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  • 1
    Electronic Resource
    Electronic Resource
    The contribution of hyperglycaemia and hypoinsulinaemia to the insulin resistance of streptozotocin-diabetic rats (1992)
    Springer
    Diabetologia 35 (1992), S. 310-315 
    Details
    ISSN: 1432-0428
    Keywords: Streptozotocin diabetes ; hyperglycaemia ; phlorizin ; insulin treatment ; glucose utilization index ; 2-deoxy-D-glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relative contribution of hyperglycaemia and hypoinsulinaemia was evaluated in rats made diabetic by streptozotocin administration. Four groups of rats were studied: untreated normal rats; streptozotocin-diabetic; streptozotocin-diabetic treated with phlorizin (0.4 mg/kg body weight per day); streptozotocin-diabetic mildly treated with insulin (0.7 IU/day). In all groups, insulin action (responsiveness) was assessed with the euglycaemic (5.3 mmol/l) hyperinsulinaemic (524 mU/l) clamp technique combined with 3H-2-deoxy-D-glucose method, enabling determination of the glucose utilization index in various tissues. Responsiveness of the overall glucose utilization process to insulin was reduced by 28% in streptozotocin-diabetic rats (12.0±1.2 vs 16.5±0.6 mg·kg−1·min−1, p〈0.001). This was associated with a significant reduction (p〈0.05) in the glucose utilization index in all muscles studied (average=17.0 vs 32.1 ng·mg of tissue−1·min−1), in the heart (19.6 vs 39.5 ng·mg−1·min−1), brown adipose tissue (98.9 vs 178.0 ng·mg−1·min−1), skin (6.4 vs 13.1 ng·mg−1·min−1). Phlorizin treatment normalized plasma glucose levels without affecting those of insulin, and restored overall glucose utilization to normal (16.6±1.0mg·kg−1·min−1). This normalization was accompanied by a normalization of the glucose utilization index in all muscle types studied (29.2 ng·mg−1·min−1), in the heart (50.0ng·mg−1·min−1), brown adipose tissue (157.2 ng·mg−1·min−1), and skin (10.0 ng·mg−1·min−1). White adipose tissue, brain and gut were not affected. Mild insulin treatment with persistent hyperglycaemia was not able to significantly ameliorate glucose disposal (14.5±0.9 mg·kg−1·min−1) or the glucose utilization index of most individual tissues (muscle=18.4; heart=36.2; brown adipose tissue=148.0; skin=7.7 ng· mg−1· min−1). These data show that correction of hyperglycaemia in streptozotocin-diabetic rats normalizes insulin action, while partial correction of the hypoinsulinaemia fails to do so.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401197
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of non-esterified fatty acid oxidation in glucocorticoid-induced peripheral insulin resistance in vivo in rats (1993)
    Springer
    Diabetologia 36 (1993), S. 899-906 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF02374470
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  • 3
    Electronic Resource
    Electronic Resource
    Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1202-1208 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00399793
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  • 4
    Electronic Resource
    Electronic Resource
    Ocular complications in the old and glucose-intolerant genetically obese (fa/fa) rat (1990)
    Springer
    Diabetologia 33 (1990), S. 137-144 
    Details
    ISSN: 1432-0428
    Keywords: Obese fa/fa rat ; non-insulin-dependent diabetes ; oral glucose tolerance ; diabetic microangiopathy ; retinal capillary
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Genetically obese fatty (fa/fa) male rats with abnormal oral glucose tolerance associated with initial hyperinsulinaemia as well as control lean (FA/FA) rats were investigated for the development of retinal microangiopathies. The animals were kept on a standard or sucrose supplemented diet. When tested at 60 weeks, the glucose intolerance of fa/fa rats was accompanied by an insulin response that was now either comparable to that of lean rats (standard diet) or close to nil (sucrose supplemented diet). At killing (68 weeks of age), retinal vasculature was examined by electron microscopy and morphological changes were quantitatively assessed by ultrastructural morphometry. A retinal microangiopathy was observed in all mutant animals which was more pronounced in the sucrose fed group, and which was characterized by: (1), an increase in focal thickenings and in nodules of the basement membrane adjacent to the perivascular glial cells; (2), a decrease in the number of pericyte nulei with concomitant signs of early degenerative cytoplasmic changes of pericytes; (3), an increase in the pinocytic activity of endothelial cells, indicative of presumptive changes in vascular permeability; (4), an increase in the number of intercellular endothelial junctions; (5), the presence of numerous stimulated platelets within capillaries. The fa/fa rat may thus be considered as a suitable model for studying the pathophysiology of ocular complications, in particular retinopathy accompanying non-insulin-dependent diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404039
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  • 5
    Electronic Resource
    Electronic Resource
    Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1202-1208 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00399793
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Central nervous system and peripheral abnormalities: clues to the understanding of obesity and NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. S169 
    Details
    ISSN: 1432-0428
    Keywords: Hyperinsulinaemia ; hypercorticosteronaemia ; glucose and lipid handling ; Neuropeptide Y ; corticotropin-releasing factor ; autonomic nervous system ; insulin resistance ; lipogenesis ; local cerebral glucose utilization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To study the impact on glucose handling of the observed hyperinsulinaemia and hypercorticism of the genetically obese fa/fa rats, simplified animal models were used. In the first model, normal rats were exposed to hyperinsulinaemia for 4 days and compared to saline-infused controls. At the end of this experimental period, the acute effect of insulin was assessed during euglycaemic-hyperinsulinaemic clamps. White adipose tissue lipogenic activity was much more insulin responsive in the “insulinized” than in the control groups. Conversely muscles from “insulinized” rats became insulin resistant. Such divergent consequences of prior “insulinization” on white adipose tissue and muscle were corroborated by similar divergent changes in glucose transporter (GLUT 4) mRNA and protein levels in these respective tissues. In the second model, normal rats were exposed to stress levels of corticosterone for 2 days. This resulted in an insulin resistance of all muscle types that was due to an increased glucose-fatty acid cycle, without measurable alteration of the GLUT 4 system. In genetically obese (fa/fa) rats, local cerebral glucose utilization was decreased compared to lean controls. This could be the reason for adaptive changes leading to increased levels in their hypothalamic neuropeptide Y levels and median eminence corticotropin-releasing-factor. Thus, in a third model, neuropeptide Y was administered intracerebroventricularly to normal rats for 7 days. This produced hyperinsulinaemia, hypercorticosteronaemia, as well as most of the metabolic changes observed in the genetically obese fa/fa rats, including muscle insulin resistance. These data together suggest that the aetiology of obesity-insulin resistance of genetically obese rodents has to be searched within the brain, not peripherally.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400841
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of a β-adrenergic agonist on glucose transport and insulin-responsive glucose transporters (GLUT4) in brown adipose tissue of control and obese fa/fa rats (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 52-58 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00374733
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    Paper (German National Licenses)
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