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  • 1
    Electronic Resource
    Electronic Resource
    Increased insulin action in the rat after protein malnutrition early in life (1991)
    Springer
    Diabetologia 34 (1991), S. 559-564 
    Details
    ISSN: 1432-0428
    Keywords: Insulin action ; insulin secretion ; low protein diet ; malnutrition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of a limited period of low protein feeding in young rats on insulin secretion and insulin action during adult-age has been studied. Four-week-old rats were maintained for 4 weeks on isocaloric diets containing 5% protein (low protein) or 15% protein (control). The low protein rats gained weight at a considerably lower rate than the control rats. This was obtained in the absence of any decrease of spontaneous food intake. Basal plasma insulin levels were decreased (p〈0.01) by 40% in low protein rats. However, the glucose-stimulated insulin secretion obtained in vivo after an i.v. glucose load remained normal. The basal plasma glucose level in the low protein rats was only marginally decreased (by 20%). The tolerance to i.v. glucose was found to be slightly enhanced in the low protein rats as compared to the control rats as shown by a significantly increased K value (p}〈0.01). In vivo insulin action in the low protein rats was investigated using the euglycaemic-hyperinsulinaemic clamp technique in conjunction with isotopic measurements of glucose turnover. The overall glucose utilization rate was normal in the basal state but significantly increased (p〈0.05) when measured at a submaximal plasma insulin level. The basal hepatic glucose production in the low protein rats was similar to that in the control rats. During the clamp studies, the suppression of endogenous glucose production was found to be similar in the low protein rats and the control rats but this was obtained at significantly lower (p〈0.01) steady-state insulin levels in the low protein group than in the control group. In conclusion, the current results indicate that the modest improvement of glucose tolerance which is revealed in the low protein rats results from changes in the insulin action upon the target tissues: both the insulin-mediated glucose uptake by peripheral tissues and the ability of insulin to suppress hepatic glucose output are enhanced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400273
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  • 2
    Electronic Resource
    Electronic Resource
    In vivo insulin resistance in streptozotocin-diabetic rats — evidence for reversal following oral vanadate treatment (1989)
    Springer
    Diabetologia 32 (1989), S. 185-190 
    Details
    ISSN: 1432-0428
    Keywords: Streptozotocin-diabetic rats ; glucose production ; glucose utilisation ; insulin resistance ; vanadate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hepatic glucose production and peripheral glucose utilisation were measured in vivo with the euglycaemic-hyper-insulinaemic clamp technique in rats rendered severely diabetic with streptozotocin (45 mg/kg) and in control rats. The rats were studied in the post-absorptive state while anaesthetised. The basal glucose production and glucose utilisation were significantly higher (p〈0.001) in diabetic rats 9 days after streptozotocin administration. During the clamp studies, suppression of glucose production by the liver induced by submaximal or maximal insulin levels was significantly less (p〈0.01 and p〈0.001 respectively) effective in diabetic rats as compared to control rats. Glucose utilisation was significantly lower following both submaximal (p〈0.01) or maximal (p〈0.001) hyperinsulinaemia as compared to control rats. Oral administration of vanadate (0.2mg/ml in drinking water) for a 20-day period in diabetic rats lowered their plasma glucose levels to normal near values within 4 days, normalised plasma insulin levels, and increased pancreatic insulin stores. The rate of glucose disappearance (K value) and in vivo glucose-induced insulin secretion as estimated during an i.v. glucose tolerance test were not significantly improved. In control rats, vanadate treatment did not significantly affect any of the above parameters. In vanadate treated diabetic rats, basal glucose production was normalised. Following submaximal or maximal hyperinsulinaemia, glucose production was suppressed normaly. Basal glucose utilisation was restored and returned to normal values during submaximal hyperinsulinaemia. However, during maximal hyperinsulinaemia, glucose utilisation still remained significantly lower (p〈0.05) as compared to vanadate-treated control rats. Vanadate treatment in control rats did not affect significantly any of the above parameters. These results show an insulin-like effect of vanadate upon glucose metabolism in vivo in the liver and peripheral tissues of diabetic rats, leading to normalisation of glycaemia in the absence of any significant improvement of insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265092
