Fetal growth and the physiological control of glucose tolerance in adults: a minimal model analysis

2000 ◽  
Vol 278 (4) ◽  
pp. E700-E706 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Vivienne M. Moore ◽  
Ian F. Godsland ◽  
Richard A. Cockington ◽  
Jeffrey S. Robinson ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Body Mass ◽  
Fetal Growth ◽  
Minimal Model ◽  
Adult Life ◽  
Fat Distribution ◽  
Birth Size

Although there is now substantial evidence linking low birthweight with impaired glucose tolerance and type 2 diabetes in adult life, the extent to which reduced fetal growth is associated with impaired insulin sensitivity, defective insulin secretion, or a combination of both factors is not clear. We have therefore examined the relationships between birth size and both insulin sensitivity and insulin secretion as assessed by an intravenous glucose tolerance test with minimal model analysis in 163 men and women, aged 20 yr, born at term in Adelaide, South Australia. Birth size did not correlate with body mass index or fat distribution in men or women. Men who were lighter or shorter as babies were less insulin sensitive ( P = 0.03 and P = 0.01, respectively), independently of their body mass index or body fat distribution. They also had higher insulin secretion ( P = 0.007 and P = 0.006) and increased glucose effectiveness ( P = 0.003 and P = 0.003). Overall glucose tolerance, however, did not correlate with birth size, suggesting that the reduced insulin sensitivity was being compensated for by an increase in insulin secretion and insulin-independent glucose disposal. There were no relationships between birth size and insulin sensitivity or insulin secretion in women. These results show that small size at birth is associated with increased insulin resistance and hyperinsulinemia in young adult life but that these relationships are restricted to the male gender in this age group.

Effect of body mass index and fat distribution on insulin sensitivity, secretion, and clearance in nonobese healthy men.

1992 ◽  
Vol 75 (1) ◽  
pp. 170-175 ◽  
Author(s):  
C Walton ◽  
I F Godsland ◽  
A J Proudler ◽  
C V Felton ◽  
V Wynn
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Fat Distribution ◽  
Healthy Men

scholarly journals Impaired Insulin Secretion in the Turner Metabolic Syndrome

2004 ◽  
Vol 89 (7) ◽  
pp. 3516-3520 ◽  
Author(s):  
Vladimir K. Bakalov ◽  
Margaret M. Cooley ◽  
Michael J. Quon ◽  
Mei Lin Luo ◽  
Jack A. Yanovski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Body Mass Index ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Cell Function ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Glucose Challenge

Abstract An increased prevalence of impaired glucose homeostasis (IGH) and diabetes mellitus is reported in monosomy X, or Turner syndrome (TS). To determine whether IGH is an intrinsic feature of this syndrome, independent of obesity or hypogonadism, we compared results of a standard oral glucose challenge in age- and body mass index-matched women with TS and with karyotypically normal premature ovarian failure (POF). Fasting glucose levels were normal in both groups, but glucose values after oral glucose challenge were higher in TS [2-h glucose, 135 ± 36 mg/dl (7.5 ± 2.0 mmol/liter) in TS and 97 ± 18 mg/dl (5.4 ± 1.0 mmol/liter) in POF; P < 0.0001]. Glucose-stimulated insulin secretion was lower in TS; e.g. the initial insulin response (ΔI/ΔG30) was decreased by 60% compared with POF (P < 0.0001). We also compared responses to a standard iv glucose tolerance test in women with TS and in age- and body mass index-matched normal women and found that the insulin area under the curve was 50% lower in women with TS (P = 0.003). Insulin sensitivity measured by the quantitative insulin sensitivity check index was higher in women with TS compared with both control groups. Thus, IGH is not secondary to obesity or hypogonadism in TS, but it is a distinct entity characterized by decreased insulin secretion, suggesting that haploinsufficiency for X-chromosome gene(s) impairs β-cell function and predisposes to diabetes mellitus in TS.

Minimal model-derived insulin sensitivity, insulin secretion and glucose tolerance: relationships with blood rheology

2012 ◽  
Vol 51 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Jean-Frédéric Brun ◽  
Emmanuelle Varlet-Marie ◽  
Eric Raynaud de Mauverger ◽  
Jacques Mercier
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Minimal Model ◽  
Blood Rheology

Effect of Dapagliflozin on Insulin Secretion and Insulin Sensitivity in Patients with Prediabetes

2018 ◽  
Vol 128 (08) ◽  
pp. 506-511 ◽  
Author(s):  
Alejandra M. Ramírez-Rodríguez ◽  
Manuel González-Ortiz ◽  
Esperanza Martínez-Abundis
Keyword(s):  
Body Mass Index ◽  
Body Weight ◽  
Uric Acid ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Waist Circumference ◽  
Body Mass ◽  
Fasting Glucose ◽  
Controlled Clinical Trial ◽  
Double Blind

