Effects of oral vanadyl treatment on diabetes-induced alterations in the heart GLUT-4 transporter.

Vanadyl sulfate was administered orally during a 10-week trial period to streptozotocin-diabetic and control male rats to test the hypothesis that chronic vanadyl supplementation would prevent the decline in cardiac muscle cell glucose transporter protein (GLUT-4) that otherwise manifests in conjunction with insulin deficiency. Isolated cardiac myocytes and cardiac sarcolemmal vesicles were prepared from heart tissue of rats that had been maintained on the following regimens: untreated control, oral vanadyl-supplemented control (0.6 mg/ml), untreated diabetic (streptozotocin-induced; 60 mg/kg), and vanadyl-supplemented diabetic. Myocytes isolated from untreated diabetic rat hearts had decreased rates of glucose oxidation. Chronic, oral administration of vanadyl to diabetic rats maintained glucose oxidation rates of cardiac myocytes at control levels. Immunoblot analyses revealed that total cardiac myocyte and sarcolemmal GLUT-4 glucose transporter protein levels were significantly lower in the diabetic group relative to control. Vanadyl treatment of diabetic rats produced a normalization of both sarcolemmal GLUT-4 and total cardiac myocyte levels towards control levels. The reduction of GLUT-4 mRNA levels seen with untreated diabetes was also completely prevented with vanadyl treatment. These results demonstrate that chronic-oral vanadyl sulfate supplementation limits the decline in glucose oxidative capacity of cardiac myocytes that otherwise manifests in the untreated diabetic state. This action of vanadyl may occur via a mechanism that is linked to the preservation of sarcolemmal GLUT-4 protein levels.

Substrate-dependent alteration in O2 consumption and energy metabolism in vascular smooth muscle.

Energy metabolism and the substrate utilization pattern of intact porcine carotid artery were investigated in the presence or absence of glucose and/or octanoate during the phases of isometric contraction induced by K+ depolarization. During the early phase of contraction, there was a rapid increase in the rate of O2 uptake that was independent of the rate of force generation but dependent on the availability of intracellular pyruvate, the source of which was glucose and not glycogen. Lactate production increased linearly from the onset of contractile stimulation and was not suppressed by octanoate oxidation. There was no alteration from the basal resting state in the concentrations of the metabolites of the tricarboxylic acid cycle in the presence or absence of octanoate. During the phase of steady-state force maintenance, O2 consumption was increased compared with the basal unstimulated rate but was not increased when glucose and octanoate were present, which is consistent with the Crabtree effect. This was associated with increased aerobic lactic acid production and inhibition of the tricarboxylic acid cycle at the citrate synthase step. Alteration of the high-energy phosphate content could not account for the pattern of O2 consumption during contraction under different substrate conditions. In the absence of glucose, the energy from octanoate oxidation could substitute for the energy ordinarily derived from aerobic glycogen and lactic acid production. It is concluded that energy metabolism of vascular smooth muscle is coordinated during contraction by integration of the pathways of aerobic glycolysis and oxidative phosphorylation.

The antiadrenergic effect of cyclopentyladenosine on myocardial contractility is reduced in vivo in diabetic rats.

The aim of this study was to test the hypothesis that the antiadrenergic action of adenosine is reduced in diabetes. This was determined by evaluating the effect of experimental diabetes mellitus on the in vivo myocardial antiadrenergic action of cyclopentyladenosine, and adenosine A1-receptor agonist. Changes in heart rate and ventricular performance in response to infusion of dobutamine, a beta 1-adrenergic agonist, were determined in the absence and presence of cyclopentyladenosine, in anesthetized, 10- to 12-week male diabetic (60 mg/kg streptozotocin), insulin-treated diabetic and control rats. Intravenous dobutamine (16 micrograms/kg) increased +dP/dtmax and -dP/dtmax in control rats from 7,706 +/- 553 and 5,449 +/- 403 mmHg/s (1 mmHg = 133.3 Pa) to 19,170 +/- 465 and 8,855 +/- 317 mmHg/s, respectively. In diabetic rats dobutamine increased +dP/dtmax and -dP/dtmax from 5,733 +/- 541 and 4,016 +/- 426 to 15,015 +/- 1,521 and 7,039 +/- 809 mmHg/s, respectively. Cyclopentyladenosine significantly attenuated dobutamine-stimulated increases in +dP/dtmax and -dP/dtmax in both control and diabetic rats in a dose-dependent (0.1-3.0 micrograms/kg) manner. Cyclopentyladenosine potency to attenuate dobutamine-enhanced +dP/dtmax was reduced significantly (p < 0.05) in diabetic rats compared with controls (ID50, 1.07 vs. 0.59 micrograms/kg, respectively) with no change in efficacy. The magnitude of cyclopentyladenosine inhibition of dobutamine-enhanced -dP/dtmax was greater in control than diabetic rats (81 vs. 54%, respectively), but ID50 values were not different. Insulin treatment of diabetic rats prevented the observed changes. These data suggest that the antiadrenergic action of adenosine is compromised in diabetes and that this may contribute to the development of diabetic cardiomyopathy.

