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  • 1
    Electronic Resource
    Electronic Resource
    Oral vanadate decreases muscle insulin resistance in obese fa/fa rats (1992)
    Springer
    Diabetologia 35 (1992), S. 522-527 
    Details
    ISSN: 1432-0428
    Keywords: Vanadate ; insulin resistance ; hyperinsulinaemic clamps ; fa/fa rats ; obesity ; glucose metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Oral vanadate has been reported as improving glucose homeostasis in genetically obese and hyperinsulinaemic fa/fa rats. It has also been shown that these beneficial effects could not be ascribed to the decrease in body weight induced by the treatment, or to changes in insulin counterregulatory hormones. The present study examined therefore whether the effects of vanadate could be attributed to a direct correction of the severe insulin resistance of these animals. fa/fa Rats chronically treated with vanadate were compared to both control rats fed ad libitum and pair-fed rats. The three groups were studied in the basal state and during euglycaemic hyperinsulinaemic clamps. Slightly lower plasma glucose levels were always maintained in vanadate-treated rats in conjunction with markedly lower plasma insulin levels either during basal or clamp studies. During the clamp, the glucose infusion rate required to maintain glycaemia at basal values was consistently higher in vanadate-treated rats than in the other two groups. Experiments using [6-3H]glucose as tracer showed that this was not due to a greater inhibition of hepatic glucose production by insulin, but corresponded to a larger increment in peripheral glucose disposal. The stimulation of overall glucose metabolic clearance induced by insulin was 129% and 41% higher in vanadate-treated than in control and pair-fed rats respectively. Similar experiments with 2-deoxy-[1-3H]glucose as tracer showed that the larger increase in insulin-mediated glucose clearance occurred in various types of muscle. The action of insulin was particularly impressive on the cardiac muscle of vanadate-treated rats. In conclusion, the beneficial effects of vanadate on glucose homeostasis in obese hyperinsulinaemic fa/fa rats involve a sustained improvement of the impaired sensitivity to insulin in muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400479
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Oral selenate improves glucose homeostasis and partly reverses abnormal expression of liver glycolytic and gluconeogenic enzymes in diabetic rats (1996)
    Springer
    Diabetologia 39 (1996), S. 3-11 
    Details
    ISSN: 1432-0428
    Keywords: Selenium ; glycolytic enzymes ; gluconeogenic enzymes ; gene expression ; streptozotocin-diabetic rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Selenium is a trace element that exerts certain insulin-like actions in vitro. In this study, we evaluated its in vivo effects on the glucose homeostasis of rats made diabetic and insulin-deficient by streptozotocin. Na2SeO4 was administered ad libitum in drinking water and/or food for 10 weeks. The elevated plasma glucose levels (~ 25 mmol/l) and glucosuria (~ 85 mmol/day) of untreated rats were decreased by 50 and 80%, respectively, by selenate treatment. The beneficial effect of selenate was also evident during oral and intravenous glucose tolerance tests: the integrated glucose responses were decreased by 40–50% as compared to those in untreated rats. These effects were not due to an increase in plasma insulin levels. Compared to non-diabetic rats, pancreatic insulin reserves were reduced by more than 90% in treated and untreated diabetic rats. The hepatic activities and mRNA levels of two key glycolytic enzymes, glucokinase and l-type pyruvate kinase were blunted in diabetic rats. They increased ~ two- to threefold after selenate treatment, to reach 40–75% of the values in non-diabetic rats. In contrast, elevated activity and mRNA levels of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase, were reduced by 40–65% after selenate administration. Since selenate induced a moderate decrease in body weight due to an anorexigenic effect, we checked that there was no improvement of glucose homeostasis or hepatic glucose metabolism in an additional group of calorie-restricted diabetic rats, which was weight-matched with the selenate group. In addition, no obvious toxic side-effects on the kidney or liver were observed in the rats receiving selenate. In conclusion, selenate induces a sustained improvement of glucose homeostasis in streptozotocin-diabetic rats by an insulin-like action, which involves partial correction of altered pretranslational regulatory mechanisms in liver metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400407
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  • 3
    Electronic Resource
    Electronic Resource
    Phlorizin treatment of diabetic rats partially reverses the abnormal expression of genes involved in hepatic glucose metabolism (1993)
    Springer
