Insulin secretion and carbohydrate metabolism in experimental protein malnutrition.
In order to study the evolution of endocrine and metabolic changes in protein malnutrition, we created a replica of this human syndrome in a primate model. This model was free from stress factors like infestations, and infections and provided an opportunity to study the details more closely. Our results showed that definite endocrine and metabolic changes are established by six weeks of protein deprivation. The study demonstrated that protein deprivation results in decreased fasting blood glucose levels associated with diminution in fasting, and total insulin output when presented with a glucose load. There is also deterioration of carbohydrate tolerance. It is suggested that decreased fasting blood glucose is a consequence of impaired breakdown and/or depletion of glycogen stores, and hepatic dysfunction secondary to fatty infiltration. The exact cause of decrease in insulin output remains to be clearly elucidated. The carbohydrate intolerance is attributed to insulin lack, hepatic dysfunction and decreased glucose disposal consequent to protein deprivation.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D050260:Carbohydrate Metabolism; D004032:Diet; D004195:Disease Models, Animal; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D008253:Macaca mulatta; D011488:Protein Deficiency / Q000378:metabolism*; D011502:Protein-Energy Malnutrition / Q000378:metabolism*
D001786:Blood Glucose; D001798:Blood Proteins; D007328:Insulin