Search PubMed⌕ Search

Biomedical subjects

D E James

Publications and source records attributed to D E James.

At least 127 records · Page 7Linked to original sources
PubMed1984

The effect of exercise training on glycogen, glycogen synthase and phosphorylase in muscle and liver.

It is thought that exercise training in both man and the rat results in a protective effect against the depletion of carbohydrate stores during exercise (glycogen-sparing). However there has been no comprehensive study of the effects of training on glycogen anabolic and catabolic enzymes with liver or muscle. The aim of this study was to examine whether changes in these enzymes occur and whether these changes may provide an explanation for the glycogen-sparing which results from exercise training. Male rats were trained by a treadmill running program at three different workloads. In addition, there were three control groups: free eating (SF), food restricted (SR), and one SF with a single bout of exercise prior to sacrifice. Exercise training was associated with a 60-150% increase in glycogen synthase and phosphorylase and a 50-70% increase in glycogen content in soleus, an intermediate muscle, but not in extensor digitorum longus (EDL), a white muscle nor in liver. The increase in glycogen synthase and phosphorylase in intermediate muscle was proportional to the degree of training and there was a significant correlation between glycogen content, glycogen synthase, and phosphorylase activity in intermediate muscle. Cytochrome c oxidase activity, an indicator of respiratory capacity, increased 50% in gastrocnemius of trained rats and was significantly correlated with glycogen synthase and phosphorylase in soleus. These results indicate a significant effect of exercise training on glycogen anabolic and catabolic enzymes in intermediate muscle, with no significant effects in white muscle or liver. The changes do not provide an explanation for glycogen-sparing, but are consistent with improved capacity of intermediate muscle for rapid glycogen mobilisation and repletion.

Animals↗
PubMed1984

Effect of exercise training on whole-body insulin sensitivity and responsiveness.

Exercise training causes a decline in basal and glucose-stimulated plasma insulin levels and improves glucose tolerance. Furthermore evidence has been presented for effects on both insulin receptors and postreceptor events. However, it is unclear how these changes affect the in vivo dose-response relationship between insulin levels and whole-body glucose utilization. The aim was to examine the effect of exercise training on this relationship and distinguish between changes in insulin sensitivity and responsiveness. Euglycemic clamps were performed in trained (ET, running 1 h/day for 7 wk), sedentary (CON), and sedentary food-restricted ( SFR ) rats. ET rats showed no increase in maximal net glucose utilization in response to insulin (ET 29.5 +/- 0.6 vs. CON 28.2 +/- 1.5 mg X kg-1 X min-1, NS), whereas insulin sensitivity was increased as indicated by the insulin concentration causing half-maximal stimulation (ED50) (49 +/- 20 for ET and 133 +/- 30 mU/l for CON). Thus 7 wk of moderate exercise training resulted in a significant shift of whole-body insulin sensitivity to place ED50 well within the physiological range of insulin concentrations. This would undoubtedly result in improved glucose disposal in the postprandial state and emphasizes the potential benefit of exercise in obesity and type II diabetes.

Animals↗
PubMed1983

In vivo insulin sensitivity in the rat determined by euglycemic clamp.

Our aim was to develop the glucose clamp (GC) technique in the conscious rat for assessment of in vivo insulin sensitivity. A 2-h euglycemic GC could be performed in chronically cannulated rats using 625 microliter blood. Overnight-fasted rats were infused with porcine insulin (1.67 mU . kg-1 . h-1). Insulin levels of 41 +/- 2 (SE) mU/liter were produced in rats aged 91 +/- 4 days with a 60- to 120-min glucose infusion rate (GIR60-120) of 10.6 +/- 0.6 mg . kg-1 . min-1 (n = 9) during euglycemia. GIR60-120 was significantly (P less than 0.025) reduced in rats aged greater than 130 days (mean, 169 +/- 16 days) to 7.7 +/- 1.2 mg . kg-1 . min-1 (n = 7). Metabolic clearance rate of porcine insulin (46 +/- 3 ml . kg-1 . min-1) and GIR60-120 compared with plateau plasma insulin levels are higher than values reported in humans. The latter may be due to suppression of a higher basal hepatic glucose production or increased potency of porcine compared with native insulin. We conclude that the GC can be accomplished in the rat. When combined with tracer administration and subsequent killing, it should provide a quantitative in vivo measurement of insulin sensitivity in individual tissues.

Animals↗
PubMed1983

Effect of acute exercise and prolonged training on insulin response to intravenous glucose in vivo in rat.

Physical training causes hypoinsulinemia and enhanced insulin sensitivity. Insulin sensitivity is also enhanced by a single bout of exercise. However, changes in beta-cell responsiveness with acute exercise are ill defined. To clarify these relationships intravenous glucose tolerance tests were performed in 1) physically trained rats (3 different levels), 48 h after the last bout of exercise; 2) untrained rats, 0.5, 4, and 24 h after a single bout of exercise; or 3) sedentary control rats. The total area under the glucose-stimulated insulin response curve (GSIR) was negatively correlated with total distance run during training (r = -0.45, P less than 0.05), whereas glucose tolerance was improved (P less than 0.005 vs. controls) with intensive training. GSIR was suppressed by 38% (P less than 0.01 vs. controls) 0.5 h after a single bout of exercise. This effect persisted for 4 h but was not present after 24 h. These results indicate that a single bout of exercise induces suppression of GSIR which lasts less than 24 h. In contrast, physical training induces prolonged suppression (for at least 48 h) of GSIR, proportional to the intensity of training, and improved glucose tolerance.

Animals↗
PubMed1981

Insulin precipitation in artificial infusion devices.

Precipitation of insulin is a problem with mechanical insulin infusion devices. Therefore conditions affecting insulin precipitation have been studied in a recirculating system using a peristaltic pump. Acetate buffer favoured precipitation and a pH of 2, 3 or 8 resulted in no less (and often more) precipitation than a pH of 7 using either acetate of phosphate buffer. However, no precipitation occurred in a phosphate buffered neutral preparation after ten days of pumping through tubing pretreated with EDTA. In comparison at pH 7, using acetate buffer with untreated tubing, more than 95% of insulin was precipitated in ten days. A heavy metal-insulin association appears to be a major factor in the precipitation. However, some formation of insulin fibrils is probable as the precipitate is autocatalytic and partially acid insoluble. Phosphate buffered highly purified porcine insulin is suitable for relatively prolonged infusion if metal ion contamination of the delivery system is minimised.

Buffers↗
PubMed1981

Rapid pulsatile corticosterone secretion in the rat is not confirmed.

We attempted to confirm and extend a previous suggestion by other workers that, in the rat, corticosterone may be released as a series of very short pulses with a period of one minute. We measured the corticosterone concentration in the blood of chronically cannulated, unanaesthetised male rats, repeatedly, at ten second intervals, for periods of up to 25 minutes while the rats were engaged in normal activity or sleep or were subject to acute or chronic stress. We could find no evidence of the proposed rapid pulsatile secretion and suggest that the earlier finding may have been artifactual.

Adrenal Glands↗