Fatty acid, tricarboxylic acid cycle metabolites, and energy metabolism in vascular smooth muscle.

The influence of octanoate on O2 consumption, tricarboxylic acid (TCA) cycle intermediates, and high-energy phosphates was examined in intact resting porcine carotid artery to investigate the role of fatty acid in energy metabolism and its integration with glucose metabolism in vascular smooth muscle. Incubation of resting arteries with octanoate (0.5 mM), which was previously shown to inhibit aerobic glycolysis (6), inhibited lactate production by 64% and increased O2 consumption by 30%. The increase in O2 consumption with octanoate was approximately equal to that calculated to account for the ATP production lost by inhibition of aerobic lactate production by octanoate. In glucose-free medium, the level of high-energy phosphate was reduced but was restored when octanoate was included in the incubation medium. This was associated with an increase in O2 consumption. These results suggest that the energy requirements of resting carotid artery can be largely met by the oxidative metabolism of fatty acid. Octanoate induced anaplerosis of the TCA cycle, as indicated by a 70% increase in the level of citrate. Extracellular glucose was necessary for octanoate-induced anaplerosis, probably by providing the extra carbon via pyruvate carboxylation, whereas a coupled transamination involving aspartate was a less important anaplerotic mechanism.

Relation of glycosylated hemoglobin to in vivo cardiac function in response to dobutamine in spontaneously diabetic BB Wor rats.

The contribution of metabolic control to in vivo myocardial contractile function in response to beta 1-adrenergic stimulation was determined in the spontaneously diabetic BB Wor rat. The study involved a group of insulin-dependent BB Wor rats showing marked variations in metabolic control, assessed by the level of glycosylated hemoglobin (gHb). These diabetic BB rats were divided into moderate and severe (%gHb > 14), diabetic groups. A group of Wistar rats and diabetes-resistant BB Wor rats served as controls. In vivo myocardial contractile function was measured under basal conditions and after i.v. dobutamine infusions in anesthetized rats, using a catheter-tip pressure transducer inserted into the left ventricle. No dramatic differences in heart rate with dobutamine stimulation were observed between the moderate, severe diabetic, and diabetes-resistant groups. However, heart rate was lower in Wistar control rats compared with these groups. Systolic left ventricular pressure was depressed in severe diabetic rats compared with Wistar controls. In addition, positive dP/dt was significantly less in the severe diabetic group at the highest doses of stimulation, whereas negative dP/dt was depressed under basal conditions and remained so with increasing doses of dobutamine. In the diabetic group maximal systolic left ventricular pressure, rate-pressure product, and negative dP/dt responses to dobutamine were all inversely correlated with gHb. These results indicate that changes in metabolic control of the insulin-dependent BB diabetic rat can contribute to a depressed myocardial contractile function.

Metabolic compatibility of abattoir and human corneas: an ex vivo 31P nuclear magnetic resonance spectroscopic study of intact tissues.

This study establishes the metabolic similarities and differences of intact abattoir corneas and the human cornea ex vivo, using 31P nuclear magnetic resonance spectroscopy. Phosphorylated sugars (SP), inorganic orthophosphate (Pi), phosphodiesters, ATP, ADP, and the nucleoside diphosphosugars and dinucleotides (NS&DN) were quantitated. The intracorneal pH also was determined. In addition, metabolic indices ATP/Pi, ATP/ADP, ATP/(ADP + Pi), SP/Pi, the phosphorylation potential, and the 31P energy modulus were calculated. Significant differences were observed between the abattoir and human corneas in phosphorylated sugars, NS&DN, and intracorneal pH, as well as in the indices ATP/ADP and SP/Pi. The overall energy status as measured by the 31P energy modulus was significantly higher in the bovine cornea when compared to the porcine and human corneas, suggestive of a very high energy reserve in the bovine cornea.

Effects of anabolic steroids and endurance exercise on cardiac performance.

