Visceral and Subcutaneous Adiposity: Are Both Potential Therapeutic Targets for Tackling the Metabolic Syndrome?

Abstract

The metabolic syndrome represents a constellation of co-morbidities that include central adiposity, insulin resistance, dyslipidemia and hypertension, which results from an elevated prevalence of obesity. An increased abdominal adiposity is observed in upper-body obesity with preferential accumulation of fat in the visceral depot, which renders these individuals more prone to metabolic and cardiovascular problems. The pathophysiology of the metabolic syndrome seems to be closely associated to an elevated efflux of free fatty acids from the visceral fat compartment and a dysregulation of the expression of adipose tissue-derived factors (also termed "adipokines"). Weight reduction and increased physical activity represent the main approach to tackle the "diabesity" epidemic. Nonetheless, taking advantage of the different biochemical and molecular characteristics of visceral and subcutaneous adipose tissue may open up novel pharmacological strategies to combat the metabolic and cardiovascular derangements accompanying the metabolic syndrome.

Insulin sensitivity: modulation by nutrients and inflammation

“…It is also possible that this adipose tissue microhypoxia exacerbates the proinflammatory nature of the newly recruited macrophages, resulting in further activation of hypoxia-sensitive pathways and amplification of the inflammatory state. These events appear to be more pronounced in visceral adipose tissue compared with subcutaneous fat depots, as expansion of visceral fat has a uniquely adverse effect on insulin sensitivity (93).…”

Antagonism of T-type calcium channels inhibits high-fat diet–induced weight gain in mice

“…In contrast, treatment with a T-type antagonist dose-dependently increased lean mass to levels significantly different from those observed with fenfluramine. Body composition improvements may also be more relevant to the disease process than net weight reduction, including whether visceral or subcutaneous fat is selectively altered (46)(47)(48)(49)(50). Future efforts will be required to explore these changes in more detail.…”

Dead adipocytes, detected as crown-like structures, are prevalent in visceral fat depots of genetically obese mice

“…Obesity is frequently associated with metabolic syndrome; insulin resistance is widely suspected as the central starting event of the condition (1). Although the adipose organ of obese animals and humans is increased at both subcutaneous and visceral sites, visceral fat alone is responsible for the metabolic consequences of obesity (5)(6)(7)(8)(9). The reasons for this effect are unclear.…”