We previously reported that a chronic supplementation with myo-
inositol (MI) improved
insulin sensitivity and reduced fat accretion in mice. We then tested the potency of such dietary intervention in the prevention of
insulin resistance in C57BL/6 male mouse fed a high-fat diet (HFD). In addition, some abnormalities in
inositol metabolism were reported to be associated with
insulin resistance in several animal and human studies. We then investigated the presence of such anomalies (i.e. inosituria and an
inositol intra-tissue depletion) in this diet-induced
obesity (DIO) mouse model, as well as the potential benefit of a MI supplementation for
inositol intra-tissue deficiency correction. HFD (60 % energy from fat) feeding was associated with inosituria and
inositol intra-tissue depletion in the liver and kidneys. MI supplementation (0·58 mg/g per d) restored
inositol pools in kidneys (partially) and liver (fully). HFD feeding for 4 months induced ectopic
lipid redistribution to liver and muscles, fasting hyperglycaemia and hyperinsulinaemia,
insulin resistance and
obesity that were not prevented by MI supplementation, despite a significant improvement in
insulin sensitivity parameter K
insulin tolerance test and a reduction in white adipose tissue (WAT) mass ( - 17 %, P< 0·05). MI supplementation significantly reduced
fatty acid synthase activity in epididymal WAT, which might explain its beneficial, but modest, effect on WAT accretion in HFD-fed mice. Finally, we found some abnormalities in
inositol metabolism in association with a diabetic phenotype (i.e.
insulin resistance and fasting hyperglycaemia) in a DIO mouse model. Dietary MI supplementation was efficient in the prevention of
inositol intra-tissue depletion, but did not prevent
insulin resistance or
obesity efficiently in this mouse model.