Acute exercise reduces insulin resistance-induced TRB3 expression and amelioration of the hepatic production of glucose in the liver of diabetic mice.

Full 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. Copyright 2009 Wiley-Liss, Inc.

Author information

Author/s: Lima, Athos F (AF); Ropelle, Eduardo R (ER); Pauli, José R (JR); Cintra, Dennys E (DE); Frederico, Marisa J S (MJ); Pinho, Ricardo A (RA); Velloso, Lício A (LA); De Souza, Cláudio T (CT);

Affiliation: Universidade Cruzeiro do Sul, Unicsul, São Paulo, SP, Brazil.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Journal of cellular physiology (J Cell Physiol), published in United States. (Language: eng)

Reference: 2009-Oct; vol 221 (issue 1) : pp 92-7

Dates: Created 2009/07/29; Completed 2009/08/28;

PMID: 19492410, status: MEDLINE (last retrieval date: 8/28/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Cell Cycle Proteins - metabolism
Diabetes Mellitus, Experimental - enzymology; metabolism; physiopathology
Diet
Fasting
Glucose - biosynthesis
Glycogen - metabolism
Insulin - metabolism
Insulin Resistance

Insulin Resistance
Liver - enzymology; metabolism; physiopathology
Male
Mice
Mice, Obese
Phosphoenolpyruvate Carboxykinase (ATP) - metabolism
Physical Conditioning, Animal
Proto-Oncogene Proteins c-akt - metabolism
Signal Transduction

Associated Chemicals: Cell Cycle Proteins (0) ; TRB3 protein, mouse (0) ; Insulin (11061-68-0) ; Glucose (50-99-7) ; Glycogen (9005-79-2) ; Proto-Oncogene Proteins c-akt (EC 2.7.1.37) ; Phosphoenolpyruvate Carboxykinase (ATP) (EC 4.1.1.49)

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