ABSTRACT
An in vivo response of glucose oxidation to growth hormone has been demonstrated. Hypophysectomized rats were found to oxidize glucose at rates significantly higher than normal rats. Treatment with growth hormone 1 h before injection of 14C-U-glucose, 14C-6-glucose, or 14C-1-glucose caused a return to a normal oxidation pattern. This acute response was independent of insulin action but clearly time-dependent since no change from untreated hypophysectomized rats appeared when growth hormone was given at various times prior to administration of labeled glucose. The response observed for 14C-6-glucose was comparable to that observed for 14C-1-glucose with regard to dynamics but differed with respect to total 14C recovered as 14CO2. The cumulative percent 14CO2 recovered from oxidation of 14C-6-glucose 1 h after growth hormone injection exceeded that recovered from oxidation of 14C-1-glucose. These results suggest a change in glucose oxidation by a route that cannot be explained solely by changes in either the hexose monophosphate or Embden-Meyerhof pathways.
Subject(s)
Glucose/metabolism , Growth Hormone/pharmacology , Pituitary Gland/physiology , Animals , Hypophysectomy , Insulin/pharmacology , Male , Oxidation-Reduction , Pyruvates/metabolism , Rats , Time Factors , Uridine Diphosphate Glucuronic Acid/metabolismABSTRACT
The rate of appearance of radioactive carbon dioxide after injection of 14C-U-glucose, 14C-3,4-glucose, 14C-1-pyruvate, 14C-2-pyruvate, and 14C-1-acetate was measured in untreated, insulin-treated, and bovine growth hormone (bGH)-treated rats and compared to the results obtained from normal rats. The CO2 specific activity (SA) curve obtained from normal rats (mean of four experiments) injected with 14C-U-glucose reached a maximum value of 487 in 50 min and fell exponentially to near zero levels by 5 h. In contrast, the curve for untreated diabetic rats reached a peak of 247 in 17 min. In normal rats, 75% of the injected 14C was recovered as CO2 in 5 h compared to recovery of 31% by diabetic rats. Daily administration of 2 U protamine zinc insulin (PZI)/100 g body weight to diabetic rats returned these measurements to normal levels. A single injection of 400 microgram bGH (1.5 USP U/mg) into each diabetic rat 2 h before the start of the experiment yielded an SA curve and a percent recovery value comparable to results found with insulin treatment. The chronology of the insulin-like effect of the bGH was pertinent since other time intervals (including chronic bGH treatment) produced no similarity. Experiments carried out with 14C-3,4-glucose, 14C-1-pyruvate, 14C-2-pyruvate, and 14C-1-acetate suggest that bGH affects the glycolytic pathway at some point between the phosphorylation of glucose and the formation of pyruvate.
Subject(s)
Diabetes Mellitus, Experimental/metabolism , Glucose/metabolism , Growth Hormone/pharmacology , Insulin/pharmacology , Acetates/metabolism , Animals , Blood Glucose/metabolism , Carbon Dioxide/metabolism , Cattle , Fatty Acids, Nonesterified/blood , Male , Pyruvates/metabolism , RatsABSTRACT
An in vivo response of ornithine decarboxylase activity to growth hormone has been demonstrated. In hypophysectomized rats, found to oxidize ornithine at rates comparable to those of normal rats, an acute treatment of growth hormone 4 hours before injection of L-ornithine-1-14C caused a 39% increase in the peak specific activity of carbon dioxide and a 24% increase in the 14CO2 recovered in 5 hours. However, response was not observed when growth hormone was administered chronically rather than acutely.
