Visceral Fat - Abdominal Fat

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Generality

Visceral fat - also known as abdominal fat - is the part of fatty 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 the intramuscular one, which is instead distributed among the muscle fibers (the latter also seems to be significantly correlated to the insulin) resistance).

Abdominal Obesity

The excess 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 its hormones (called precisely androgens).

The need to differentiate this form of obesity from the gynoid one - typical of the female sex and characterized by fatty deposits concentrated in the lower half of the abdomen, in the gluteal and femoral regions - derives from the different influence of the two phenotypes on cardiovascular risk. It is therefore not a question of a simple topographic differentiation, but of a distinction of great physiopathological significance.

Health hazards

Among the two types of obesity, the abdominal one has clearly proved to be more dangerous, so much so as to be considered one of the most important risk factors for morbidity and mortality due to cardiovascular diseases, 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).

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 tissue, or rather of the adipose organ. We have seen, in particular, that abdominal fat has different characteristics compared to the subcutaneous one, both from the cellular point of view and in terms of the effects that these cells perform on the endocrine-metabolic balance of the organism. In fact, it has been shown that 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 appetite and energy balance, immunity, angiogenesis, insulin sensitivity and lipid metabolism.

One of the best known adipokines, adiponectin, improves insulin sensitivity and has anti-inflammatory activity; its levels, unlike those of many other adipokines, are lower in the obese than in normal weight. By contrast, excess 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 ASP (stimulating activity on triglyceride synthesis and inhibition of fatty acid oxidation).

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

The number of macrophages present in adipose tissue is proportional to the degree of obesity, or rather to the hypertrophy of 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 raising the atherosclerotic risk. This gas promotes lipolysis and is a stimulus for the proliferation of brown fat cells, which, unlike 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 local angiogenesis and mitochondriogenesis (which would probably prevent the aforementioned death of adipocytes due to hypoxia due to excessive lipid accumulation), is inhibited by TNF-α, an adipokine released in large quantities by white adipose tissue visceral hypertrophic and macrophages attacking it.

The particular anatomical location of visceral fat causes the adipokines and other released substances to 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 entire body.

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

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

To try to explain the correlation between excess of omental fat and type II diabetes, it has been shown that the high flow of fatty acids, coming from visceral and liver-directed adipocytes, increases the production of VLDL (which as we know can be later transformed into dangerous LDL - bad cholesterol, which predispose to the atheromatous process). It also promotes gluconeogenesis and reduces hepatic clearance of insulin, resulting in increased levels of this hormone in the circulation. In addition to fatty acids from visceral adipose deposits, it is also necessary to take into account the action of the adipokines themselves. Interleukin-6, for example, at the liver level 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 muscle cells. As a result there is an increase in blood glucose, in response to which the pancreas increases the release of insulin. The double hepato-pancreatic contribution to hyperinsulinemia means that large amounts of insulin are present in circulation despite the high glycemic values; in these cases we speak of insulin resistance, that is of a condition characterized by the reduced biological response of the tissues to the 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 of glucose metabolism that range from impaired fasting glucose to reduced glucose tolerance to overt diabetes. These alterations, together with those equally negative on lipid metabolism, account for the greater cardiovascular risk of the subject with visceral obesity compared to normal weight.