Abstract Aim To evaluate the effect of dapagliflozin on insulin secretion and insulin sensitivity in patients with prediabetes. Methods A randomized, double-blind, placebo-controlled clinical trial was carried out in 24 adults diagnosed with prediabetes and without pharmacological treatment. Patients were randomly assigned into two groups of 12 patients each to receive 10 mg of oral dapagliflozin or placebo once a day during 12 weeks. At baseline and at the end of the study, anthropometric and metabolic measurements were evaluated, including the first phase of insulin secretion, total insulin secretion, and insulin sensitivity. Results After dapagliflozin administration, there were significant decreases in body weight (80.8±16.3 vs. 77.8±14.9 kg, p=0.019), body mass index (30.3±3.5 vs. 29.2±3.1 kg/m2, p=0.023), waist circumference (100.6±13.5 vs. 96.2±11.8 cm, p=0.003), fasting glucose (5.9±0.4 vs. 5.1±0.3 mmol/L, p<0.001) and uric acid (334.3±70.8 vs. 262.9±60.7 mmol/L, p=0.032), with a tendency to increase the insulin sensitivity (1.94±0.72 vs. 2.63±1.04, p=0.064). Conclusion Dapagliflozin administration in patients with prediabetes decreased body weight, body mass index, waist circumference, fasting glucose, and uric acid, with a tendency to increase the insulin sensitivity without changes in insulin secretion.

Insulin sensitivity, insulin secretion, and glucose effectiveness in subjects with impaired glucose tolerance: A minimal model analysis

Metabolism ◽  
1994 ◽  
Vol 43 (6) ◽  
pp. 714-718 ◽  
Author(s):  
Ataru Taniguchi ◽  
Yoshikatsu Nakai ◽  
Mitsuo Fukushima ◽  
Hiroo Imura ◽  
Hitomi Kawamura ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Minimal Model ◽  
Model Analysis ◽  
Glucose Effectiveness

scholarly journals Glucose tolerance, insulin resistance and insulin secretion in young south Indian adults: Relationships to parental size, neonatal size and childhood body mass index

2010 ◽  
Vol 87 (2) ◽  
pp. 283-292 ◽  
Author(s):  
Palany Raghupathy ◽  
Belavendra Antonisamy ◽  
Finney S. Geethanjali ◽  
Julia Saperia ◽  
Samantha D. Leary ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Mass Index ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Body Mass ◽  
Childhood Body Mass Index ◽  
South Indian

scholarly journals Insulin Sensitivity Measured with the Oral Minimal Model is lower in Obese Subjects Who Report omitting their Breakfast

2019 ◽  
pp. 134-145
Author(s):  
Brun JF ◽  
Delbos C ◽  
Gimet F ◽  
Raynaud de Mauverger E ◽  
Mercier J
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Minimal Model ◽  
Cross Sectional Study ◽  
Oral Glucose ◽  
Sectional Study ◽  
Cross Sectional ◽  
Obese Subjects ◽  
Oral Minimal Model

Introduction: Omitting the breakfast has been reported to promote weight gain and to impair insulin sensitivity. However this latter effect was only assessed with simple surrogates. We thus aimed at verifying if insulin sensitivity is lowered in individuals who omit their breakfast with a more quantitative assessment, using the “Oral Minimal Model” (OMM) i.e., an extension of Bergman’s minimal model to oral glucose tolerance-tests, in a cross-sectional study of a population exhibiting the full range of body mass indices.Materials and methods: We selected on our database of patients, explored for weight and/or eating disorders, 27 individuals omitting their breakfast (defined on the basis of an alimentary standardized questionnaire) and compared them to 103 matched subjects taking a hyperglucidic breakfast. The breakfast was analyzed with the OMM for the assessment of insulin sensitivity. Insulin secretion was assessed with a previously reported procedure, allowing the calculation of the parameters of phase 1 and 2 of insulin secretion of Cobelli and Mari’s models. In addition, it is already known that Mari’s model provides an index of post stimulatory potentiation of insulin secretion. Disposition indices (product of SI and insulin secretion parameters) were also determined.Results: In the 27 subjects omitting their breakfast compared to the 103 matched subjects the difference in insulin sensitivity was not found. No difference in insulin secretion parameters is detected. Homeostasis between insulin secretion and insulin sensitivity appears to be functional. However when splitting the sample in categories of BMI the expected difference appears in the range 30-40. In this subgroup (Omitting (n=9) BMI: 35.4±0.99 vs. non-omitting (n=47) BMI: 34.1±0.37 kg/m²) insulin sensitivity was lower in individuals omitting their breakfast (4.32 10-4 min-1/(μU/ml)± 0.94 vs. 9.33±1.84, p=0.03). Despite a slight increase in insulin levels and in the overall insulin secretion rate, a decrease in potentiation and in disposition index was evidenced in individuals omitting their breakfast. The lowering effect of omitting the breakfast on insulin sensitivity is thus evidenced in obese subjects in this sample (but not in those with a BMI below 30). This impairment in insulin sensitivity resulted in a decrease of glucose tolerance by 34%. This finding, based on a cross-sectional study but using a sophisticated measurement, is in agreement with the previous report that omission of the breakfast may induce resistance to insulin. It suggests that the worsening effect on SI that was experimentally found in an interventional study in healthy women becomes important enough in obese subjects to be detected in a cross-sectional study, and that this effect associates a decrease in SI and an incomplete adaptation of insulin release to this reduction in SI, and thus a decrease in glucose tolerance.

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