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  • 1
    Electronic Resource
    Electronic Resource
    Paradoxical inhibition of insulin secretion by glucose in non-insulin-dependent diabetic patients (1995)
    Springer
    Acta diabetologica 32 (1995), S. 1-6 
    Details
    ISSN: 1432-5233
    Keywords: Non-insulin-dependent diabetes ; Hyperglycaemic clamp ; paradoxical beta-cell response ; insulin secretion ; C-peptide secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In young healthy individuals, an i.v. glucose bolus leads to an immediate increase in plasma insulin, whereas in non-insulin-dependent diabetic patients this early response is diminished, lacking or even negative. In the present study, we sought to determine whether negative responses were also present during square-wave glucose stimulation (transition from 18 to 25 mM), whether they represented a decrease in beta-cell secretion, whether they were accompanied by an altered response to arginine (5 gl-arginine bolus), and whether they were a consequence of ageing rather than of diabetes. A group of 12 patients (aged 53±2 years, mean±SE) with non-insulin-dependent diabetes (D) and 12 matched healthy controls (C; aged 47±1 years) were evaluated twice at an interval of 3 months. Other baseline values were body mass index (BMI) 28±1 (D) and 26±1 (C) kg/m2, fasting C-peptide 0.85±0.12 (D) and 0.92±0.10(C) nmol/l, and fasting P-glucose 12.3±0.9 (D) and 5.8±0.1 (C) mM,P〈0.05. Paradoxical responses (a decrease of two or more times the SD of the analysis within 15 min of increasing the glucose concentration) were seen in five diabetic patients for insulin (22±8%) and in nine diabetic patients for C-peptide (13±3%), but never in the healthy controls. Plasma glucose increased and protein decreased similarly, whether the responses were paradoxical or not. Paradoxial responses were reproduced after three months. Responses to arginine did not correlate with responses to glucose. In summary, in contrast to healthy matched controls, 40–75% of non-insulin-dependent diabetics show a marked initial decrease in beta-cell secretion upon square-wave glucose stimulation. This is probably specific to glucose stimulation, as it did not occur in response to arginine stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581036
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  • 2
    Electronic Resource
    Electronic Resource
    The effect of moderate exercise on postprandial glucose homeostasis in NIDDM patients (1997)
    Springer
    Diabetologia 40 (1997), S. 447-453 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin sensitivity ; physical activity ; insulin ; C-peptide ; non-esterified fatty acids; glycerol ; glucose turnover.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of exercise on glycaemia in the post-prandial state was studied for the first time in non-insulin-dependent diabetic (NIDDM) patients. Meal-induced glucose responses were followed for 8 h in 9 diet-treated patients with NIDDM. Subjects consumed a standardized breakfast and 4 h later a standardized lunch. They were studied in the resting state (control day (CD)) and on another day 45 min of bicycle exercise (53 ± 2 % V˙O 2 max (mean ± SEM)) was performed 45 min after breakfast (exercise day (ED)). On day 3 (diet day (DD)), the breakfast meal was reduced corresponding to the extra energy expenditure during the exercise period on ED. Responses were calculated as areas under the plasma concentration curve (AUC) during 4 h after either breakfast (B-AUC) or lunch (L-AUC). B-AUC for glucose was identical on ED (215 ± 63 mmol/l · 240 min) and DD (219 ± 60 mmol/l · 240 min) and on these days lower (p 〈 0.05) than on CD (453 ± 78 mmol/l · 240 min). L-AUC for glucose on CD, ED and DD did not differ significantly. B-AUCs for both insulin and C-peptide were also significantly lower on ED and DD as compared to CD (Insulin: 31337 ± 8682, 26092 ± 6457 and 47649 ± 15046 mmol/l · 240 min, respectively. C-peptide: 99 ± 19, 104 ± 26 and 195 ± 31 pmol/ml · 240 min, respectively). Rate of appearance (Ra) for glucose was unaffected by exercise whereas rate of disappearance (Rd) increased significantly. No differences in Ra or Rd were observed after lunch. In conclusion, postprandial exercise of moderate intensity decreases glycaemia and plasma insulin levels after breakfast in NIDDM patients, but this effect does not persist during and after the following lunch meal. Reduction of breakfast caloric intake has the same effect on postprandial glycaemia and insulin secretion as an equivalent exercise-induced increase in caloric expenditure. [Diabetologia (1997) 40: 447–453]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050699
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    The effect of intense exercise on postprandial glucose homeostasis in Type II diabetic patients (1999)
    Springer
    Diabetologia 42 (1999), S. 1282-1292 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin sensitivity; physical activity; insulin; free fatty acids; glucose turnover.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The influence of postprandial high intensity exercise on glycaemia was studied in patients with Type II diabetes mellitus. Methods. Patients who were treated by diet only (n = 8) ate a standardised breakfast and 4 h later a standardised lunch. They were studied in the resting state (control day) and on another day (exercise day) when they did intermittent exercised at high intensity after breakfast) (4 bouts including 3 min at 56.5 ± 3.9 % V˙.O2 max (means ± SEM), 4 min at 98.3 ± 5.1 % V˙.O2 max and 6 min of rest). Responses were calculated as areas under the plasma concentration curve (AUC) during 4 h after either breakfast or lunch. Results. Breakfast-AUCs for glucose, insulin and C peptide were lower (p 〈 0.05) on the exercise day compared with the control day (glucose: 538 ± 94 vs 733 ± 64 mmol · l–1· 240 min; insulin: 16 ± 4 vs 22 ± 3 pmol · ml–1· 240 min; C peptide: 143 ± 22 vs 203 ± 29 pmol · ml–1· 240 min). After breakfast glucose appearance was unaffected by exercise, whereas disappearance and clearance increased (p 〈 0.05). Muscle glycogen was diminished by exercise (p 〈 0.05). After lunch no differences were observed between experiments. Exercise-induced reductions in glucose, insulin and C peptide responses were similar (p 〉 0.05) in this study of intermittent, high intensity exercise and in a previous study of isocaloric but prolonged moderate (45 min at 53 ± 2 % V˙.O2 max) postprandial exercise. Conclusion/interpretation. Postprandial high intensity exercise does not deteriorate glucose homeostasis but reduces both glucose concentrations and insulin secretion. The effect of exercise is related to energy expenditure rather than to peak exercise intensity. Finally, postprandial exercise does not influence glucose homeostasis during a subsequent main meal. [Diabetologia (1999) 42: 1282–1292]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051440
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    Paper (German National Licenses)
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