Obesity-Related Metabolic Syndrome: Mechanisms of Sympathetic Overactivity

Table 1

Effects of insulin resistance, ghrelin, and some adipokines on endocrine and metabolic functions in the pathogenesis of the MetS.

	General effects	Effects on sympathetic nervous system	In vitro/animal studies (references)	Human studies (references)
Insulin resistance	Direct antinatriuretic action	(i) Its intracerebral administration increases sympathetic outflow; (ii) Induces sympathetic overactivity; (iii) Stimulates SNS to increase cardiac output	[46–50]	[39, 49, 56–58]
Leptin	(i) Levels correlate with adipose tissue mass; (ii) Satiating factor decreases food intake; (iii) Physiological regulation of feeding behavior trough hypothalamic receptors	Vasocontractile effect related to SNS activation	[90, 92, 95, 97, 103, 104, 109, 110]	[90, 91, 99, 100, 102, 107, 111]
NEFAs	Levels are increased in obesity and inversely correlated with insulin sensitivity	Induce a central activation of MNSA in lean subjects	[115–118]	[114, 119, 122]
Adiponectin	(i) Levels are inversely related to obesity, DM, and insulin resistant states; (ii) Ameliorates obesity-related hypertension		[127, 128, 132, 133]	[129, 131]
Ghrelin	(i) Its infusion decreases blood pressure and HR; (ii) Improves endothelial function; (iii) Promotes weight gain and increases appetite	Its infusion increases SNS activity	[136, 137, 141, 143]	[140, 142, 144]