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            <funder>This work was supported by INSERM and INSA-Lyon. M.L. CROZE, R.E. VELLA and L. HADJI were recipient for grants from the French "Ministère de la Recherche et de la Technologie".</funder>
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            <idno type="halRefHtml">&lt;i&gt;Journal of Nutritional Biochemistry&lt;/i&gt;, 2013, 24 (2), pp.457-66. &lt;a target="_blank" href="https://dx.doi.org/10.1016/j.jnutbio.2012.01.008"&gt;&amp;#x27E8;10.1016/j.jnutbio.2012.01.008&amp;#x27E9;&lt;/a&gt;</idno>
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                <term xml:lang="en">myo-inositol</term>
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                <term xml:lang="en">fat mas</term>
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              <p>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&lt;.005) compared with controls. The decrease in white adipose tissue deposition was due to a decrease in adipose cell volume (-33%, P&lt;.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.</p>
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