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.
Highlights
Adipose tissue, once seen as a mere passive reservoir for energy storage, today is considered a highly active endocrine and metabolic structure that react to over-nutrition with expansion and to energy deficit releasing lipids (Rutkowski et al, 2015)
These findings provide direct evidence of sympathetic discharge of nerves to interscapular BAT (IBAT) after PGE1 injection, supporting the hypothesis of a functional involvement of the ventromedial hypothalamus (VMH), a key structure in the control of sympathetic activity and food intake (Thornhill and Halvorson, 1994), as a consequence of the stimulatory effect of PGE1 upon the preoptic-anterior hypothalamus (PO/AH) (Thornhill and Halvorson, 1994)
We have briefly focused on the relationship between autonomic nervous system (ANS) and orexins in the control of body weight, according to the theory of the “thermoregulatory hypothesis” of food intake
Summary
Giovanni Messina 1, 2*†, Anna Valenzano 1 †, Fiorenzo Moscatelli 1, Monica Salerno 1, Antonio Lonigro 1, Teresa Esposito 2, Vincenzo Monda 2, Gaetano Corso 1, Antonietta Messina 2, Andrea Viggiano 3, Antonio I. 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 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, and by the increase or decrease of the sympathetic outflow to selected WAT depots, in response to different lipolytic requirements of these two conditions. 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
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