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Acute exercise reduces insulin resistance‐induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice
Authors:Athos F Lima  Eduardo R Ropelle  José R Pauli  Dennys E Cintra  Marisa JS Frederico  Ricardo A Pinho  Lício A Velloso  Cláudio T De Souza
Institution:1. Universidade Cruzeiro do Sul, Unicsul, S?o Paulo, SP, Brazil;2. Departamento de Clínica Médica, FCM, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil;3. Curso de Educa??o Física—Modalidade Saúde, Departamento de Biociências, UNIFESP, Santos, SP, Brazil;4. Exercise Biochemistry and Physiology Laboratory, Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil
Abstract:TRB3 (a mammalian homolog of Drosophila) is emerging as an important player in the regulation of insulin signaling. TRB3 can directly bind to Ser/Thr protein kinase Akt, the major downstream kinase of insulin signaling. Conversely, physical exercise has been linked to improved glucose homeostasis and enhanced insulin sensitivity; however, the molecular mechanisms by which exercise improves glucose homeostasis, particularly in the hepatic tissue, are only partially known. Here, we demonstrate that acute exercise reduces fasting glucose in two models diabetic mice. Western blot analysis showed that 8 h after a swimming protocol, TRB3 expression was reduced in the hepatic tissue from diet‐induced obesity (Swiss) and leptin‐deficient (ob/ob) mice, when compared with respective control groups at rest. In parallel, there was an increase in insulin responsiveness in the canonical insulin‐signaling pathway in hepatic tissue from DIO and ob/ob mice after exercise. In addition, the PEPCK expression was reduced in the liver after the exercise protocol, suggesting that acute exercise diminished hepatic glucose production through insulin‐signaling restoration. Thus, these results provide new insights into the mechanism by which physical activity improves glucose homeostasis in type 2 diabetes. J. Cell. Physiol. 221: 92–97, 2009. © 2009 Wiley‐Liss, Inc
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