Alloxan-induced hyperglycemia in rats is reduced by 16,16-dimethyl-PGE2.
Female rats were treated with subcutaneous 16,16-dimethyl-PGE2 (1-75 micrograms/kg) for 24, 18, and 0.5 h prior to and 6, 24, and 48 h after intravenous beta cell destruction. Protection was assessed by morphological examination of beta cells and the level of fasting hyperglycemia seen 72 h after alloxan treatment. Prostaglandin reduced the degree of alloxan-induced hyperglycemia in a dose-dependent fashion but had no demonstrable effect on morphological assessment of beta cell destruction. However, prostaglandin treatment by itself induced transient (0-2 h) hyperglycemia that could be correlated inversely with the level of fasting blood glucose observed 72 h after alloxan treatment. Administration of oral glucose, which mimics the prostaglandin-induced hyperglycemia, afforded protection against alloxan challenge comparable to that produced by the prostaglandin. Thus, it appears that reduction of alloxan-induced hyperglycemia by 16,16-dimethyl-PGE2 may be linked to the transient hyperglycemia produced prior to alloxan administration.
D015064:16,16-Dimethylprostaglandin E2 / Q000627:therapeutic use*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000473:pathology; D005260:Female; D005951:Glucose Tolerance Test; D007515:Islets of Langerhans / Q000473:pathology; D011459:Prostaglandins E, Synthetic / Q000627:therapeutic use*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D001786:Blood Glucose; D011459:Prostaglandins E, Synthetic; D015064:16,16-Dimethylprostaglandin E2