Modulation of hypothalamic S6K1 and S6K2 alters feeding behavior and systemic glucose metabolism

Author:

Tavares Mariana Rosolen12,Lemes Simone Ferreira2,de Fante Thais2,Saenz de Miera Cristina3,Pavan Isadora Carolina Betim12,Bezerra Rosangela Maria Neves1,Prada Patricia Oliveira4,Torsoni Marcio Alberto2,Elias Carol Fuzeti3,Simabuco Fernando Moreira12

Affiliation:

1. 1Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

2. 2Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

3. 4Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, USA

4. 3Laboratory of Molecular Research in Obesity (LABIMO), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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.

Publisher

Bioscientifica

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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