Increased insulin sensitivity and basal insulin effectiveness in postprandial reactive hypoglycaemia

Glucose clamp experiments have shown that patients with reactive postprandial hypoglycaemia (PRH) frequently have an increased glucose disposal, but the relative involvement of insulin sensitivity (SI) and glucose effectiveness (Sg) in this process remains unknown. The minimal model approach was use...

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Bibliographic Details
Published in:Acta diabetologica 1996-03, Vol.33 (1), p.1-6
Main Authors: BRUN, J. F, BOUIX, O, MONNIER, J. F, BLACHON, C, JOURDAN, N, BACCARA, M. T, FEDOU, C, ORSETTI, A
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Blood Glucose - drug effects
Blood Glucose - metabolism
Eating
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Female
Glucose - metabolism
Glucose Clamp Technique
Glucose Tolerance Test
Humans
Hypoglycemia - blood
Hypoglycemia - physiopathology
Insulin - pharmacology
Male
Medical sciences
Reference Values
Tumors. Hypoglycemia
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Summary:Glucose clamp experiments have shown that patients with reactive postprandial hypoglycaemia (PRH) frequently have an increased glucose disposal, but the relative involvement of insulin sensitivity (SI) and glucose effectiveness (Sg) in this process remains unknown. The minimal model approach was used to compare 13 patients in whom moderate reactive hypoglycaemia ( < 3.3 mmol) had been previously diagnosed and 13 matched controls. The intravenous glucose tolerance test (IVGTT, 0.5 g/kg glucose IV) with 0.02 U/kg insulin given at the 19th min and frequent sampling over 180 min shows that PRH patients exhibit a higher glucose tolerance coefficient Kg (2.99 +/- 0.26 vs 2.19 +/- 0.12; P < 0.02), higher SI [22.9 +/- 6.4 vs 7.18 +/- 0.14 min-1/(microU/ml). 10(-4); P < 0.01] and higher Sg (3.84 +/- 0.35 vs 2.92 +/- 0.79 min-1. 10(-2); P < 0.05). The increase in Sg is explained by an increase in its component basal insulin effectiveness (BIE: 1.2 +/- 0.27 min-1.10(-2) in PRH subjects vs 0.58 +/- 0.07; P < 0.05) rather than an increase in Sg at zero insulin. The increase in BIE results from the high values of SI. In 4 PRH subjects SI and Sg were within the normal range, and the increase in Kg evidenced in the 9 others was explained by an increase in SI alone in 3 cases, in Sg alone in 1 case, and both SI and Sg in 5 cases. Thus, in sedentary subjects, the previously reported rise in tissue glucose assimilation is mainly explained by an increased insulin-mediated glucose disposal rather than non-insulin-mediated glucose disposal.
ISSN:0940-5429
1432-5233
DOI:10.1007/BF00571932