TO THE EDITOR:
The study by Lottati and colleagues on the effect of omentectomy on insulin resistance provides more evidence for the sinister role of visceral fat (1). Although there is a strong association between excess visceral, as opposed to subcutaneous, fat and insulin resistance and related cardiovascular diseases, no clear mechanism for this association has been established (2).
A possible explanation for this could lie in the recent observation that adipocytes in white body fat are often poorly perfused with blood and that adipocyte hypoxia is common. In response to this hypoxic stress, the adipocytes secrete a spectrum of pro-inflammatory cytokines, or adipokines. These adipokines are intimately linked to the genesis of insulin resistance, type 2 diabetes, and cardiovascular disease (3). Excess visceral fat is associated with increased circulating adipokines (4).
Omental fat, like all intra-abdominal visceral fat, and unlike subcutaneous fat, is subject to the intra-abdominal pressure. In man, this is normally about 7 mm Hg but rises to ≥18 mm Hg in morbid obesity (5). This intra-abdominal pressure will reduce the arterial perfusion pressure gradient of the visceral fat by an equivalent amount. Relative to a typical mean arterial blood pressure of 85 mm Hg, this reduction could be as much as 20%. The lower perfusion pressure will decrease blood flow and oxygen flux to the visceral fat. In turn, this will lead to more adipocyte hypoxia. Consequently visceral adipocytes may tend to be more hypoxic than subcutaneous adipocytes.
This mechanism could explain the increased adipokine secretion of visceral adipocytes and could account for the association of increased visceral fat mass with insulin resistance, type 2 diabetes and cardiovascular disease. Thus, the reduction in visceral fat mass by omentectomy could bring about a reduction in excess adipokine secretion with consequent improvement in insulin sensitivity as observed by Lottati et al.