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  • 3
    Electronic Resource
    Electronic Resource
    Impairment of the mitochondrial oxidative response to D-glucose in pancreatic islets from adult rats injected with streptozotocin during the neonatal period (1990)
    Springer
    Diabetologia 33 (1990), S. 654-660 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic islets ; insulin release ; streptozotocin ; glucose metabolism ; leucine metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreatic islets removed from adult rats injected with streptozotocin during the neonatal period display an impaired secretory response to D-glucose and, to a lesser extent, to L-leucine. Despite normal to elevated hexokinase and glucokinase activities in the islets of these glucose-intolerant animals and despite normal mitochondrial binding of the hexokinase isoenzymes, the metabolic response to a high concentration of D-glucose is severely affected, especially in terms of D-[6-14C]glucose oxidation. Thus, the ratio in D-[6-14C]glucose oxidation/D-[5-3H]glucose utilization is much less markedly increased in response to a rise in hexose concentration and, at a high concentration of D-glucose (16.7 mmol/l), less markedly decreased by the absence of Ca2+ and presence of cycloheximide in diabetic than control rats. This metabolic defect contrasts with (1) a close-to-normal or even increased capacity of the islets of diabetic rats to oxidize D-[6-14C]glucose, [2-14C]pyruvate, L-[U-14C]glutamine and L-[U-14C]leucine at low, non-insulinotropic, concentrations of these substrates; (2) a lesser impairment of the oxidation of L-[U-14 C]leucine tested in high concentration (20 mmol/l), the effect of Ca2+ deprivation upon the latter variable being comparable in diabetic and control rats; (3) an unaltered transamination of either [2-14 C]pyruvate or L-[U-14C]leucine; and (4) a modest perturbation of glycolysis. The most obvious alteration in glycolysis consists in a lesser increase of the glycolytic flux in response to a rise of D-glucose concentration in diabetic than control rats, this coinciding with an apparent decrease in affinity of glucokinase for the hexose. It is speculated that the preferential impairment of the metabolic and secretory response to D-glucose may be mainly attributable to an altered coupling between calcium accumulation and the stimulation of oxidative events in Beta-cell mitochondria of diabetic rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400566
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  • 4
    Electronic Resource
    Electronic Resource
    In vivo and in vitro increased pancreatic beta-cell sensitivity to glucose in normal rats submitted to a 48-h hyperglycaemic period (1993)
    Springer
    Diabetologia 36 (1993), S. 589-595 
    Details
    ISSN: 1432-0428
    Keywords: Glucose infusion ; in vivo insulin secretion ; in vitro insulin secretion ; beta-cell sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the importance of the level and the duration of glucose stimulation on the in vivo and in vitro insulin response to glucose in normal rats previously submitted to hyperglycaemia. Rats were made hyperglycaemic by a 48-h glucose infusion. Glucose-induced insulin secretion was investigated in vivo by a 20-min hyperglycaemic clamp and in vitro by the isolated perfused pancreas technique, 3 h after the end of the in vivo glucose infusion. In glucose-infused rats, as compared to controls, in vivo incremental plasma insulin values above baseline integrated over the 20-min hyperglycaemic clamp (ΔI) were five times higher during 8 mmol/l glucose clamp, only two times higher in 11 mmol/l glucose clamp and no different in 16.5 mmol/l. Compared to the controls, in vitro incremental plasma insulin concentration above baseline integrated over a 20-min period (ΔI) in glucose-infused rats was 16 times higher in response to 2.8 mmol/l glucose, two times higher in response to 5.5 mmol/l, similar in response to 8.3 mmol/l and significantly lower in response to 16.5 mmol/l. In conclusion, our data suggest that a 48-h hyperglycaemic period results in an increased response of the pancreatic beta cell to low glucose. The response is immediately maximal and can not be increased with higher glucose concentrations. This situation could explain the apparent minimal effect of high concentrations on in vitro insulin secretion in previously hyperglycaemic rats and may provide insights into the sequence of events leading to the impairment of beta-cell function in Type 2 (non-insulin-dependent) diabetes mellitus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404066
