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By decreasing the ability of circulating leptin to enter brain interstitial fluid, where it can bind to neuronal leptin receptors, impaired leptin transport across endothelial cells of the blood–brain barrier is one potential mechanism. Several studies indicate that, like insulin9, leptinuptakeintothebrainisfacilitatedbyleptinreceptorsexpressedby endothelial cells35 in the blood–brain barrier that function as leptin transporters. Whether dysfunction of this transport process can lead to obesity remains to be determined, but the finding that obese humans have leptin levels in cerebrospinal fluid that are low in comparison to plasma36 is consistent with this possibility.
Reduced leptin-receptor signal transduction is another potential cause of leptin resistance. This has been documented not only in the brain of rodents bearing mutant leptin receptors, but also as an acquired response to leptin-receptor activation. Like some other cytokine receptors, activation of the leptin receptor induces expression of a protein that inhibits further leptin signal transduction, termed ‘suppressor of cytokine signalling-3’ (SOCS-3)37. The potential contribution of SOCS-3 to acquired forms of leptin resistance and obesity is an active area of study.
Upon activation of leptin receptors in the brain, a series of integrated neuronal responses is probably required for food intake and energy balance to be affected. Failure of one or more neuronal systems in this circuit to respond to the leptin signal will therefore manifestasleptinresistance.Thekeyrolethattheseneuronaleffector pathways have in energy homeostasis makes them an important priority for study and is the focus of the following discussion.
Neuropeptide effectors of adiposity signals
Several distinct hypothalamic neuropeptide-containing pathways have emerged as candidate mediators of leptin and insulin action in the CNS (Table 1).
Neuropeptide Y stimulates food intake