Central insulin may up-regulate thyroid activity by suppressing neuropeptide Y release in the paraventricular nucleus.
Down-regulation of thyroid activity during underfeeding or diabetes - and upregulation during overfeeding - have not been adequately explained. Experimental findings suggest that hypothalamic secretion of thyrotropin releasing hormone (TRH) is modulated by feeding status; neuropeptide Y may be a key mediator of this modulation. I propose that insulin, acting centrally as a signal of carbohydrate availability, promotes TRH secretion by inhibiting release of neuropeptide Y in the paraventricular nucleus. This mechanism may contribute to the weight loss reported during administration of certain insulin-sensitizing agents, and observed during low-fat diets.
McCarty
M F
MF
Nutrition 21, San Diego, CA 92109, USA.
D000818:Animals; D003920:Diabetes Mellitus / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000502:physiology*; D008954:Models, Biological; D009478:Neuropeptide Y / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009748:Nutrition Disorders / Q000503:physiopathology; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology*; D013961:Thyroid Gland / Q000502:physiology* / Q000503:physiopathology; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism / Q000502:physiology
D007328:Insulin; D009478:Neuropeptide Y; D013973:Thyrotropin-Releasing Hormone