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  • 5
    Electronic Resource
    Electronic Resource
    Metabolic, Ionic, and Secretory Response to D-Glucose in Islets from Rats with Acquired or Inherited Non-Insulin-Dependent Diabetes
    Amsterdam : Elsevier
    Biochemical Medicine and Metabolic Biology 50 (1993), S. 301-321 
    Details
    ISSN: 0885-4505
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/bmmb.1993.1072
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  • 6
    Electronic Resource
    Electronic Resource
    Study of hexose transport, glycerol phosphate shuttle and Krebs cycle in islets of adult rats injected with streptozotocin during the neonatal period
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 83 (1992), S. 95-104 
    Details
    ISSN: 0303-7207
    Keywords: Glycerol phosphate shuttle ; Hexose transport ; Pancreatic islet ; Streptozotocin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0303-7207(92)90150-5
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of high sucrose diet on insulin secretion and insulin action: a study in the normal rat (1987)
    Springer
    Diabetologia 30 (1987), S. 252-258 
    Details
    ISSN: 1432-0428
    Keywords: High sucrose feeding ; insulin secretion ; perfused pancreas ; insulin action ; insulin-glucose clamp technique ; glucose production ; glucose utilization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of chronic high sucrose feeding for 1 month on in vivo and in vitro insulin secretion and on in vivo insulin action were studied in normal male rats. As compared to the standard chow diet, the high sucrose diet induced excess in vivo insulin response to an intravenous glucose load; the high sucrose diet also slightly improved glucose tolerance, as demonstrated by significantly higher rate of glucose disappearance (p〈0.02). The increased insulin secretion in response to glucose in vivo seems to be related to an hyper-reactivity of the pancreatic B cell to glucose, since it was still observed in vitro with the isolated perfused pancreas preparation. By contrast, B cells of sucrose-fed rats exhibited in vitro a normal response to arginine and a significantly lowered (p〈0.05) response to acetylcholine. The insulin action in the sucrose-fed rats was quantified in vivo with the insulin-glucose clamp technique. The effects of different concentrations of insulin on glucose production and glucose utilization were studied in anaesthetized rats while in the postabsorptive state. The basal glucose utilization was found significantly higher (p〈0.001) in sucrose-fed rats. During the clamp studies the glucose utilization induced by submaximal (400 μU/ml) or maximal (7500 μU/ml) insulin levels was significantly more important (p〈0.02) in the sucrose-fed rats than in the chow-fed rats. This suggests that insulin-mediated glucose uptake is enhanced over a large range of plasma insulin levels in the sucrose-fed rats. In the basal state hepatic glucose production was significantly higher (p〈0.001) in sucrose-fed rats. During the clamp studies, the suppression of glucose production induced by submaximal or maximal insulin levels was significantly less effective (p〈0.05) in the sucrose-fed rats as compared to chow-fed rats, thus suggesting that the liver becomes resistant to insulin action after sucrose feeding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00270424
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of high sucrose diet on insulin secretion and insulin action. A study in rats with non-insulin-dependent diabetes induced by streptozotocin (1987)
    Springer
    Diabetologia 30 (1987), S. 666-673 
    Details
    ISSN: 1432-0428
    Keywords: High sucrose feeding ; rats with non-insulin-dependent diabetes ; insulin secretion ; perfused pancreas ; insulin action ; insulin-glucose clamp technique ; glucose production ; glucose utilisation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of chronic high sucrose feeding for 1 month on in vivo and in vitro insulin secretion and on in vivo insulin action were studied in rats with non-insulin-dependent diabetes. As compared to the standard diet, the high sucrose diet induced an increase of the in vivo insulin response to an intravenous load and deteriorated the glucose tolerance as attested by significantly lower rates of glucose disppearance (K values, p〈0.001). The increased insulin secretion in response to glucose in vivo seems to be related to a