This study examined the effects of anabolic steroids and exhaustive endurance exercise, and the combination of both treatments on in vitro cardiac contractile function. Fifty-two male Sprague-Dawley rats were randomly assigned, in groups of 13, to one of the four groups: sedentary control (C), steroid-treated (ST), exercise-trained (E), and exercise plus steroid treated (E+S). Nandrolone decanoate was administered to the steroid-treated groups every 7-9 days during the 10 weeks study, while the C and E groups received glycerol injection on these occasions. The exercised rats ran on a treadmill wearing a collar weight (2-3% of body weight) for 50 min, 5 days a week. In vitro ventricular performance was assessed in isolated Langendorff perfused hearts in response to increasing left ventricular balloon volumes. Left ventricular +dP/dt, dP/dt at 60 mmHg developed pressure, tension time index, and Emax (slope of the pressure-volume curves) were significantly (p < 0.05) lowered in the E+S group, as compared to the C, E, or ST group. Meanwhile, the E group exhibited a higher (p < 0.05) left ventricular systolic pressure (LVSP) than the C and E+S groups. No significant differences in dP/dt/P, heart weight (wt), and heart wt to body wt ratio were detected among the four groups. Rats subjected to endurance exercise or anabolic steroid treatment alone exhibited no change in LV function.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dietary fish oil on cardiovascular responsiveness to adrenergic agonists in spontaneously hypertensive rat.

To test the hypothesis that dietary fish oil supplementation decrease systolic blood pressure in hypertensive rats by modifying cardiovascular responsiveness to adrenergic agonists, spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) received either a corn or fish oil diet, 5% (g/kg) for 10 weeks. Mean aortic pressure was lower in fish oil treated (161 +/- 7 mm Hg (1 mmHg = 133.3 Pa)) than corn oil treated (191 +/- 6 mmHg) SHR. Although dietary fish oil supplementation decreased responsiveness to norepinephrine in isolated thoracic aorta from SHR, there was no change in cardiovascular responsiveness to the beta 1 agonist dobutamine or the alpha 1 agonist phenylephrine when these adrenergic agonists were administered in vivo. However, dietary fish oil did decrease the spontaneous basal tone in aorta from both SHR and WKY. This study provides further evidence that dietary fish oil lowers blood pressure in an animal model genetically predisposed to hypertension. However, the mechanism for this decrease in mean aortic pressure in vivo does not appear to be related to modification of cardiovascular responsiveness to alpha 1- or beta 1-adrenergic agonists and may be related to a decrease in basal vasomotor tone.

Effects of exercise training and anabolic steroids on plantaris and soleus phospholipids: a 31P nuclear magnetic resonance study.

1. The purpose of this study was to examine the effect of exercise, anabolic steroid treatment, and a combination of both treatments on the phospholipid composition of predominantly fast twitch (plantaris) and slow twitch (soleus) skeletal muscles. The 4 experimental groups analyzed were sedentary control (C), steroid-treated (S), exercise-trained (E), and exercise plus steroid-treated (ES). 2. Among the 11 phospholipids quantitated, for the plantaris muscle, phosphatidylcholine was reduced in ES relative to C, while phosphatidylethanolamine and phosphatidylethanolamine plasmalogen were elevated in E and ES relative to C. For the soleus muscle, phosphatidylserine was reduced in S and E relative to C, and cardiolipin was elevated in E relative to C. 3. Of the 27 metabolic indices calculated for the plantaris, 15 changed significantly among E and ES relative to S and C, while for the soleus, only three indices changed among the four groups, two among E and ES relative to S and C and one between S and C. 4. For the plantaris muscle, the results are consistent with an exercise-induced alteration of membrane phospholipid composition that increases ion translocation activity. For the soleus muscle, this membrane alteration essentially does not take place. 5. Steroid treatment had little to no statistically significant effect on plantaris and soleus muscle phospholipid systems, regardless of the imposed regimen.

Cadmium-induced attenuation of coronary blood flow in the perfused rat heart.

