Chronic treatment with myo-inositol reduces white adipose tissue accretion and improves insulin sensitivity in female mice

J Nutr Biochem. 2013 Feb;24(2):457-66. doi: 10.1016/j.jnutbio.2012.01.008. Epub 2012 May 30.

Abstract

Type 2 diabetes is a complex disease characterized by a state of insulin resistance in peripheral tissues such as skeletal muscle, adipose tissue or liver. Some inositol isomers have been reported to possess insulin-mimetic activity and to be efficient in lowering blood glucose level. The aim of the present study was to assess in mice the metabolic effects of a chronic treatment with myo-inositol, the most common stereoisomer of inositol. Mice given myo-inositol treatment (0.9 or 1.2 mg g(-1) day(-1), 15 days, orally or intraperitoneally) exhibited an improved glucose tolerance due to a greater insulin sensitivity. Mice treated with myo-inositol exhibited a decreased white adipose tissue accretion (-33%, P<.005) compared with controls. The decrease in white adipose tissue deposition was due to a decrease in adipose cell volume (-33%, P<.05), while no change was noticed in total adipocyte number. In skeletal muscle, in vivo as well as ex vivo myo-inositol treatment increased protein kinase B/Akt phosphorylation under baseline and insulin-stimulated conditions, suggesting a synergistic action of myo-inositol treatment and insulin on proteins of the insulin signalling pathway. Myo-inositol could therefore constitute a viable nutritional strategy for the prevention and/or treatment of insulin resistance and type 2 diabetes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / drug effects
  • Adipose Tissue, White / cytology
  • Adipose Tissue, White / drug effects*
  • Administration, Oral
  • Animals
  • Female
  • Glucose Tolerance Test
  • Inositol / pharmacology*
  • Insulin / metabolism
  • Insulin Resistance* / physiology
  • Insulin Secretion
  • Mice
  • Muscle, Skeletal / drug effects
  • Oncogene Protein v-akt / metabolism
  • Phosphorylation / drug effects
  • Signal Transduction / drug effects

Substances

  • Insulin
  • Inositol
  • Oncogene Protein v-akt