Acute exercise suppresses hypothalamic PTP1B protein level and improves insulin and leptin signaling in obese rats
Autor: | Vagner R. R. Silva, Eloize C Chiarreotto-Ropelle, Gustavo D. Pimentel, Luciana Santos Souza Pauli, Cláudio T. De Souza, P O Prada, Carlos K. Katashima, José Rodrigo Pauli, José B.C. Carvalheira, Eduardo Rochete Ropelle, Dennys E. Cintra, Paty K. Picardi |
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Rok vydání: | 2013 |
Předmět: |
Leptin
Male medicine.medical_specialty Physiology Endocrinology Diabetes and Metabolism medicine.medical_treatment Blotting Western Hypothalamus Mice Obese Inflammation Physical exercise chemistry.chemical_compound Mice Random Allocation Physiology (medical) Internal medicine Physical Conditioning Animal medicine Animals Insulin Obesity Rats Wistar Protein Tyrosine Phosphatase Non-Receptor Type 1 Leptin receptor business.industry Interleukin-6 digestive oral and skin physiology Tyrosine phosphorylation Immunohistochemistry Rats Specific Pathogen-Free Organisms Endocrinology chemistry Signal transduction medicine.symptom business Corticosterone hormones hormone substitutes and hormone antagonists Signal Transduction |
Zdroj: | American journal of physiology. Endocrinology and metabolism. 305(5) |
ISSN: | 1522-1555 |
Popis: | Hypothalamic inflammation is associated with insulin and leptin resistance, hyperphagia, and obesity. In this scenario, hypothalamic protein tyrosine phosphatase 1B (PTP1B) has emerged as the key phosphatase induced by inflammation that is responsible for the central insulin and leptin resistance. Here, we demonstrated that acute exercise reduced inflammation and PTP1B protein level/activity in the hypothalamus of obese rodents. Exercise disrupted the interaction between PTP1B with proteins involved in the early steps of insulin (IRβ and IRS-1) and leptin (JAK2) signaling, increased the tyrosine phosphorylation of these molecules, and restored the anorexigenic effects of insulin and leptin in obese rats. Interestingly, the anti-inflammatory action and the reduction of PTP1B activity mediated by exercise occurred in an interleukin-6 (IL-6)-dependent manner because exercise failed to reduce inflammation and PTP1B protein level after the disruption of hypothalamic-specific IL-6 action in obese rats. Conversely, intracerebroventricular administration of recombinant IL-6 reproduced the effects of exercise, improving hypothalamic insulin and leptin action by reducing the inflammatory signaling and PTP1B activity in obese rats at rest. Taken together, our study reports that physical exercise restores insulin and leptin signaling, at least in part, by reducing hypothalamic PTP1B protein level through the central anti-inflammatory response. |
Databáze: | OpenAIRE |
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