Visceral fat

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Generality

Visceral fat - also known as abdominal fat - is the part of adipose tissue concentrated within the abdominal cavity and distributed between the internal organs and the trunk.

Visceral fat differs from subcutaneous fat - concentrated in the hypodermis (the deepest layer of the skin) - and from intramuscular fat, which is instead distributed among the muscle fibers (the latter also seems to be significantly correlated with insulin. resistence).

Abdominal obesity

The "excess of abdominal fat is defined by the terms" central obesity "," abdominal obesity "and" android obesity ". With this last term we want to underline the typical association of visceral fat with the male sex and his hormones (called precisely androgens).

The need to differentiate this form of obesity from the gynoid one - typical of the female sex and characterized by adipose accumulations concentrated in the lower half of the abdomen, in the gluteal and in the femoral regions - derives from the different influence of the two phenotypes on cardiovascular risk. it is therefore a simple topographical differentiation, but rather a distinction with a great physiopathological significance.

Health hazards

Of the two types of obesity, abdominal obesity has clearly proved to be more dangerous, so much so that it is considered one of the most important risk factors for cardiovascular disease morbidity and mortality, as well as one of the main risk factors for type II diabetes. The exaggerated accumulation of central fat is also associated with the metabolic and cardiovascular complications typical of the metabolic syndrome (hypertension, hyperlipidemia, hepatic steatosis, atherosclerosis and the aforementioned type II diabetes).

The epidemiological evidence on the dangerousness of visceral fat has been confirmed in more recent times, thanks to the growing amount of studies on the endocrine function of the tissue, or rather of the adipose organ. It has been seen, in particular, that abdominal fat has different characteristics than to the subcutaneous one, both under the cellular profile and under the aspect of the effects that these cells carry out on the endocrine-metabolic equilibrium of the organism. In fact, it has been shown that the white adipocytes of visceral fat are particularly active in the release of adipokines, substances with local (paracrine), central and peripheral (endocrine) effects. Through the direct or indirect release of these substances, visceral fat controls the "appetite and energy balance, immunity, angiogenesis, insulin sensitivity and lipid metabolism."

One of the best known adipokines, adiponectin, improves insulin sensitivity and is endowed with anti-inflammatory activity; its levels, unlike those of many other adipokines, are lower in the obese than in the normal weight. On the other hand, the excess of visceral fat increases the release of substances such as interleukin 6 (IL-6), resistin and TNF-α (cytokines with pro-inflammatory activity), PAI-1 (pro-thrombotic effect ) and the ASP (stimulating activity on the synthesis of triglycerides and inhibitory on the oxidation of fatty acids).

The excessive volumetric increase of adipocytes, caused by the conspicuous accumulation of triglycerides, determines their death and consequent lysis by macrophages, which attack the lipid vacuoles with a further increase in the inflammatory state of the organism (the levels of protein C also rise. reactive, currently considered an important cardiovascular risk factor).

The number of macrophages present in the adipose tissue is proportional to the degree of obesity, or rather to the hypertrophy of the adipocytes typically associated with obesity. Thus there is a sort of foreign body reaction, with consequent chronic inflammation which, if perpetuated over time, predisposes to important metabolic diseases.

The reduction in the synthesis and release of nitric oxide, a gas with a powerful vasodilatory action, contributes to further elevating the atherosclerotic risk. This gas promotes lipolysis and is a stimulus for the proliferation of brown adipose cells, which, unlike the white ones, do not accumulate lipids but burn them, either to maintain body temperature in cold environments, or to get rid of food excesses that would alter the " metabolic balance. The synthesis of nitric oxide, also active in angiogenesis and in local mitochondrionesis (which would probably prevent the aforementioned death of adipocytes due to hypoxia from excessive lipid accumulation), is inhibited by TNF-α, an adipokine released in large quantities from the hypertrophic visceral white adipose tissue and the macrophages that attack it.

The particular anatomical location of visceral fat ensures that the adipokines and other substances released flow directly into the portal venous system, which transports them to the liver. The prominent metabolic role played by this gland helps to explain the great influence of visceral fat on the health of the whole organism.

A typical feature of visceral fat is the greater sensitivity to lipolytic stimuli, since the action of omental lipoprotein-lipase is 50% greater than that of subcutaneous fat. This means that in case of weight loss, the first fat to be " burned "is the visceral one.

The excess of abdominal fat is directly related to the circumference of the waist. In particular, the cardiovascular risk becomes clinically relevant when the threshold values ​​of 102 cm of circumference at the umbilical level in men and 88 cm in women are reached.

To try to explain the correlation between excess omental fat and type II diabetes, it has been shown that the high flow of fatty acids, coming from visceral adipocytes and going to the liver, increases the production of VLDL (which, as we know, can be subsequently transformed into the dangerous LDL - bad cholesterol, which predispose to the atheromatous process). It also promotes gluconeogenesis and reduces the hepatic clearance of insulin, with a consequent increase in the levels of this hormone in the circulation. In addition to fatty acids from visceral adipose deposits, we must also and in any case take into account the action of the adipokines themselves. Interleukin-6, for example, in the liver stimulates gluconeogenesis and triglyceride secretion, with compensatory hyperinsulinemia.

The high presence of free fatty acids in the circulation causes these nutrients to "compete" with glucose for entry into cells, particularly in muscle cells. As a result, an increase in blood sugar occurs, in response to which the pancreas increases the release of insulin. The double hepato-pancreatic contribution to hyperinsulinemia means that despite the high glycemic values, large amounts of insulin are present in the circulation; in these cases, we speak of insulin resistance, that is a condition characterized by the reduced biological response of the tissues to "insulin action. Not surprisingly, the surgical removal of visceral adipose tissue in moderately obese rats is able to normalize insulin resistance.

Insulin resistance and hyperinsulinemia are responsible for all those alterations in glucose metabolism ranging from impaired fasting glycaemia, to impaired glucose tolerance, up to overt diabetes.These alterations, together with the equally negative ones on lipid metabolism, account for the greater cardiovascular risk of the subject with visceral obesity compared to normal weight.