slight increase of the pancreatic B-cell reactivity to glucose, since it was still observed in vitro with the isolated perfused pancreas preparation. By contrast, B cells of sucrose-fed rats exhibited in vitro a significantly lowered (p〈0.01) response to acetylcholine and arginine. The insulin action in the sucrose-fed diabetic rats was quantified in vivo with the insulin-glucose clamp technique. The effects of different concentrations of insulin on glucose production and glucose utilisation were studied in anaesthetized rats while in the postabsorptive state. The basal glucose utilisation was found significantly higher (p〈0.001) in sucrose-fed rats. During the clamp studies the glucose utilisation induced by submaximal (450 mU/l) insulin level was significantly less important (p〈0.01) in the sucrose-fed rats than in the chow-fed rats. Following a maximal hyperinsulinaemia (5000 mU/l) the glucose utilisation was similar in both groups. This suggests that insulin-mediated glucose uptake is decreased over the range of submaximal plasma insulin levels in the sucrose-fed diabetic rats. In the basal state hepatic glucose production was significantly higher (p〈0.001) in sucrose-fed rats. During the clamp studies, the suppression of glucose production induced by submaximal or maximal insulin levels was significantly less effective (p〈0.01) in the sucrose-fed rats as compared to chow-fed rats, thus suggesting that the liver becomes resistant to insulin action after sucrose feeding. Finally, these results suggest that restriction of complex carbohydrates in favor of sucrose in insulin-deficient rats leads to metabolic events likely to develop insulin resistance in target tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277326
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  • 9
    Electronic Resource
    Electronic Resource
    Long-term gliclazide treatment improves the in vitro glucose-induced insulin release in rats with Type 2 (non-insulin-dependent) diabetes induced by neonatal streptozotocin (1989)
    Springer
    Diabetologia 32 (1989), S. 577-584 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes ; gliclazide therapy ; insulin release ; insulin content ; B-cell desensitization to glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neonatal rats treated with streptozotocin on the day of birth (n0-STZ) or on day 5 (n5-STZ) exhibited when fully grown a very mild or frank basal hyperglycaemia respectively and a specific failure of insulin release in response to glucose. To determine whether short (1 day) or long-term (30 days) gliclazide treatment modifies the pancreatic insulin content and the B-cell response to secretagogues, diabetic rats were given oral gliclazide (10 mg/kg per day) and compared to control diabetic and non-diabetic rats. Insulin secretion in the isolated perfused pancreas was studied the day after the last gliclazide administration. In severely hyperglycaemic n5-STZ rats (plasma glucose levels 〉16 mmol/l) long-term gliclazide treatment did not lower the plasma glucose values, did not affect the pancreatic insulin stores, nor did it significantly modify the insulin release in vitro in response to glucose or arginine. In moderately hyperglycaemic n5-STZ rats (plasma glucose levels 〈16 mmol/l) the plasma glucose levels declined progressively reaching 8 mmol/l as a mean at the end of the gliclazide therapy. In the n5-STZ rats responsive to gliclazide the pancreatic insulin stores were increased twofold as compared to values in untreated n5-STZ rats, however, this difference did not reached significance and the pancreatic in sulin stores in the responsive gliclazide treated rats remained depleted by 76% compared to normal insulin stores. In the n0-STZ rats (very mild hyperglycaemia) the long-term gliclazide treatment did not significantly modify the plasma glucose levels or the pancreatic insulin stores. After the 30-day gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (1) the in vitro glucose-induced insulin secretion was increased three to fivefold, (2) the response to arginine which was basically increased in the untreated diabetic rats was again amplified two to threefold, (3) the insulin release in response to gliclazide was unchanged. In conclusion, long-term gliclazide therapy augments stimulated insulin secretion in these two rat models of Type 2 (non-insulin-dependent) diabetes and does not induce any refractoriness to acute sulfonylurea stimulation. The improvement of B-cell function observed here was not related to the concomitant variations of hyperglycaemia and/or pancreatic insulin content
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00285331
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