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Article Dans Une Revue Molecular and Cellular Endocrinology Année : 2012

Hypothalamic serotonin-insulin signaling cross-talk and alterations in a type 2 diabetic model.

Résumé

Serotonin and insulin are key regulators of homeostatic mechanisms in the hypothalamus. However, in type 2 diabetes, the hypothalamic responsiveness to serotonin is not clearly established. We used a diabetic model, the Goto Kakizaki (GK) rats, to explore insulin receptor expression, insulin and serotonin efficiency in the hypothalamus and liver by means of Akt phosphorylation. Insulin or dexfenfluramine (stimulator of serotonin) treatment induced Akt phosphorylation in Wistar rats but not in GK rats that exhibit down-regulated insulin receptor. Studies in a neuroblastoma cell line showed that serotonin-induced Akt phosphorylation is PI3-kinase dependent. Finally, in response to food intake, hypothalamic serotonin release was reduced in GK rats, indicating impaired responsiveness of this neurotransmitter. In conclusion, hypothalamic serotonin as insulin efficiency is impaired in diabetic GK rats. The insulin-serotonin cross-talk and impairment observed is one potential key modification in the brain during the onset of diabetes.

Dates et versions

hal-00720430 , version 1 (24-07-2012)

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Citer

Ioannis K. Papazoglou, Flavien Berthou, Nicolas Vicaire, Claude Rouch, Eirini M. Markaki, et al.. Hypothalamic serotonin-insulin signaling cross-talk and alterations in a type 2 diabetic model.. Molecular and Cellular Endocrinology, 2012, 350 (1), pp.136-44. ⟨10.1016/j.mce.2011.12.007⟩. ⟨hal-00720430⟩
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