    Diabetologia 36 (1993), S. 292-298 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; phlorizin ; glucagon ; hepatic glucose metabolism ; gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Liver insulin resistance and glucagon-stimulated hepatic glucose production are characteristics of the diabetic state. To determine the potential role of glucose toxicity in these abnormalities, we examined whether phlorizin treatment of streptozotocin-diabetic rats resulted in altered expression of genes involved in key steps of hepatic glucose metabolism. By inhibiting renal tubular glucose reabsorption, phlorizin infusion to diabetic rats induced normoglycaemia, did not significantly alter low circulating insulinaemia, but caused a marked decrease in hyperglucagonaemia. Glucokinase and L-type pyruvate kinase mRNA levels were reduced respectively by 90% and 70% in fed diabetic rats, in close correlation with changes in enzyme activities. Eighteen days of phlorizin infusion partially restored glucokinase mRNA and activity (40% of control levels), but had no effect on L-type pyruvate kinase mRNA and activity. In contrast to the glycolytic enzymes, mRNA and activity of the gluconeogenic enzyme, phospoenolpyruvate carboxykinase were increased (10- and 2.2-fold, respectively) in fed diabetic rats. Phlorizin administration decreased phospoenolpyruvate carboxykinase mRNA to values not different from those in control rats, while phospoenolpyruvate carboxykinase activity remained 50% higher than that in control rats. The 50% rise in liver glucose transporter (GLUT 2) mRNA and protein, produced by diabetes, was also corrected by phlorizin treatment. In conclusion, we propose that phlorizin treatment of diabetic rats may induce a partial shift of the predominating gluconeogenesis, associated with hepatic glucose overproduction, into glycolysis, by correction of impaired pre-translational regulatory mechanisms. This could be essentially mediated through improved pancreatic alpha-cell function and subsequent lowering of hyperglucagonaemia. These observations suggest that glucagon-stimulated hepatic glucose production may result, in part, from glucose toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400230
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  • 4
    Electronic Resource
    Electronic Resource
    Tissue-specific correction of lipogenic enzyme gene expression in diabetic rats given vanadate (1994)
    Springer
    Diabetologia 37 (1994), S. 1065-1072 
    Details
    ISSN: 1432-0428
    Keywords: Key words Vanadium ; lipogenic enzymes ; gene expression ; streptozotocin-diabetic rats.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vanadium is a potent insulinomimetic agent. In vivo, its blood glucose lowering action in insulin-deficient diabetic rats is associated with corrected expression of genes involved in hepatic glucose metabolism. In this study, we investigated whether vanadate treatment also reverses the impaired expression of genes coding for key enzymes of lipogenesis in diabetic liver and white adipose tissue. Oral administration of vanadate to streptozotocin-rats caused a 55 % fall in plasma glucose levels after feeding without modifying low insulinaemia. It also partially corrected the low thyroid hormone concentrations. In untreated diabetic animals, hepatic mRNA levels of acetyl-CoA carboxylase and fatty acid synthase were reduced by more than 80 and 90 %, respectively, in close correlation with changes in enzyme activities. Three weeks of vanadate treatment totally restored acetyl-CoA carboxylase mRNA and partially restored fatty acid synthase mRNA (71 % of control levels). The activities of both lipogenic enzymes were increased 3.5 to 4-fold, to reach 45 to 65 % of control values. By contrast, in white adipose tissue, vanadate modified neither expression nor activity of both lipogenic enzymes, which remained blunted (〈 10 % of control levels). In conclusion, vanadate treatment partially restores the activities of two key lipogenic enzymes in liver, but not in white adipose tissue, of diabetic rats. This correction results from a reversal of impaired pre-translational regulatory mechanisms possibly mediated by an improvement of thyroid function and a selective restoration of liver glycolytic flux. [Diabetologia (1994) 37: 1065–1072]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418369
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  • 5
    Electronic Resource
    Electronic Resource
    Repercussions of chronic protein-calorie malnutrition on glucose homeostasis in the rat (1987)
    Springer
    Diabetologia 30 (1987), S. 946-951 
    Details
    ISSN: 1432-0428
