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  • 1
    ISSN: 1432-0428
    Keywords: Glucose infusion ; pregnant rats ; fetus ; plasma insulin ; fetal body weight ; lipid synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mild hyperglycaemia was induced in unrestrained pregnant rats from day 20.5 to day 23.5 of pregnancy, using a continuous glucose infusion. Control rats were infused with distilled water. In post-mature fetuses from glucose-infused rats, raised plasma glucose and insulin concentrations were related to increased body weight (6.03±0.07 g) and total carcass fat (2.02±0.04% of fresh weight) compared with control fetuses of the same age (5.35±0.07 and 1.5±0.04 g, respectively). Concurrently, the rate of lipogenesis in the carcass, estimated from the incorporation of tritium from tritiated water into fatty acids, was significantly increased in fetuses from glucose infused rats compared with control rats (6.00±0.34 versus 2.62±0.27 and 3H2O · h-1 · g tissue-1, respectively).
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Glucose infusion ; pregnant rats ; prolonged pregnancy ; fetus ; plasma insulin ; plasma glucagon ; liver phosphoenolpyruvate carboxykinase ; liver glycogen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Continuous glucose infusion was used to induce mild hyperglycaemia in unrestrained pregnant rats during the last three days of pregnancy. Control pregnant rats were infused with distilled water. Fetuses were studied after normal or prolonged pregnancy. Fetuses from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a rise in the glucagon/insulin ratio from 6.5 to 67 in fetuses from control rats and from 1.3 to 13 in fetuses from glucose-infused rats. Concurrently in fetuses from control rats, liver phosphoenolpyruvate carboxykinase activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser extent. These results show that both the A and B cells of the rat fetal pancreas are sensitive to chronic glucose stimulation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: BB rat ; diabetes ; glucose intolerance ; insulin sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In diabetes-prone BB rats, 30 to 50% of animals undergo autoimmune destruction of the pancreatic B-cells leading to a short period of glucose intolerance, followed by an abrupt onset of diabetes. We have examined whether the glucose intolerance period and the onset of diabetes are associated with changes in insulin sensitivity, using the euglycaemic hyperinsulinaemic clamp coupled with [3-3H] glucose infusion. Glucose intolerant rats were detected by a transient glycosuria one hour after an oral glucose load performed every four days. Insulin sensitivity studied in these rats the day following their detection was normal. Other diabetes-prone BB rats were tested daily and studied on the first day of glycosuria. In the basal state, glucose production was increased in diabetic rats (11.3±1.1 vs 7.1±0.8mg·min−1·kg−1, p〈0.05). Tissue glucose utilization was similar in diabetic and control rats (8.3±0.5 vs 7.1±0.8mg·min−1·kg−1) despite a three fold higher glycaemia in the diabetic rats. During the hyperinsulinaemic clamps, glycaemia was clamped at 6.1–6.6 mmol/l in diabetic and control rats. A decreased insulin sensitivity was observed in diabetic rats at submaximal (200 μU/ml) and maximal (1500 μU/ml) insulin concentrations for both inhibition of hepatic glucose production and stimulation of glucose utilization. No autoantibodies against insulin could be detected in the plasma of diabetic rats. Plasma concentrations of glucagon, catecholamines, ketone bodies and fatty acids were similar in control and diabetic rats during the clamp studies. Our results suggest that the decrease of basal insulin concentration is responsible for the insulin resistance in the diabetic BB rat at onset of diabetes, either directly or through the increased glycaemia.
    Type of Medium: Electronic Resource
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  • 4
    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
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 68 (1976), S. 19-22 
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Slight gestational hyperglycaemia ; high gestational hyperglycaemia ; fetus ; insulin release ; perifused pancreas ; leucine ; arginine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Unrestrained pregnant rats were infused with glucose during the last week of pregnancy to produce slight or high gestational hyperglycaemia. Control rats were infused with distilled water. Insulin secretion of the fetuses at term was studied in vitro using a perifusion system. Compared with controls, perifused pancreases of slightly hyperglycaemic fetuses showed a similar pattern of insulin secretion in response to 10 mmol/l leucine. Arginine-induced insulin secretion at 20 mmol/1 was higher than in controls. In both groups, 10 mmol/l a-ketoisocaproate had a poor stimulatory effect on insulin release, and 5 mmol/1 D-glyceraldehyde was ineffective in eliciting insulin secretion. In highly hyperglycaemic fetuses all the secretagogues, with the exception of arginine, which induced a sustained monophasic insulin secretory response, had no effect on insulin release. These data show that long-term exposure of fetal B cells to high plasma glucose levels in utero suppresses or alters further insulin secretory response not only to glucose but also to other nutrient secretagogues. The partially spared insulin secretory response to arginine suggests that the defect may concern stimulus-secretion coupling rather than insulin releasing machinery.
    Type of Medium: Electronic Resource
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