The present studies were undertaken to test the hypothesis that cadmium alters myocardial metabolism, producing effects on coronary blood flow. Hearts isolated from adult, male Sprague-Dawley rats were control-equilibrated and then treated with Cd (0.1-100 microM). Myocardial O2 consumption (MVO2), lactate production, contractile activity, and coronary flow were determined at regular intervals. Parallel experiments were also performed in hearts administered 0.5 mM KCN to compare the effects of cadmium on myocardial lactate release with that of a known inhibitor of mitochondrial respiration. Coronary flow decreased significantly in response to Cd. This effect was dose-related (ED50 = 0.4 microM Cd), achieving maximal levels within the initial 5 min of exposure and persisting thereafter. Cd treatment also significantly decreased myocardial contractile activity [ED50 = 2.4 microM Cd (+dP/dt)] and MVO2 in a dose-dependent manner. This latter effect was time-dependent with an ED50 value of 2.1 microM at 5 min, as compared to a value of 0.5 microM Cd at 30 min. Lactate levels measured in the coronary effluent were unaffected by Cd treatment, except at the highest dose. Collectively, the results of this study failed to support a metabolic mechanism as the basis for the observed changes in coronary flow in response to cadmium administration. Instead, these results suggest an alternative hypothesis that Cd disturbs coronary flow via a mechanism involving direct actions on the coronary vasculature.

NMR spectroscopy study of heart phospholipids. An exercise and anabolic steroids effect.

Because 31P NMR spectral analysis of phospholipid (PL) is an accurate and rapid technique for resolving the quantity of PL resonances and involving minimum chemical manipulations that may affect the integrity of the tissue (24-26), we studied the effect of anabolic steroid injection, exercise training, or a combination of both treatments on whole heart phospholipids using 31P NMR spectral analysis. Male Sprague-Dawley rats were randomly assigned to 4 groups of 11 each: sedentary control (C), steroid-treated (ST), exercise-trained (E), and exercise plus steroid-treated (ES). The ST and ES rats were administered nandrolone decanoate by i.m. injection every 7-9 d during the 10 wk study, while the C and E rats were injected with glycerol. The exercise rats ran on a treadmill, wearing a collar weight for 50 min/day, 5 days/wk. There was a significant difference in body wt among the four groups at the conclusion of the study; however, no significant differences in heart wt or in the ratio of heart wt:body wt were observed among the four groups. Myocardial phospholipid profiles of the exercise-trained rats were significantly (p less than 0.05) different from those of the untrained rats. The changes were enhanced somewhat by the steroid treatment. The profiles differed in the relative amounts of four of the nine myocardial phospholipids detected: phosphatidylcholine, phosphatidylethanolamine (PE), PE plasmalogen, and phosphatidylserine. We conclude that the observed changes in whole heart phospholipid compositions are due to experimental treatment specifically from exhaustive exercise and not from anabolic steroids or cardiac hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential effects of fatty acids on glycolysis and glycogen metabolism in vascular smooth muscle.

The effects of fatty acids of different chain lengths on aerobic glycolysis, lactic acid production, glycogen metabolism and contractile function of vascular smooth muscle were investigated. Porcine carotid artery segments were treated with 50 microM iodoacetate and perchloric acid tissue extracts were then analyzed by 31P-NMR spectroscopy to observe the accumulation of phosphorylated glycolytic intermediates so that the activity of the Embden-Myerhof pathway could be tracked under various experimental paradigms. Aerobic glycolysis and lactate production in resting arteries were almost completely inhibited with 0.5 mM octanoate, partially inhibited with 0.5 mM acetate and unaffected by 0.5 mM palmitate. Inhibition of glycolysis by octanoate was not attributable to inhibition of glucose uptake or glucose phosphorylation. Basal glycogen synthesis was unchanged with palmitate and acetate, but was inhibited by 52% with octanoate incubation. The characteristic glycogenolysis which occurs upon isometric contraction with 80 mM KCl in the absence of fatty acid in the medium was not demonstrable in the presence of any of the fatty acids tested. Glycogen sparing was also demonstrable in norepinephrine contractions with octanoate and acetate, but not with palmitate. Additionally, norepinephrine-stimulated isometric contraction was associated with enhanced synthesis of glycogen amounting to 6-times the basal rate in medium containing octanoate. Contractile responses to norepinephrine were attenuated by 20% in media containing fatty acids. Thus, fatty acids significantly alter metabolism and contractility of vascular smooth muscle. Fatty acids of different chain lengths affect smooth muscle differentially; the pattern of substrate utilization during contraction depends on the contractile agonist and the fatty acid present in the medium.

Phosphorylase b kinase and phosphorylase a phosphatase activities in contracting vascular smooth muscle: stimulation by fatty acid.

