Ascorbic acid metabolism in diabetes mellitus.
Competition for membrane transport between glucose and ascorbic acid (AA) has been shown in vitro in human lymphocytes, granulocytes, and fibroblasts. Therefore, we examined the effects of acute administration of i.v. glucose on AA levels in mononuclear (MNL) and polymorphonuclear leukocytes (PMN) and on leukocyte chemotaxis. Plasma glucose and AA, MNL AA, PMN AA, and chemotaxis by MNL and PMN were measured before and after i.v. glucose in fasted normal male volunteers. A decline in AA occurred in PMN as well as MNL, but decreases in AA induced acutely by transient hyperglycemia were not associated with changes in chemotaxis. However, under conditions of prolonged hyperglycemia maintained by a glucose clamp technique, significant changes (p less than 0.01) in chemotaxis by both PMN and MNL were observed after 210 and 240 min, with changes in chemotaxis to several chemoattractants significantly correlated with decreases in intracellular AA after 240 min (p less than 0.05). These results are consistent with the hypothesis that chronic hyperglycemia may be associated with intracellular deficits of leukocyte AA, an impaired acute inflammatory response, and altered susceptibility to infection and faulty wound repair in patients with diabetes.
D000328:Adult; D000368:Aged; D001205:Ascorbic Acid / Q000097:blood*; D001786:Blood Glucose / Q000378:metabolism; D002630:Chemotactic Factors / Q000494:pharmacology; D002634:Chemotaxis, Leukocyte; D003920:Diabetes Mellitus / Q000097:blood*; D005947:Glucose; D006801:Humans; D008214:Lymphocytes / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology; D009504:Neutrophils / Q000502:physiology
D001786:Blood Glucose; D002630:Chemotactic Factors; D005947:Glucose; D001205:Ascorbic Acid