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Low salt intake modulates insulin signaling, JNK activity and IRS-1^ser307 phosphorylation in rat tissues

Patrícia Oliveira Prada

Patrícia Oliveira Prada Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Michella Soares Coelho

Michella Soares Coelho Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Henrique Gottardello Zecchin

Henrique Gottardello Zecchin Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Miriam Sterman Dolnikoff

Miriam Sterman Dolnikoff Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Alessandra Lia Gasparetti

Alessandra Lia Gasparetti Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Luzia Naôko Shinohara Furukawa

Luzia Naôko Shinohara Furukawa Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Mario José Abdalla Saad

Mario José Abdalla Saad Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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Joel Claudio Heimann

Joel Claudio Heimann Departamento de Clínica Médica da Universidade Estadual de Campinas, Campinas, Brazil
Departamento de Farmacologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil
Departamento de Clínica Médica, Divisão de Nefrologia, Laboratório de Hipertensão Experimental da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

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A severe restriction of sodium chloride intake has been associated with insulin resistance and obesity. The molecular mechanisms by which the low salt diet (LS) can induce insulin resistance have not yet been established. The c-jun N-terminal kinase (JNK) activity has been involved in the pathophysiology of obesity and induces insulin resistance by increasing inhibitory IRS-1^ser307 phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1^ser307 phophorylation in liver, muscle and adipose tissue by immunoprecipitation and immunoblotting in rats fed with LS or normal salt diet (NS) during 9 weeks. LS increased body weight, visceral adiposity, blood glucose and plasma insulin levels, induced insulin resistance and did not change blood pressure. In LS rats a decrease in PI3-K/Akt was observed in liver and muscle and an increase in this pathway was seen in adipose tissue. JNK activity and IRS-1^ser307 phosphorylation were higher in insulin-resistant tissues. In summary, the insulin resistance, induced by LS, is tissue-specific and is accompanied by activation of JNK and IRS-1^ser307 phosphorylation. The impairment of the insulin signaling in these tissues, but not in adipose tissue, may lead to increased adiposity and insulin resistance in LS rats.

Article Type:: Research Article

DOI:: https://doi.org/10.1677/joe.1.06028

Volume/Issue:: Volume 185: Issue 3

Free access

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

Mariana Rosolen Tavares

Mariana Rosolen Tavares Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil
Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Simone Ferreira Lemes

Simone Ferreira Lemes Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Thais de Fante

Thais de Fante Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Cristina Saenz de Miera

Cristina Saenz de Miera Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, USA

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Isadora Carolina Betim Pavan

Isadora Carolina Betim Pavan Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil
Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Rosangela Maria Neves Bezerra

Rosangela Maria Neves Bezerra Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Patricia Oliveira Prada

Patricia Oliveira Prada Laboratory of Molecular Research in Obesity (LABIMO), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Marcio Alberto Torsoni

Marcio Alberto Torsoni Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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Carol Fuzeti Elias

Carol Fuzeti Elias Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, USA

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Fernando Moreira Simabuco

Fernando Moreira Simabuco Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil
Laboratory of Metabolic Disorders (LABDIME), School of Applied Sciences (FCA), University of Campinas (UNICAMP), Limeira, São Paulo, Brazil

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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.