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Modulation of hypothalamic S6K1 and S6K2 alters feeding behavior and systemic
glucose metabolism.
Authors Tavares MR, Lemes SF, de Fante T, Saenz de Miera C, Pavan ICB, Bezerra RMN,
Prada PO, Torsoni MA, Elias CF, Simabuco FM
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal The Journal of endocrinology
Year 2020
Date Published 1/1/2020
Volume : Pages 244 : 71 - 82
PubMed Reference 31557728
Abstract The mTOR/S6Ks signaling is one of the intracellular pathways important for
metabolic control, acting both peripherally and centrally. In the hypothalamus,
mTOR/S6Ks axis mediates the action of leptin and insulin and can modulate the
expression of neuropeptides. We analyzed the role of different S6Ks isoforms in
the hypothalamic regulation of metabolism. We observed decreased food intake and
decreased expression of agouti-related peptide (AgRP) following
intracerebroventricular (icv) injections of adenoviral-mediated overexpression
of three different S6Ks isoforms. Moreover, mice overexpressing p70-S6K1 in
undefined periventricular hypothalamic neurons presented changes in glucose
metabolism, as an increase in gluconeogenesis. To further evaluate the
hypothalamic role of a less-studied S6K isoform, p54-S6K2, we used a Cre-LoxP
approach to specifically overexpress it in AgRP neurons. Our findings
demonstrate the potential participation of S6K2 in AgRP neurons regulating
feeding behavior.


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