    Keywords: Protein-calorie malnutrition ; glucose tolerance ; hypoglycaemia ; insulin secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The characteristics, progressivity and reversibility of the changes in glucose homeostasis brought about by chronic protein-calorie malnutrition were studied in the rat. Four-week-old male rats received a control diet (15% protein) or a low-protein diet (5% protein) until the age of 28 weeks. Other rats received the low-protein diet until 12–15 weeks, and then the control diet. In malnourished rats, fasting plasma glucose levels and both fasting and fed plasma insulin levels were lower than in control rats. At the age of 15 weeks, tolerance to oral glucose was slightly poorer, whereas tolerance to intravenous glucose was slightly better in rats receiving the low-protein diet than in control rats. During both tests the insulin response of malnourished rats was severely blunted. This inhibition largely exceeded the small decrease in their pancreatic insulin reserves. Similar results were obtained when the same test was repeated 9 weeks later. If the rats were transferred from a low-protein to a control diet for these 9 weeks, the changes in glucose tolerance were partially corrected, but the insulin response remained inhibited. Though hepatic glycogen stores were increased in malnourished rats, i. v. glucagon or arginine caused a smaller rise in plasma glucose levels than in control rats. The insulin response was also impaired and, unlike the glucose response, was not restored by 6 weeks on a control diet. The hypoglycaemia induced by intravenous insulin was more sustained in malnourished than in control rats, but this abnormality was corrected by refeeding a control diet for 6 weeks. The results thus show that chronic protein-calorie malnutrition in the rat severely impairs insulin secretion, but only mildly alters glucose tolerance, likely because of an associated high sensitivity to insulin. These changes do not aggravate with time and are only partially reversed by several weeks on a control diet.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00295879
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  • 6
    Electronic Resource
    Electronic Resource
    Tissue-specific correction of lipogenic enzyme gene expression in diabetic rats given vanadate (1994)
    Springer
    Diabetologia 37 (1994), S. 1065-1072 
    Details
    ISSN: 1432-0428
    Keywords: Vanadium ; lipogenic enzymes ; gene expression ; streptozotocin-diabetic rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vanadium is a potent insulinomimetic agent. In vivo, its blood glucose lowering action in insulin-deficient diabetic rats is associated with corrected expression of genes involved in hepatic glucose metabolism. In this study, we investigated whether vanadate treatment also reverses the impaired expression of genes coding for key enzymes of lipogenesis in diabetic liver and white adipose tissue. Oral administration of vanadate to streptozotocin-rats caused a 55% fall in plasma glucose levels after feeding without modifying low insulinaemia. It also partially corrected the low thyroid hormone concentrations. In untreated diabetic animals, hepatic mRNA levels of acetyl-CoA carboxylase and fatty acid synthase were reduced by more than 80 and 90%, respectively, in close correlation with changes in enzyme activities. Three weeks of vanadate treatment totally restored acetyl-CoA carboxylase mRNA and partially restored fatty acid synthase mRNA (71% of control levels). The activities of both lipogenic enzymes were increased 3.5 to 4-fold, to reach 45 to 65% of control values. By contrast, in white adipose tissue, vanadate modified neither expression nor activity of both lipogenic enzymes, which remained blunted (〈10% of control levels). In conclusion, vanadate treatment partially restores the activities of two key lipogenic enzymes in liver, but not in white adipose tissue, of diabetic rats. This correction results from a reversal of impaired pre-translational regulatory mechanisms possibly mediated by an improvement of thyroid function and a selective restoration of liver glycolytic flux.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418369
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    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Effects of vanadate on the expression of genes involved in fuel homeostasis in animal models of Type I and Type II diabetes (1995)
    Springer
    Molecular and cellular biochemistry 153 (1995), S. 121-124 
    Details
    ISSN: 1573-4919
    Keywords: vanadium compounds ; insulin-dependent diabetes ; insulin-independent diabetes ; gene expression in liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Vanadium is a trace element that has raised increasing interest in diabetology since the discovery of its insulin-like propertiesin vitro andin vivo. This brief article reviews the most recent data concerning the beneficial effects of vanadium compounds on fuel homeostasis in animal models of insulinopenic (Type I) or insulin-resistant (Type II) diabetes. These studies open obvious therapeutic possibilities in diabetes, and more particularly, in states of insulin resistance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01075926
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    Paper (German National Licenses)
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