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: Intestinal glucose uptake in normal, untreated and insulin-treated diabetic dogs. Author: Alada AR, Falokun PO, Oyebola DD. Journal: Afr J Med Med Sci; 2005 Jun; 34(2):147-56. PubMed ID: 16749339. Abstract: The study was carried out on fasted, anaesthetized diabetic and non-diabetic dogs. Diabetes was induced by i.v injection of alloxan (60 mg/kg). A vein draining a segment of the upper jejunum was cannulated for blood flow measurements, and blood samples were obtained for determination of glucose content of arterial and venous blood. Glucose uptake was calculated as the product of jejunal blood flow and arterio-venous glucose difference ((A-V) glucose. The results showed that following induction of diabetes, there were significant increases in jejunal blood flow, (A-V) glucose and jejunal glucose uptake when compared with non-diabetic dogs. For instance, the glucose uptake increased from 23.10+/-2.34 to 178.40+/-6.93 mg/min. When the diabetic dog was challenged with different doses of insulin (2.5, 5.0, 7.5, 10.0 iu/kg), the blood glucose levels and the intestinal glucose uptake decreased in a dose-dependent manner. In normal dogs, insulin administration caused negative glucose uptake at the lower dose (5.0 iu/ kg) while at the higher dose, 8.0 iu/kg, insulin caused just a transient negative glucose uptake. From the results, it was concluded that the small intestine increased its glucose uptake in response to the hyperglycemia in alloxan-induced diabetes and when the blood glucose was reduced with insulin the intestine also reduced its glucose uptake accordingly. The result of insulin administration in normal dogs suggests that glucose uptake by the gut cannot be explained on the basis of blood glucose concentration alone.[Abstract] [Full Text] [Related] [New Search]