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  • Glucose transport  (2)
  • glycogen synthesis  (2)
  • in vivo glucose uptake  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 730 (1983), S. 49-56 
    ISSN: 0005-2736
    Keywords: (Rat diaphragm) ; Cytochalasin B ; Glucose transport ; Microsome ; Plasma membrane
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Glucose effects ; insulin effects ; glycogen synthesis ; glycogen degradation ; glycolytic intermediates ; hepatic glucose production
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of glucose and of insulin on hepatic glucose production and metabolism has been studied in fed anaesthetized rats during hyperinsulinaemic clamp combined with various steady state levels of glycaemia (6.8±0.1, 9.3±0.1, 11.8±0.1 mmol/l). Hepatic glucose production was measured using constant infusion of D-[6-3H] glucose. At the end of each clamp the liver was freeze clamped, and enzyme activities and metabolites were measured. Hepatic glucose production was totally suppressed in all the groups receiving insulin. In the group with steady-state normoglycaemia, the suppression of hepatic glucose production was accompanied by a decrease in the levels of glucose-6-phosphate, an increase in those of fructose 2,6-bisphosphate and glycolytic intermediates, but without change in glycogen level or glycogen synthase and phosphorylase. In contrast, in the groups with steady-state hyperglycaemia, phosphorylase a was inactivated, and glycogen synthase activated. Under these conditions, glucose-6-phosphate levels were also decreased and those of fructose 2,6-bisphosphate and glycolytic intermediates were higher than in the group with steady-state normoglycaemia. A slight drop in the level of cAMP was also observed which may contribute, with hyperglycaemia, to the inactivation of phosphorylase. Incorporation of tritiated water into liver glycogen paralleled the activation of glycogen synthase and the accumulation of glycogen. The data indicate that, at normoglycaemia, insulin may suppress hepatic glucose production by channeling glucose-6-phosphate into the glycolytic pathway; at higher levels of glycaemia, a decreased rate of glycogenolysis and an increased rate of glycogen synthesis due to phosphorylase a inactivation and synthase activation may contribute to the decreased level of glucose-6-phosphate, and to a sparing and a net synthesis of glycogen.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Muscle ; glucocorticoids ; insulin resistance ; glucose transport ; glucose transporter ; glucose fatty-acid cycle ; lipid oxidation ; glycogen synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism by which glucocorticoids induce insulin resistance was studied in normal rats administered for 2 days with corticosterone then tested by euglycaemic hyperinsulinaemic clamps. Corticosterone administration induced a slight hyperglycaemia, hyperinsulinaemia and increased non-esterified fatty acid levels. It impaired insulin-stimulated total glucose utilization (corticosterone 15.7±0.7; controls 24.6±0.8 mg·kg−1·min−1), as well as residual hepatic glucose production (corticosterone 4.9±1.0; controls 2.0±0.7 mg·kg−1·min−1). During the clamps, insulin did not decrease the elevated non-esterified fatty acid levels in corticosterone-administered rats (corticosterone 1.38±0.15, controls 0.22±0.04 mmol/l). Corticosterone administration decreased the in vivo insulin-stimulated glucose utilization index by individual muscles by 62±6%, and the de novo glycogen synthesis by 78±2% (n=8–9 muscles). GLUT4 protein and mRNA levels were either unchanged or slightly increased by corticosterone administration. Inhibition of lipid oxidation by etomoxir prevented corticosterone-induced muscle but not hepatic insulin resistance. In conclusion, glucocorticoid-induced muscle insulin resistance is due to excessive nonesterified fatty acid oxidation, possibly via increased glucose fatty-acid cycle ultimately inhibiting glucose transport, or via decreased glycogen synthesis, or by a direct effect on glucose transporter translocation or activity or both.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Intracerebroventricular (i.c.v.) ; neuropeptide Y (NPY) ; food intake ; body weight gain ; in vivo glucose uptake ; muscle insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four- and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-d-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebro-ventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Key words Intracerebroventricular (i. c. v.) ; neuropeptide Y (NPY) ; food intake ; body weight gain ; in vivo glucose uptake ; muscle insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four- and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-d-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebroventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported. [Diabetologia (1994) 37: 1202–1208]
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2013
    Keywords: β-Adrenergic agonist ; Glucose transport ; GLUT4 ; Brown adipose tissue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A β-adrenergic agonist specific for brown adipose tissue, Ro 16-8714, was administered to control and obese insulin-resistant fa/fa rats and glucose utilisation measured in brown adipose tissue using the euglycaemic hyperinsulinaemic clamp combined with the injection of 2-deoxyglucose. Treatment with the β-agonist increased basal and insulin-stimulated glucose utilization in both groups, resulting in an increased effect of the hormone in treated animals. This effect is specific for brown adipose tissue and is not found in other insulin-sensitive tissue. The total number of insulin-responsive glucose transporters (GLUT4) measured in crude membrane preparations was similar in the two groups when expressed per total tissue. They were, however, decreased in the fa/fa group when expressed per milligram of tissue. Acute treatment with the ß-adrenergic agonist increased the total number of GLUT4 in both groups. The agonist also increased the amount of mRNA coding for GLUT4 suggesting an effect on the transcription and/or on the stability of GLUT4 mRNA.
    Type of Medium: Electronic Resource
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