The first phase insulin response to intravenous glucose is highly reproducible

Rayman, G.; Clark, P. M. S.; Schneider, Eric F.; Hales, C. N.

doi:10.1007/bf00400209

Cited by 37 publications

(18 citation statements)

References 8 publications

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“…We have shown that this measurement of first phase insulin release is highly reproducible [11]. In addition the first phase insulin response has been shown to correlate with both the pancreatic insulin content and beta-cell mass [14].…”

Section: Discussionmentioning

confidence: 79%

Fetal growth and insulin secretion in adult life

et al. 1994

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Summary Recent studies suggest that NIDDMislinked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/1, p = 0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/1,p = 0.02) and correlated with fasting insulin level (p = 0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in prenatal life. [Diabetologia (1994) 37: 592-596] Key words NIDDM, insulin secretion, fetal growth, programming.Recent research has suggested that NIDDM may originate through impaired development in fetal life and early infancy. Among 370 men aged 64 years living in Hertfordshire, England, the percentage who had either NIDDM or impaired glucose tolerance was highest in those who had lowest birthweights or weights at age i year [1]. This finding was confirmed by a subsequent study of men and women aged 46 to 54 years who were born in Preston, England, where the association was shown to be due to babies who were small regardless of their gestational age rather than babies who were born

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Section: Discussionmentioning

confidence: 79%

Fetal growth and insulin secretion in adult life

et al. 1994

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“…3 additionally shows results of an oGTT of son I using a 100-g glucose load, demonstrating an impaired response to this challenge. ivGTTs have been established to provide a sensitive index of ␤ cell function, particularly with regard to the rapid first-phase insulin response (28). Therefore, results of ivGTTs were evaluated for insulin secretion, especially the first-phase peak, and glucose elimination.…”

Section: Resultsmentioning

confidence: 99%

“…For ivGTTs, 0.33 g glucose/kg body wt was injected intravenously as a 40% solution into the right antecubital vein within 2 min. Blood for insulin and C-peptide was drawn from a permanent cannula placed into the left radial vein while keeping the hand in a water bath at 44 Њ C, to obtain arterialized blood as suggested elsewhere (28). Samples were drawn at 0, 1, 2, 3, 4, 5, 6, 8, 10, 20, 40, and 60 min.…”

Section: Methodsmentioning

confidence: 99%

Deficiency of phosphofructo-1-kinase/muscle subtype in humans impairs insulin secretion and causes insulin resistance.

Ristow¹,

Vorgerd²,

Möhlig³

et al. 1997

J. Clin. Invest.

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Non-insulin-dependent diabetes mellitus (NIDDM) is caused by peripheral insulin resistance and impaired ␤ cell function. Phosphofructo-1-kinase (PFK1) is a rate-limiting enzyme in glycolysis, and its muscle subtype (PFK1-M) deficiency leads to the autosomal recessively inherited glycogenosis type VII Tarui's disease. It was evaluated whether PFK1-M deficiency leads to alterations in insulin action or secretion in humans.A core family of four members was evaluated for PFK1-M deficiency by DNA and enzyme-activity analyses. All members underwent oral and intravenous glucose tolerance tests (oGTT and ivGTT) and an insulin-sensitivity test (IST) using octreotide.Enzyme PFK1-M deficiency causes impaired insulin secretion in response to glucose, demonstrating its participation in islet glucose metabolism, and peripheral insulin resistance. These combined metabolic sequelae of PFK-1 deficiency identify it as a candidate gene predisposing to NIDDM. ( J.

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“…Insulin sensitivity (Si) has been found to be closely correlated to the glucose disposal rate measured by the euglycemic hyperinsulinemic clamp (40)(41)(42). Furthermore, the reproducibility of Si and the acute insulin response to glucose has been found to be sufficient (43,44). One further advantage of the FSIGT is the simultaneous estimation of insulin secretion, insulin sensitivity, and glucose-mediated glucose disposal.…”

Section: Discussionmentioning

confidence: 99%

Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. A novel compensatory mechanism.

Alford²,

et al. 1994

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20 normoglycemic first degree relatives of non-insulin-dependent diabetes mellitus (NIDDM) patients were compared with 20 matched subjects without any family history of diabetes using the intravenous glucose tolerance test with minimal model analysis of glucose disappearance and insulin kinetics. Intravenous glucose tolerance index (Kg) was similar in both groups (1.60±0.14 vs 1.59±0.18, x 10-2 minm-, NS). However, insulin sensitivity (Si) was reduced (3.49±0.43 vs 4.80±0.61, x 10-4 mind per mU/liter, P = 0.05), whereas glucose effectiveness (Sg) was increased (1.93±0.14 vs 1.52±0.16, X 10-2 min-, P < 0.05) in the relatives. Despite insulin resistance neither fasting plasma insulin concentration (7.63±0.48 vs 6.88±0.45, mU/liter, NS) nor first phase insulin responsiveness (Phil) (3.56±0.53 vs 4.13±0.62, mU/liter min' per mg/dl, NS) were increased in the relatives. Phil was reduced for the degree of insulin resistance in the relatives so that the Phil x Si index was lower in the relatives (11.5±2.2 vs 16.7±2.0, x 10-4 min 2 per mg/dl, P < 0.05). Importantly, glucose effectiveness correlated with Kg and with basal glucose oxidation but not with total glucose transporter 4 (GLUT4) content in a basal muscle biopsy. In conclusion we confirm the presence of insulin resistance in first degree relatives of NIDDM patients. However, insulin secretion was altered and reduced for the degree of insulin resistance in the relatives, whereas glucose effectiveness was increased. We hypothesize that increased glucose effectiveness maintains glucose tolerance

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The first phase insulin response to intravenous glucose is highly reproducible

Cited by 37 publications

References 8 publications

Fetal growth and insulin secretion in adult life

Fetal growth and insulin secretion in adult life

Deficiency of phosphofructo-1-kinase/muscle subtype in humans impairs insulin secretion and causes insulin resistance.

Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. A novel compensatory mechanism.

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