Facebook
Twitter
LinkedIn
Email
 |
Checking for direct PDF access through Ovid | |
Excerpt
The existence of an inflammatory state involving the adipose tissue and its potential role in obesity and associated complications has been shown in a recent study, which found that the white adipose tissue (WAT) produces tumor necrosis factor alpha (TNFα), a proinflammatory cytokine. Hence, there are two scientific evidences of human obesity as a chronic inflammatory illness: the well-described moderate increase of inflammatory factors in the circulation of obese subjects and, now, the identification of macrophage cells infiltrating the WAT, which may enhance the low-grade chronic inflammation associated with obesity. The mechanism of this macrophage infiltration, however, remains undefined.
It has been suggested that this low-grade inflammatory state is associated with metabolic and cardiovascular complications of obesity, and it has been shown that weight loss can help improve this state by significantly decreasing circulating inflammatory molecules and macrophage cells in WAT depots. Weight loss, however modest, may improve numerous complications of obesity, including diabetes, hypertension, heart disease, and polycystic ovarian syndrome, as numerous data indicate that decreasing energy intake and increasing physical activity may be effective in reducing overall inflammation. Weight loss has also been associated with reduction of endothelial stress and, with a very low calorie diet (VLCD), a reduction of cytokines derived from adipose tissue. In a recent study, after 4 wk of VLCD (average 5-6 kg weight loss), the proinflammatory gene expression profile of the subcutaneous WAT of obese patients became closer to that of nonobese subjects. Improvement in the inflammatory profile also increases the expression of anti-inflammatory factors.
The authors concluded that the discovery of the low-grade inflammatory state in obesity and of the macrophage infiltration in WAT opens new perspectives in the research of the psychopathological mechanism involved in the development of obesity comorbidities, their evolution, and maintenance. They suggested that future studies should try to identify the molecular mechanisms of the inflammatory state and of the very early signals of macrophage infiltration into WAT so as to control the interaction of macrophages with adipocytes and other target tissues.
