- 10-19-2011, 07:07 PM
"In spite of our progress in understandingleptin resistance and obesity, critical questions remainunanswered. In particular, how does elevated leptin lead toleptin resistance? Although both leptin receptors and leptin
signaling are down regulated by chronically elevated leptin,the degree of down-regulation of either component isinsufficient to account for largely absent leptin responses.Could selective leptin resistance in the CNS explain thisdiscrepancy? Emerging evidence suggests that leptinsignaling is preferentially reduced in the arcuate nucleus ofthe hypothalamus and not in other regions such as theventromedial, dorsomedial and/or premammilary nucleusof the hypothalamus that also express leptin receptors (49).By what mechanism(s) is the leptin resistance prevented inthese other nuclei? If we can understand the nature ofleptin resistance and develop new ways to reverse thatresistance, we can unleash the potent fat reducing potentialof leptin, and leptin may once again referred to as the “antiobesityhormone”.
A study from 2007 kinda articulates difference between circulating vs ARC nucleus levels in modulation of adiposy.
These datademonstrate that chronic vanadium administrationenhances the weight-reducing effects of centrallyadministered leptin in lean animals. The underlying
mechanism appears to involve enhanced hypothalamicleptin signal transduction.
- 10-19-2011, 07:19 PM
- 10-19-2011, 07:44 PM
10-20-2011, 05:27 PM
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