The activities of phosphorylase b kinase and phosphorylase a phosphatase were determined during the phases of KCl-induced contraction in porcine carotid artery. Phosphorylase b kinase exhibited a biphasic pattern with activity increasing 70% above basal levels during the early phase of active force generation (45 s into contraction) followed by a decline in activity during the phase of steady-state tension maintenance. Phosphorylase a phosphatase was stimulated simultaneously with phosphorylase b kinase, with activity increasing 100% over basal levels at 45 s into contraction, but remaining elevated at 30 min. Incubation of arteries in 0.5 mM palmitate resulted in a 30% increase in basal activity of phosphorylase b kinase and 117% augmentation of basal phosphatase activity, with no further increase in activity of either enzyme with contraction. The results indicate that both the kinase and phosphatase are subject to regulation during contractile activation of the muscle, possibly by similar but not identical mechanisms.

Phosphatic metabolites, intracellular pH and free [Mg2+] in single, intact porcine carotid artery segments studied by 31P-NMR.

Superfused porcine carotid artery segments (approximately 7 cm lengths) were analyzed by 31P-NMR spectroscopic methods to characterize the 31P spectrum of arterial smooth muscle and to determine the influence of passive stretch (intraluminal pressurization, 95-100 mmHg) on cellular phosphatic metabolite levels, intracellular pH and free magnesium concentration ([Mg2+free]i). Equilibrated, single, intact arteries were studied under steady-state, constant flow conditions at 37 degrees C. Phosphoethanolamine, phosphocholine, inorganic phosphate (Pi), phosphocreatine (PCr) and nucleoside triphosphates (NTP), primarily ATP, were the principle metabolites detected in the 31P-NMR spectrum of intact arterial smooth muscle. The concentration of these metabolites and intracellular pH, as determined from the referenced chemical shift of Pi, were unaffected by pressurization. The PCr:Pi ratios determined for nonpressurized (flaccid) and pressurized arteries were 1.2 +/- 0.1 and 1.3 +/- 0.3, respectively. Intracellular pH averaged 7.02 +/- 0.02 (mean +/- 1 S.D.) for flaccid arteries vs. 7.03 +/- 0.05 for pressurized arteries. The upfield chemical shift of the beta-ATP peak, which has been described in other types of smooth muscle, was also observed in these experiments. Interestingly, pressurization significantly shifted the resonance position of this peak, which was interpreted to represent a change in [Mg2+free]i. The average [Mg2+free]i of flaccid artery preparations was computed to be 0.54 +/- 0.03 x 10(-3) M, as compared to 0.99 +/- 0.10 x 10(-3) M for pressurized arteries. This change in [Mg2+free]i was evident within the first hour following pressurization and persisted thereafter. These findings suggest that altering the resting length of vascular smooth muscle produces a change in [Mg2+free]i. This shift in free Mg2+ levels may act as a metabolic signal triggering a change in vascular smooth muscle metabolism, an effect which has been reported to occur in smooth muscle in response to stretch.

Effects of altering carbohydrate metabolism on energy status and contractile function of vascular smooth muscle.

Substrate-dependent changes in vascular smooth muscle energy metabolism and contractile function were investigated in isolated porcine carotid arteries. In media containing glucose glycogen catabolism accounted for all the estimated high-energy phosphate turnover that occurred in conjunction with contraction induced by 80 mM KCl. However, in glucose-free media glycogen catabolism accounted for only a portion of the estimated ATP utilization in resting and contracting arteries, even though glycogen stores were not depleted. The glycogenolysis and lactate production that ordinarily accompanies contraction was completely inhibited by 5 mM 2-deoxyglucose (2-DG). However, there was no decrease in the high-energy phosphate levels when compared to control resting arteries similarly treated with 2-DG. The results suggest that an endogenous non-carbohydrate source may be an important substrate for energy metabolism. Treatment of arteries with 50 microM iodoacetate (IA) in media containing glucose resulted in a marked reduction of high energy phosphate levels and an accumulation of phosphorylated glycolytic intermediates, as demonstrated by 31P-NMR spectroscopy. In glucose-free media, 50 microM IA had only a slight effect on high-energy phosphate levels, while glycogenolysis proceeded unhindered. With 1 mM IA in glucose-free media, the oxidative metabolism of glycogen was inhibited as evidenced by the depletion of high-energy phosphates and the appearance of sugar phosphates in the 31P-NMR spectra. Thus, the titration of enzyme systems with IA reveals a structural partitioning of carbohydrate metabolism, as suggested by previous studies.

Fatty acid alters glycogen metabolism in contracting vascular smooth muscle.

