Leptin, the satiety hormone produced by adipocytes, acts on which hypothalamic neurons to suppress appetite, and what is its primary intracellular signaling mechanism?

• A Acts on NPY/AgRP neurons via Gq-PLC-IP3 signaling to stimulate feeding behaviour
• B Acts on orexin neurons via cAMP-PKA to inhibit orexin release, reducing wakefulness and appetite
• C Acts directly on peripheral adipocytes via PPAR-gamma activation to reduce lipid storage
• D Acts on POMC/CART neurons via JAK2-STAT3 signaling, stimulating alpha-MSH production that activates MC4R to suppress appetite ✓

Explanation

Leptin binds leptin receptors (Ob-Rb) on hypothalamic neurons, primarily activating JAK2-STAT3 signaling. In POMC/CART neurons, leptin stimulates production of alpha-MSH (alpha-melanocyte stimulating hormone), which activates melanocortin-4 receptors (MC4R) on downstream neurons to suppress appetite and increase energy expenditure. Simultaneously, leptin inhibits NPY/AgRP neurons (which are orexigenic). Leptin deficiency causes severe early-onset obesity, as in Ob/Ob mice.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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