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Biomedical subjects

J C Shipp

Publications and source records attributed to J C Shipp.

At least 37 records · Page 2Linked to original sources
PubMed1977

Accumulation of myocardial triglycerides ketotic diabetes; evidence for increased biosynthesis.

The accumulation of triglycerides in the myocardium of nonketotic and overtly ketotic diabetic rats was studied. There was no increase in heart triglycerides of nonketotic rats taken off insulin treatment, although the rats exhibited several indices of diabetes. In nonketotic diabetic rats untreated with insulin, myocardial triglycerides repeatedly increased and declined to control levels. In severely ketotic rats, heart triglycerides increased about threefold and did not decline with time. In order to understand the mechanism of increase in myocardial triglycerides in ketotic diabetes, the biosynthesis of triglycerides was studied with heart homogenates. The total esterification of sn-glycero-3-phosphate was unaltered, but the synthesis of diglycerides and triglycerides was increased in the myocardium of the ketotic rat. On treatment of the diabetic rats with insulin, the synthesis of di- and triglycerides in heart homogenates reverted to control values. Thus the results of the present study demonstrate that (1) a persistent increase in myocardial triglyceride content was observed only in the ketotic diabetic rat and (2) increased synthesis of triglycerides is a factor in its accumulation in the myocardium of the ketotic rat.

Animals↗
PubMed1976

Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes.

Significant alterations in heart carbohydrate and lipid metabolism are present 48 h after intravenous injection of alloxan (60 mg/kg) in rats. It has been suggested that uncoupling of oxidative phosphorylation occurs in the alloxanized rat heart in vivo, whereas normal oxidative metabolism has been demonstrated in alloxan-diabetic rat hearts perfused in vitro under conditions of adequate oxygen delivery. We examined the hypothesis that high-energy phosphate metabolism might be adversely affected in the alloxan-diabetic rat heart in vivo. Phosphocreatine and ATP were reduced by 58 and 45%, respectively (P is less than 0.001). Also, oxygen-dissociation curves were shifted to the left by 4 mmHg, and the rate of oxygen release from blood was reduced by 21% (P is less than 0.01). Insulin administration normalized heart high-energy phosphate compounds. ATP production was accelerated in diabetic hearts perfused in vitro with a well-oxygenated buffer. These studies support the hypothesis that oxidative ATP production in the alloxan-diabetic rat heart is reduced and suggest that decreased oxygen delivery may have a regulatory role in the oxidative metabolism of the diabetic rat heart.

Adenosine Diphosphate↗
PubMed1975

Effects of catecholamines on myocardial endogenous substrates and contractility.

The effects of epinephrine and norepinephrine on triglyceride and glycogen metabolism and contractility were studied in isolated perfused working rat hearts. Hearts with lipids prelabeled in vivo with [1-14C]palmitate were perfused with bicarbonate buffer containing 5.5 mM glucose, with or without 0.6 mM palmitate (3% albumin), and varying concentrations of catecholamines. Direct evidence for catecholamine-stimulated myocardial triglyceride lipolysis was obtained and, for the first time, was shown to be concentration-dependent. Also, catecholamines enhanced heart triglyceride fatty acid oxidation in concentration-dependent fashion. Stimulation of lipolysis and oxidation was observed only in hearts perfused with buffer containing glucose as the sole substrate, and was inhibited in the presence of 0.6 mM palmitate. Palmitate inhibited net glycogenolysis in the absence of catecholamines, but had little effect on epinephrine-stimulated glycogenolysis. Therefore, with free fatty acids present, mobilization of endogenous triglycerides to meet the increased metabolic demands of catecholamine stimulation is minimized; this is due, possibly, to enhanced utilization of exogenous free fatty acids and to inhibition of net lipolysis.

Animals↗
PubMed1975

Utilization of endogenous lipids and glycogen in the perfused rat heart: effects of hypoxia and epinephrine.

The interaction of hypoxia and catecholamines in the regulation of heart tissue lipid and glycogen utilization was studied in isolated perfused rat hearts with lipids prelabeled in vivo with [1-14C]palmitate. In well oxygenated hearts, epinephrine stimulated triglyceride mobilization by approximately 2-fold. In hypoxia, net mobilization of triglycerides was negligible with or without added epinephrine. Thus, the effect of hypoxia to reduce triglyceride mobilization would favor the accumulation of neutral lipid in the myocardium Glycogenolysis was markedly enhanced in hypoxic hearts and epinephrine produced little further stimulation. In well oxygenated hearts, epinephrine increased glycogen mobilization by 3-fold.

Animals↗