The purpose of this investigation was to study the effect of fatty acid on carbohydrate metabolism in contracting vascular smooth muscle. The glycogen content of porcine carotid artery incubated in media containing only glucose decreased markedly upon contraction with 80 mM KCl. In contrast, when 0.5 mM palmitate was included there was no decrease in glycogen. Furthermore, the maximal isometric force generated was 22% greater than in the absence of palmitate (P less than 0.001). Stimulation of glycogen phosphorylase a activity with contraction was also enhanced with palmitate. Palmitate had no effect on the levels of the high energy phosphates under any substrate condition. Thus, fatty acid profoundly affects glycogen metabolism and contractility in vascular smooth muscle.

Effects of ATP reduction on the pattern of force development and myosin light chain phosphorylation in intact arterial smooth muscle.

The effect of reduction of ATP content on phosphorylation of the 20 kDa light chain of myosin (MLC) and force development in intact carotid arterial smooth muscle was investigated. With reduction of ATP to 23% of control by treatment with 2-deoxyglucose there was reduction in basal, in peak and 30 min MLC phosphorylation during contraction (P less than 0.001). The rate of force development was reduced, but maximal force was the same as control. By treatment with 50 microM iodoacetate, the resting ATP content was unchanged but fell to 22% after 30 min contraction. Basal MLC phosphorylation was the same as control, but peak (P less than 0.001) and 30 min phosphorylation were lower (P less than 0.005), even though the rate and magnitude of force development were greater. The results indicate that neither rate nor magnitude of force development correlate with MLC phosphorylation. Basal and initial MLC phosphorylation may play a cooperative role in contractile function.

Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.

Because high barium concentrations (2-10 ppm) in human drinking water have been reported to be associated with elevated cardiovascular mortality, hypertension and other cardiovascular effects were sought in rats chronically exposed for 1-16 mo to drinking water containing 1, 10, or 100 ppm barium. From weaning, female Long-Evans rats were kept in a "low contamination" environment and fed a diet low in trace metals. Their drinking water was deionized, fortified with 5 essential trace metals, and either 0, 1, 10, or 100 ppm barium was added. Indirect systolic pressure of unanesthetized rats was measured in triplicate at 1, 2, 4, 8, 12, and 16 mo. Average systolic pressure increased significantly after exposure to 100 ppm barium for 1 mo or longer and after exposure to 10 ppm barium for 8 mo or longer. After 4 or 16 mo, barium exposure failed to alter organ weights or tissue concentrations of calcium, magnesium, sodium, or potassium; however, both 10 and 100 ppm barium resulted in significant increases in tissue barium. Rats exposed to 100 ppm Ba for 16 mo exhibited depressed rates of cardiac contraction and depressed electrical excitability in the heart. Hearts from these maximally exposed rats also had significantly lower ATP content and phosphorylation potential, as measured by 31P NMR spectroscopy. Although the barium-induced increase in the blood pressure of rats was modest, comparable mild hypertension in humans would have major health implications.

Species-dependent differences in ATP half-life of glucose deprived crystalline lens.

1. Significant differences were detected by 31P NMR spectroscopic techniques in the intrinsic rate of ATP hydrolysis by crystalline lenses from adult Macaca mulatta, Saimiri sciureus, Felis catus, Sus, Canis familiaris, Cavia rodentia and Oryctalagis cuniculus during exogenous glucose deprivation. 2. These differences were not attributable to differences in endogenous glycogen stores, and appear instead to emanate from comparative species differences in lenticular enzyme activities.

Improved postischemic recovery of cardiac pump function in exercised trained diabetic rats.

This study examined whether exercise training of diabetic rats (streptozocin, 55 mg/kg) would affect the ability of perfused hearts to recover pump function after 75 min of ischemia and 30 min of reperfusion. All hearts were perfused with buffer containing the diabetic plasma concentrations of glucose and free fatty acids. Four groups were studied: sedentary control, trained control, sedentary diabetic, and trained diabetic. Trained control and diabetic rats were exercised on a treadmill at 5% grade, 21 m/min, 90 min/day, 6 days/wk for 8 wk. Sedentary diabetics had significantly lower body weight and elevated plasma glucose, triacylglycerol, and cholesterol relative to both control groups. Hearts from this group exhibited depressed postischemic recovery of pump function during reperfusion. In contrast, trained diabetic rats exhibited significantly lower plasma levels of triacylglycerol and cholesterol relative to sedentary diabetics. The postischemic recovery of cardiac pump function was improved in hearts from trained diabetic rats relative to sedentary diabetics. Exercise training had no effect on control rats. These results suggest that exercise training produces an antihyperlipidemic effect in diabetic rats and improves the tolerance of the diabetic heart to ischemia.