Alloxan-induced Diabetes (alloxan-induced + diabetes)

Distribution by Scientific Domains


Selected Abstracts


C-peptide constricts pancreatic islet arterioles in diabetic, but not normoglycaemic mice

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2008
Lina Nordquist
Abstract Background Pancreatic islet blood flow is regulated separately from that of the exocrine pancreas, and a consistent finding during impaired glucose tolerance is an increased blood perfusion. The aim of the present study was to investigate whether C-peptide affects pancreatic islet arterioles in normal and diabetic mice. Materials and Methods Control and diabetic C57-Bl mice were studied after 2 weeks of alloxan-induced diabetes. Islet arterioles were dissected and microperfused with Dulbecco's modified Eagle medium (DMEM) solution. The effect of luminal application of mouse C-peptide was investigated. Results C-peptide reduced the diameter of islet arterioles from diabetic mice (,10 ± 4%, P < 0.05) compared to base-line values, whilst arterioles from normoglycaemic animals did not respond to C-peptide (P = 0.2). Conclusion These findings suggest a role for C-peptide in the regulation of islet blood flow, especially during conditions with impaired glucose tolerance. Copyright © 2007 John Wiley & Sons, Ltd. [source]


The relationship between peripheral glucose utilisation and insulin sensitivity in the regulation of hepatic glucose production: studies in normal and alloxan-diabetic dogs

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2006
M. J. Christopher
Abstract Background Hepatic glucose overproduction (HGP) of diabetes could be primary or could occur in response to the metabolic needs of peripheral (skeletal muscle (SkM)) tissues. This question was tested in normal and diabetic dogs. Methods HGP, SkM glucose uptake (Rdtissue), metabolic clearance of glucose (MCRg) and glycolytic flux (GFexog), and SkM biopsies were measured in the same dogs before and after alloxan-induced diabetes. Normal dogs were exposed to (1) an extended 20-h fast, (2) low- and high-dose glucose infusions (GINF) at basal insulinaemia, and chronic diabetic dogs were exposed to (3) hyperglycaemia, (4) phlorizin-induced normoglycaemia, and (5) poor and good diabetic control. Results (1) Prolonged fast: HGP, Rdtissue, and GFexog fell in parallel (p < 0.05). (2) Low-dose GINF: plasma glucose, insulin, Rdtissue, MCRg, and GFexog were unchanged, but HGP fell by ,40%, paralleling the supplemental GINF. (3) High-dose GINF at basal insulin: plasma glucose doubled and synchronous changes in HGP, Rdtissue, MCRg, and GFexog occurred; ICglucose, G6P, and glycogen were unchanged. (4) Hyperglycaemic diabetes: HGP was raised (p < 0.05), matching urinary glucose loss (UGL) and decreased MCRg, and maintaining normal basal Rdtissue and GFexog. SkM ICglucose was increased and glycogen decreased (both p < 0.05). (5) Phlorizin-induced normoglycaemia in diabetic dogs: HGP rose, matching the increased UGL, while maintaining normal Rdtissue and GFexog. Intramuscular substrates normalised. (6) Whole body and SkM metabolism normalised with correction of the insulin resistance and good diabetic control. Conclusion HGP reflects whether SkM is in a state of relative glucose ,excess' or absolute/relative glucose ,deprivation'. Copyright © 2005 John Wiley & Sons, Ltd. [source]


Short-term effect of acarbose on specific intestinal disaccharidase activities and hyperglycaemia in CBA diabetic mice

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 7-8 2003
D. Jureti
Summary The purpose of this study was to examine the short-term effects of 75, 100 and 150 mg of acarbose mixed in 100 g standard laboratory chow on specific intestinal disaccharidase activities and on hyperglycaemia in diabetic CBA strain mice on standard diet. The small intestine was excised and divided into three segments, from pylorus to duodenum, and two equal lengths of the jejunum and ileum of control and diabetic mice with or without added acarbose. Specific maltase and sucrase activities were determined using maltose and sucrose as substrates respectively. Increased specific activities of maltase and sucrase were detected in the intestines of CBA mice on standard laboratory diet seven days after alloxan-induced diabetes. Feeding for 7 days with 75, 100 or 150 mg acarbose uniformly mixed in 100 g standard laboratory chow, induced a decrease in the specific maltase and sucrase activities, compared with diabetic mice on standard laboratory diet. Feeding with 75 mg acarbose mixed in 100 g standard laboratory chow caused a statistically significant decrease of maltase in the duodenum and of sucrase in duodenum and jejunum, without a antihyperglycaemic effect. Feeding with 100 or 150 mg caused statistically significant decreases in specific maltase and sucrase activities in duodenum, jejunum and ileum. An antihyperglycaemic effect was observed only in the group of diabetic mice fed with 100 mg acarbose. This indicates that the antihyperglycaemic effect of acarbose involves factors other than these, related only to its inhibitory effect on disaccharidase activities. [source]


The investigation of the ultrastructural neutrophil changes in alloxan-induced diabetes in rats: response to a chemotactic challenge

CELL BIOCHEMISTRY AND FUNCTION, Issue 2 2004
Nesrin Özsoy
Abstract Experimental diabetes is one of the most popular conditions in which to study the relation between neutrophil leukocyte activity and periodontal destruction. The aetiology of neutrophil dysfunction in the gingival tissue associated with diabetes has yet to be clarified. Diabetes in rats decreases neutrophil chemotactic activity in proportion to the severity of this systemic disorder. The present study was carried out to evaluate the relationship between the severity of diabetes and the neutrophil response to two chemotactic agents, and to correlate the observed neutrophil defects with the degree of diabetes. In this study two chemotactic agents, casein (0.2,,l, 2,mg,ml,1) or N-formylmethionylleucylphenylalanine (FMLP; 0.2,,l, 10,4,M), were placed into the gingival crevices of alloxan-induced diabetic rats. Gingival biopsies were taken 15,min later and then at 5-min intervals up to 45,min and investigated by electron microscopy. Adherence and migration were observed in the rats with moderate diabetes 30,min after the application of casein. There was chemotaxis after 35,min of administration of the peptide FMLP. By 40,min neutrophils with pyknotic nuclei were observed. At 45,min neutrophils with a decreased number of granules were present. As the severity of the diabetes increased, the neutrophils degenerated and were structurally distorted. In the rats which had alloxan-induced diabetes there was abnormal periodontal damage. This damage is thought to be related to dysfunctional neutrophils. These findings many contribute to an answer to the following question: why is there an apparent variability in the susceptibilty of periodontal breakdown in diabetics? Copyright © 2003 John Wiley & Sons, Ltd. [source]