se involves progressive muscle degeneration until death at about 20 years of age, usually caused by cardiorespiratory events^(^[@ref3]^)^. For researching new therapies to improve the quality of life or discover an effective treatment for those affected by this disease, the use of animal models has major importance^(^[@ref4]^)^.

There are many animal models for studying DMD, among them, the MDX mouse and the golden retriever muscular dystrophy (GRMD) dog; however, the GRMD dog is the most appropriate^(^[@ref5]^)^ because, like in humans, it is a spontaneously occurring disease that progressively causes degeneration of muscle fibres^(^[@ref6]^)^.

Additionally, adult GRMD dogs show phenotypic characteristics similar to boys affected by DMD, such as decreased body weight and muscle quantity^(^[@ref7]^)^, differently from the mice, where the phenotype is different from the human phenotype of the same disease^(^[@ref8]^)^.

Muscle atrophy is frequently observed in patients with insulin deficiency, which leads to decreased rate of protein synthesis in skeletal muscle^(^[@ref9]^,^[@ref10]^)^. Skeletal muscle is also responsible for approximately 40 % of the total body mass and plays a major role in energy balance, since it stimulates the uptake, disposal and storage of glucose^(^[@ref11]^)^.

Glucose is the main energy source for cells, which may be obtained directly from the food or converted from other metabolites through gluconeogenesis^(^[@ref12]^)^. In single-stomached animals like dogs, dietary starches are hydrolysed enzymically in the gastrointestinal tract and the resulting glucose is absorbed and transported to the liver where the processes of glycolysis (postprandial conditions) or gluconeogenesis (fasting conditions) occur. The metabolic activities of this tissue, along with the hormonal signalling of glucagon and insulin released by α and β cells of pancreas, respectively, effectively regulate blood glucose homeostasis^(^[@ref13]^)^.

The values of plasma glucose concentrations are used as indicators o