Glucose uptake and metabolism in the human brain during hypoglycaemia assessed by in vivo magnetic resonance
Marinette van der GraafBastiaan E. de GalanDennis W. J. KlompLaura M. ParkesCees J. TackArend Heerschap
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Human brain
Carbohydrate Metabolism
Objectives The aim of this study was to evaluate the effects of Hwanggi-tang on glucose digestion, uptake, and metabolism in murine C2C12 myotubes. Methods Hwanggi-tang was prepared according to the Dong-ui-bo-gam (âªæ±é«å¯¶éâ«) prescription by 70% ethanol extraction. The effect on glucose digestion was examined by determining the inhibitory effect of Hwanggi-tang on α-glucosidase activity. We also compared and verified the gene and protein expression of genes related to glucose uptake in C2C12 myotubes treated with Hwanggi-tang or insulin. Glucose metabolism was assessed by the expression levels of associated enzymes. Results Hwanggi-tang caused a dose-dependent inhibition of α-glucosidase activity, induced glucose uptake by activation of the PI3K/Akt/mTOR pathway in the insulin signaling pathway, and promoted glucose oxidation and β-oxidation. Conclusions Hwanggi-tang exerts an anti-diabetic effect on murine myotubes by inhibiting glucose digestion and inducing glucose uptake and consumption. Keywords: carbohydrate metabolism, diabetes mellitus, herbal medicine, skeletal muscle fiber
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Digestion
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The effect of insulin and cortisol on glucose metabolism of thymus lymphocytes from adrenalectomized rats was studied. The addition of 10-8 M insulin increased glucose uptake, lactate production and the production of 14CO2 from labeled glucose at an initial concentration of 1.1 mM. Insulin stimulation of glucose metabolism was antagonized by 10-6 M Cortisol, which inhibited glucose metabolism with or without insulin present.
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The ability of iodoacetate, mannoheptulose, and 3-O-methyl glucose to alter islet cell metabolism and glucose-stimulated insulin secretion was examined. A method for the sequential analysis of the releasing and fuel function of glucose in isolated islets was applied. Insulin release was measured by radioimmunoassay and the metabolism of glucose by determining the rate of tritiated water production from [5-3H]glucose and lactate accumulation. It was found that iodoacetate, in the range of 0.2-1.0 mM, inhibited the metabolism of glucose linearly while release was not blocked until metabolism was reduced by 30-40%. The KI for both processes, release and metabolism, was the same. Pyruvate did not protect against or reverse the effects of iodoacetate. Mannoheptulose inhibited both release and metabolism half-maximally at about 5 mM when 27.5 mM glucose was used as the stimulatory agent. A mannoheptulose-resistant component of glucose metabolism, amounting to 30% of the maximal rate was observed. 3-O-Methyl glucose had no effect on insulin release but reduced glucose utilization and lactate production from low glucose. The results are discussed in light of the two prevailing hypotheses explaining glucose induced insulin release, i.e., the receptor and the metabolism hypotheses.
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The purpose of this study was to attain a better understanding of how the adipocyte transports and metabolizes glucose with and without the influence of exercise training. Rates of 2-deoxyglucose and glucose oxidation, using [1-14C]-and [6-14C]glucose, were measured in adipocytes from exercise-trained and sedentary control female rats of the same age. The trained animals were exercised by swimming, 6 h/day, 5 days/wk for 10 wk. The fat cells of the sedentary rats were significantly larger (P less than 0.005) than the trained animals and had very low rates of glucose uptake and [1-14C]- and [6-14C]glucose oxidation. The adipocytes of the trained rats were very responsive to insulin with 2-deoxyglucose rates seven times higher than those of the control animals and [1-14C]- and [6-14C]-glucose oxidation rates 14- and 13-fold (respectively) larger than control values. Comparisons of the data from exercised animals to younger sedentary rats indicates that glucose oxidation remains normal in the adipocytes of the trained animals whereas glucose transport is greatly improved. If the older sedentary controls are compared to younger animals, it can be seen that as the cell enlarges it loses its ability to take up or metabolize glucose. The combination of a loss in glucose transporting capacity with cellular enlargement and an increase in glucose uptake with exercise training suggests that movement of glucose across the cell membrane may be a limiting factor in glucose utilization in fat cells.
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