Leptin actions/effects

The answer is A. Recent research has revealed that excess visceral fat deposits secrete several factors that have direct effects on the brain as well as directly on muscle to produce peripheral insulin resistance. Some of these newly identified factors are leptin, re-sistin, and adiponectin, whose mechanisms of action are still under active investigation. Death of pancreatic beta cells is a hallmark feature of type 1 diabetes and may occur only in very advanced stages of type 2 diabetes. Excess adipose in the thighs and buttocks does not contribute as strongly to insulin resistance as does visceral fat, presumably due to a lower level of endocrine activity of such fat depots. Dysfunction of liver lipid metabolism is more a consequence of excess activity of adipose than a cause of insulin resistance. A sedentary lifestyle contributes to build-up of excess fat stores but does not act directly to induce insulin resistance. 

Villarreal D, Reams G, Freeman RH. Effects of renal denervation on the sodium excretory actions of leptin in hypertensive rats. Kidney Int. 2000 58 989-994. 

Cardiovascular Actions of Leptin Effect on Cardiomyocyte Function... 

The precise mechanism of action of CNTF in the promotion of weight loss has not been defined, but its effects appear to be mediated by various hypothalamic pathways. The weight loss from a low dose of CNTF in rodents and humans does not appear to be caused by cachectic cytokines such as interleukin-1 because no muscle wasting was observed in the CNTF-treated groups. CNTF may mediate some of its effects by coupling to downstream signaling events in the leptin pathway. In a diet-induced model of obesity, CNTF, but not leptin, was shown to stimulate phosphorylation of the cytoplasmic transcription factor... 

Alternatively, improved insulin sensitivity and lowered blood glucose with these agents in treatment of NIDDM may be an indirect effect of their action on adipose tissue. Signaling through a number of adipocyte-derived factors, including TNF-a (168), leptin (169-172), resistin (172)and adiponectin (173), is altered by PPARy activation in ways that could lead to... 

Leptin, in 10 mM glucose, opens the KATP channel and inhibits VMH GE neurons (Spanswick et ak, 1997). However, we found that the same concentration of leptin (10 nM) used here opened the KATP channel and inhibited VMN GE neurons in 2.5 mM glucose (Wang et al., 2004). However, in the presence of 2.5 or 0.1 mM glucose, leptin did not alter the action potential frequency of ARC GE neurons. Although leptin had no effect on ARC GE neurons, insulin did modulate their activity in a glucose-dependent fashion (Wang et ak, 2004). We previously showed that insulin in the presence of... 

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