 authors. The reduced production of insulin and metabolic adaptations exhibited by these animals for maintenance of glucose homeostasis can partially explain the muscle catabolism, fatty infiltration and increased liver size. Note that this information has not been previously reported in the literature. Combining the results obtained by the present study and previous studies, we can hypothesise that there is fatty infiltration of the liver as a compensatory response to low insulin secretion. Possibly, the GMRD dogs may have increased protein turnover due to higher accumulation of fatty acids in the liver by activation of lipolysis and also by increased gluconeogenesis.

Regarding age, according to the National Research Council^(^[@ref24]^)^, there is no consensus about the influence of this parameter on carbohydrate metabolism. Strasser *et al.*^(^[@ref47]^)^ have already described a lower glucose tolerance resulting from lower tissue insulin responsiveness in geriatric compared with young adult dogs. However, Lowseth *et al.*^(^[@ref48]^)^ found no significant changes in blood glucose concentrations in beagle dogs aged 3 to 14 years.

At the same time, still according to the National Research Council^(^[@ref24]^)^, geriatric dogs are considered to be, at least, 7 years old for medium breeds. In our study, the maximum age of affected dogs was 6 years old (only two dogs), which means that concerns related to variations of metabolism between G2 and G3 (where there is difference between ages) do not apply to the present experiment.

Nishio *et al.*^(^[@ref49]^)^ observed in a correlational study that glucose concentration decreased with age and decrease in creatine kinase activity, i.e. with the progress of DMD. The NEFA and ketone body concentrations increased with decreasing glucose concentration.

The authors explain that muscle degeneration may result in depletion of substrates for gluconeogenesis. In the present study, however, the affected animals presented higher values of glucose compared with carriers and c