These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Dietary components and plasma insulin responses to fasting and refeeding in genetically obese hyperglycaemic (ob/ob) mice. Author: Flatt PR, Bailey CJ. Journal: Br J Nutr; 1984 May; 51(3):403-13. PubMed ID: 6372856. Abstract: To investigate the role of dietary components in the hyperinsulinaemia of the obese hyperglycaemic (ob/ob) syndrome, plasma insulin responses to fasting and refeeding were examined in Aston ob/ob mice supplied with standard diet, non-digestible-carbohydrate test food, and isoenergetic test foods from which either carbohydrate, protein or fat was omitted. During fasting, plasma insulin concentrations fell more rapidly and to a greater extent than plasma glucose. Refeeding the standard diet raised insulin concentrations above normal, associated with a 25% compensatory increase in food intake over 24 h. Test foods supplied to previously fed or fasted mice produced glucose responses consistent with the available carbohydrate content. Carbohydrate-free food (protein and fat) provided a small insulinotropic stimulus; the effect of protein-free food (carbohydrate and fat) was greater; and the combination of carbohydrate with protein (fat-free food) evoked a marked insulin response. In contrast, insulin concentrations declined in mice given the non-digestible-carbohydrate food. Consumption of the standard diet was increased after 24 h feeding non-digestible-carbohydrate food, but was unaffected by a 30 h fast initiated 54 h previously. These results demonstrate that hyperinsulinaemia in ob/ob mice is not merely triggered by the ingestion of bulk, but depends on the type of nutrient ingested. Dietary carbohydrate appears to be the major stimulus to the hyperinsulinaemia, with an important augmentation in the presence of protein. Since direct glucose stimulation of insulin release is defective in ob/ob mice, the hyperinsulinaemia must be mediated by increased activity of the enteroinsular axis.[Abstract] [Full Text] [Related] [New Search]