Role of Autonomic Nervous System and Orexinergic System on Adipose Tissue

Abstract

Adipose tissue, defined as white adipose tissue (WAT) and brown adipose tissue (BAT), is a biological caloric reservoir; in response to over-nutrition it expands and, in response to energy deficit, it releases lipids. The WAT primarily stores energy as triglycerides, whereas BAT dissipates chemical energy as heat. In mammals, the BAT is a key site for heat production and an attractive target to promote weight loss. The autonomic nervous system (ANS) exerts a direct control at the cellular and molecular levels in adiposity. The sympathetic nervous system (SNS) provides a complex homeostatic control to specifically coordinate function and crosstalk of both fat pads, as indicated by the increase of the sympathetic outflow to BAT, in response to cold and high-fat diet, but also by the increase or decrease of the sympathetic outflow to selected WAT depots, in response to different lipolytic requirements of these two conditions. More recently, a role has been attributed to the parasympathetic nervous system (PNS) in modulating both adipose tissue insulin-mediated glucose uptake and fatty free acid (FFA) metabolism in an anabolic way and its endocrine function. The regulation of adipose tissue is unlikely to be limited to the autonomic control, since a number of signaling cytokines and neuropeptides play an important role, as well. In this review, we report some experimental evidences about the role played by both the ANS and orexins into different fat pads, related to food intake and energy expenditure, with a special emphasis on body weight status and fat mass (FM) content.

Keywords: adipose tissue; autonomic nervous system; body composition; orexin; thermogenesis.

Figure 1

A proposed model for action of central orexin on adipose tissue. LHA, lateral hypothalamic area; DMH, dorsomedial nucleus of the hypothalamus; PVN, paraventricular nucleus of the hypothalamus; LH, lateral hypothalamus; BAT, brown adipose tissue; WAT, white adipose tissue; SNS, sympathetic nervous system; UCP, uncoupling protein; EE, energy expenditure; FM, fat mass.

Figure 2

Cumulative changes in food intake, firing rate of nerves to interscapular brown adipose tissue (IBAT), IBAT and colonic temperatures. Food presentation at time 0. Intracerebroventricular injection of prostaglandin E-1 (PGE₁) or saline was made at time 0. Values are expressed as mean ± standard error.

Figure 3

Cumulative changes in food intake, temperature of interscapular brown adipose tissue (IBAT) and in core temperature. Food presentation at time 0. Intracerebroventricular injection of orexin or saline was made at time -6 h or time 0. Values are expressed as mean ± standard error.

Figure 4

A proposed model for the relationship between physical activity, resting energy expenditure, parasympathetic nervous system, and fat mass. REE, resting energy expenditure; PNS, parasympathetic nervous system; FM, fat mass.

Figure 5

Second order polynomial regression showing an inverted U-shaped relationship between percentage of body fat mass (FM) and low frequency power (LF) and high frequency power (HF).