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  • Electronic Resource  (6)
  • insulin resistance  (4)
  • food intake  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Glucose transporters: structure, function, and regulation
    Amsterdam : Elsevier
    Biochimie 73 (1991), S. 67-70 
    Details
    ISSN: 0300-9084
    Keywords: brown adipose tissue ; glucose transport ; insulin resistance ; skeletal muscle ; white adipose tissue
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0300-9084(91)90076-D
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  • 2
    Electronic Resource
    Electronic Resource
    The onset of liver glycogen synthesis in fasted-refed lean and genetically obese (fa/fa) rats (1987)
    Springer
    Diabetologia 30 (1987), S. 169-174 
    Details
    ISSN: 1432-0428
    Keywords: Liver glycogen metabolism ; fa/fa rats ; feeding ; insulin resistance ; glycolysis ; fructose-2,6-bisphosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lean and genetically obese (fa/fa) rats were fed ad libitum, or fasted for 17 h and then meal-fed for varying time intervals. During refeeding, glucose-6-phosphatase activity of lean rats declined to the low value that was present in livers of fasted obese rats and which remained unchanged in the obese group during the meal. Refeeding also resulted in increases in hepatic concentrations of glucose-6-phosphate and fractose-6-phosphate, fructose 1,6-bisphosphate, fractose-2,6-bisphosphate, α-glycerophosphate, pyruvate and lactate in lean and obese rats, absolute values being higher in the fasted obese than in the fasted lean group. Obese animals had higher postprandial portal blood insulin, glucose and lactate concentrations than lean animals. In spite of this, the rate of hepatic glycogen deposition was the same in both groups and was accompanied by similar glycogen synthase a levels. Following refeeding, phosphorylase was transiently inactivated in livers of lean but not of obese animals, while glycogen synthase was inactivated in both groups. The data suggest that (1) in lean animals refeeding was associated with a stimulation of liver glycolysis, presumably by insulin; (2) in fasted obese rats hepatic glycolysis was already in a stimulated state and was only slightly enhanced further after the meal, in keeping with their unaltered hyperinsulinaemia; (3) there was an increased turnover of liver glycogen or a resistance to insulin stimulation of glycogen synthesis in fa/fa rats during refeeding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00274223
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  • 3
    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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  • 4
    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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    Paper (German National Licenses)
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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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  • 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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