Key exogenous causes of abdominal obesity are associated with a violation of the physiological proportionality of caloric intake and the consumption of energy received - with a significant excess of consumption. With a sedentary lifestyle, unused energy in the form of triglycerides accumulates in adipocytes (cells of white adipose tissue). By the way, leads to obesity is not so much excessive consumption of fat as food rich in carbohydrates, because excess glucose under the influence of insulin is easily transformed into triglycerides. So, there are no doubts about such risk factors for obesity, as malnutrition and lack of motor activity.
One of the obvious reasons for abdominal obesity in men is alcohol. The so-called "beer belly" appears due to the fact that alcohol (including beer) gives a lot of calories without real nutritional value, and when these calories are not burned, the fat reserves in the abdominal cavity increase.
Disturbance of eating behavior is also among the reasons for being overweight: many people are accustomed to "reward themselves with food," that is, "jam" stress and any surge of emotions (the pathogenesis of this phenomenon will be discussed below).
Endogenous causes of abdominal obesity are associated with the development of a number of protein-peptide and steroid hormones, neuropeptides and neurotransmitters (catecholamines), as well as their interaction, the level of sensitivity of the conjugated receptors and the regulatory reaction of the sympathetic nervous system. Enough enough endocrine problems are genetically determined.
As noted by endocrinologists, abdominal obesity in men (who initially have more visceral fat than women) is due to a decrease in testosterone (dihydrotestosterone). Reducing the production of sex steroids, as it turned out, contributes to an increase in the number of their receptors in the tissues, but the receptor sensitivity in this case is significantly reduced, therefore, the signal transmission to the neuro receptor of the hypothalamus, which regulates the majority of endocrine processes in the body, is distorted.
Abdominal obesity in women develops, usually after the onset of menopause, and is explained by the rapid decline in the synthesis of estradiol in the ovaries. As a result, not only the catabolism of brown adipose tissue changes, but also its distribution in the body. In this case, abdominal obesity with a normal BMI (that is, with a body mass index of no more than 25) is often observed. Promotes obesity polycystic ovary, which reduces the level of female sex hormones. In addition, the risk factors for visceral obesity in women include hypothyroidism - thyroid hormone thyroid hormone deficiency and thyroid-stimulating hormone (synthesized by the pituitary gland), which play an important role in the overall metabolism.
Abdominal obesity in women after childbirth threatens those who gain more kilos during pregnancy than they should (this is typical for about 43% of pregnant women). Promotes obesity and increased weight before pregnancy, especially against a background of high levels of the prolactin hormone in the blood (which is produced during lactation and stimulates the conversion of glucose into fat). The development of abdominal obesity after childbirth can be one of the consequences of Shihan's syndrome, associated with a strong loss of blood during labor, which leads to damage to the pituitary cells.
Among the endocrine pathological changes, the following risk factors for fat accumulation in the abdominal cavity are distinguished:
- an increase in the synthesis of adrenocorticotropic hormone (ACTH) by the pituitary gland and a decrease in the production of somatotropin, beta and gamma-lipotropins;
- excess production of glucocorticoids (steroid hormones) with functional disorders of the adrenal cortex;
- an increase in the synthesis of insulin by the pancreas, while reducing the production of the hormone glucagon (stimulating lipolysis - the cleavage of triglycerides in fat cells).
In fact, the combination of these factors causes abdominal obesity in the metabolic syndrome. Abdominal obesity is part of the symptomatic complex of the metabolic syndrome and is directly related to both increased tissue resistance to insulin, the development of hyperinsulinemia and an increase in glucose from the blood, and hyperlipidemia, a high level of triglycerides in the blood and low levels of high-density lipoprotein (HDL). At the same time, according to clinical studies, in 5% of cases the metabolic syndrome is present at normal body weight, in 22% - at excess weight and in 60% of patients with abdominal obesity.
Accumulation of visceral fat in the abdominal cavity can occur with Cushing's syndrome (Isenko-Cushing's disease); with alcohol-induced pseudo-Cushing syndrome; with a benign pancreas tumor (insulinoma); with inflammatory, traumatic or radiation damage to the hypothalamus, as well as in patients with rare genetic syndromes (Lawrence-Moon, Cohen, Carpenter, etc.).
Abdominal obesity may develop in children and adolescents with neuroendocrine Fröhlich syndrome (adiposogenital dystrophy), which is the result of birth craniocerebral injuries, cerebral infestations or infectious brain damage in meningitis or encephalitis.
Obesity can lead to some medications, for example, steroids and drugs used in mental illness.
See also - Causes and pathogenesis of obesity