reduction in the transport of glucose to fat cells - adipocytes, i.e. limiting the metabolism of glucose to triglycerides. As a consequence, it threatens serious disturbances of the entire energy economy in the system.
Author: mgr farm. Nina Krawczyk
MSc in live chemistry. Edward Ozga Michalski
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10. More light on the problems of the metabolic syndrome; A Cardiothyroidological Review 2006; 1, 1: 12-26 authors: Jan Tatoń, Anna Czech, Małgorzata Bernas, Anna Rubiec-Niemirowska 11. Body degreasing - the practice of prevention and treatment of obesity; "THERAPY" No. 5 (166), MAY 2005, Page 35-44 with in
