Adipose tissue heterogeneity: implication of depot differences in adipose tissue for obesity complications

Abstract

Obesity, defined as excess fat mass, increases risks for multiple metabolic diseases, such as type 2 diabetes, cardiovascular disease and several types of cancer. Over and above fat mass per se, the pattern of fat distribution, android or truncal as compared to gynoid or peripheral, has a profound influence on systemic metabolism and hence risk for metabolic diseases. Increases in upper body adipose tissue (visceral and abdominal subcutaneous) confer an independent risk, while the quantity of gluteofemoral adipose tissue is protective. Variations in the capacity of different depots to store and release fatty acids and to produce adipokines are important determinants of fat distribution and its metabolic consequences. Depot differences in cellular composition and physiology, including innervation and blood flow, likely influence their phenotypic properties. A number of lines of evidence also support the idea that adipocytes from different anatomical depots are intrinsically different as a result of genetic or developmental events. In this chapter, we will review the phenotypic characteristics of different adipose depots and mechanisms that link their depot-specific biology to metabolic complications in men and women.

Copyright © 2012 Elsevier Ltd. All rights reserved.

Figures

Figure 1. Major adipose depots in humans

Subcutaneous adipose tissues include abdominal and gluteal, as well as femoral. Visceral adipose tissues are associated with digestive organs. Omental is attached to the stomach and mesenteric and epiploic are associated with the intestine and colon respectively. Peripheric fat surrounds the kidney and retroperitoneal fat is located in the retroperitoneal compartment.

Figure 2. Adipose signals influence systemic metabolism and appetite

Dysfunctional adipose tissue in obesity produces more proinflammatory factors (e.g. FFA, SAA, IL-6) and less antiinflammatory factors (e.g. adiponectin). These exacerbate inflammation and hence risk for metabolic diseases by affecting liver, skeletal muscle, beta-cells, as well as blood vessels. Insulin-glucose homeostasis become impaired as results of increased hepatic glucose output and muscle insulin resistance, and basal insulin secretion from pancreas is increased, most likely by FAs. Leptin and perhaps other adipokines normally regulate food intake and energy expenditure through effects on the central nervous system, but this system may become dysfunctional in the obese state. See text for more details.