A defect in insulin release in women at risk of future non-insulin-dependent diabetes

1991 ◽  
Vol 81 (2) ◽  
pp. 195-199 ◽  
Author(s):  
Anne Dornhorst ◽  
Simon G. M. Edwards ◽  
Jonathan S. D. Nicholls ◽  
Victor Anyaoku ◽  
Duncan Mclaren ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Gestational Diabetes ◽  
Plasma Glucose ◽  
Fasting Glucose ◽  
Glucose Production ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Glucose Levels ◽  
Control Subjects ◽  
Previous Gestational Diabetes

1. A study on seven Caucasian glucose-tolerant women with previous gestational diabetes and seven matched control subjects is presented. The insulin response to oral glucose, insulin sensitivity and fasting glucose production rates were measured by using a 75 g oral glucose tolerance test, an insulin tolerance test and a non-radioactive tracer, [6,6-2H]glucose, respectively. 2. Fasting plasma glucose levels were similar between the women with previous gestational diabetes and the control subjects (4.8 ± 0.3 versus 4.7 ± 0.2 mmol/l), as were fasting plasma insulin levels (median 4 m-units/l, range 1–13 m-units/l versus median 4 m-units/l, range 1–24 m-units/l). After oral glucose the 60 min plasma glucose levels in the women with previous gestational diabetes were significantly higher (8.5 ± 0.6 versus 6.7 ± 0.8 mmol/l, P < 0.05), whereas the plasma insulin level was significantly lower at both 30 min (median 23 m-units/l, range 4–47 m-units/l versus median 55 m-units/l, range 23–100 m-units/l, P < 0.02) and at 60 min (median 23 m-units/l, range 4–43 m-units/l versus median 60 m-units/l, range 16–126 m-units/l, P< 0.02). 3. Insulin sensitivity, expressed as the slope of the regression line of plasma glucose level against time after intravenous infusion of insulin (0.05 unit/kg), was similar in the women with previous gestational diabetes and the control subjects (mean slope, −0.17 ± 0.01 versus −0.17 ± 0.01). 4. Fasting glucose production rates were similar in the women with previous gestational diabetes and the control subjects (2.2 ± 0.3 versus 1.9 ± 0.1 mg min−1 kg−1). 5. Women with previous gestational diabetes, a group at risk of future non-insulin-dependent diabetes, have abnormalities of insulin release at a time when insulin sensitivity and fasting glucose production are normal.

scholarly journals Gestational diabetes and fetal outcome: a study in a tertiary care centre

2017 ◽  
Vol 6 (10) ◽  
pp. 4458
Author(s):  
V. G. Vanamala
Keyword(s):  
Birth Weight ◽  
Gestational Diabetes ◽  
Tertiary Care ◽  
Tolerance Test ◽  
Fetal Outcome ◽  
Oral Glucose ◽  
Tertiary Care Centre ◽  
Glucose Levels ◽  
The People ◽  
Urine Examination

Background: Due to urbanization and sedentary lifestyle, dietary changes, and increased obesity of the people, the incidence of GDM is steadily on the rise. It is associated with severe morbidity to the mother and the child. It is therefore imperative that an early diagnosis needs to be done so that appropriate treatment can be given.Methods: 1654 women who were included in the study were in their 24 – 28 weeks of gestation. A standardized questionnaire was formatted and details regarding the age, weight, body mass index (BMI), parity, previous medical and obstetrics history and familial history of diabetes, tests for glucose levels, complete blood picture, routine urine examination. Oral glucose tolerance test was done for all the patients after fasting overnight.Results: 87 (5.3%) of them were positive for OGTT and were considered to have Gestational Diabetes mellitus. 67.8% of the patients were in the 25-30 age group. 41.4% were pregnant for the first time and 58.6% were multi gravid. The majority of the patients had a BMI between 26-30. Most of the babies had a birth weight of above 3kgs. Out of them, 39 (44.8%) had a birth weight between 3.1-3.5kgs. <2kgs were seen in 7 (8.0%) patients.Conclusions: GDM complicates pregnancy and results in higher frequency of adverse effects in the mother and new born. Thereby, early detection can result in prompt treatment and lowering the morbidity of the fetal outcomes.

Prevalence of Hypoglycemia Following Pre-exercise Carbohydrate Ingestion Is Not Accompanied by Higher Insulin Sensitivity

2002 ◽  
Vol 12 (4) ◽  
pp. 398-413 ◽  
Author(s):  
Roy L.P.G. Jentjens ◽  
Asker E. Jeukendrup
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Glucose Tolerance Test ◽  
Time Trial ◽  
Tolerance Test ◽  
Cycle Ergometer ◽  
Submaximal Exercise ◽  
Oral Glucose ◽  
Carbohydrate Ingestion ◽  
Carbohydrate Feeding

Pre-exercise carbohydrate feeding may result in rebound hypoglycemia in some but not all athletes. The aim of the present study was to examine whether insulin sensitivity in athletes who develop rebound hypoglycemia is higher compared with those who do not show rebound hypoglycemia. Twenty trained athletes (V̇O2max of 61.8 ± 1.4 ml · kg−1 · min−1) performed an exercise trial on a cycle ergometer. Forty-five minutes before the start of exercise, subjects consumed 500 ml of a beverage containing 75 g of glucose. The exercise trial consisted of · 20 min of submaximal exercise at 74 ± 1% V̇O2max immediately followed by a time trial. Based upon the plasma glucose nadir reached during submaximal exercise, subjects were assigned to a Hypo group (<3.5 mmol/L) and a Non-hypo group (≥3.5 mmol/L). An oral glucose tolerance test was performed to obtain an index of insulin sensitivity (ISI). The plasma glucose nadir during submaximal exercise was significantly lower (p < .01) in the Hypo-group (n = 10) compared with the Non-hypo group (n = 10) (2.7 ± 0.1 vs. 4.1 ± 0.2 mmol/L, respectively). No difference was found in ISI between the Hypo and the Non-hypo group (3.7 ± 0.4 vs. 3.8 ± 0.5, respectively). The present results suggest that insulin sensitivity does not play an important role in the occurrence of rebound hypoglycemia.

Plasma Glucose, Non-Esterified Fatty Acids and Amino Acids in Huntington's Chorea

1977 ◽  
Vol 52 (3) ◽  
pp. 311-318 ◽  
Author(s):  
O. T. Phillipson ◽  
E. D. Bird
Keyword(s):  
Plasma Glucose ◽  
Plasma Concentrations ◽  
Provocation Test ◽  
Tolerance Test ◽  
Control Group ◽  
Oral Glucose ◽  
Huntington's Chorea ◽  
Plasma Tryptophan ◽  
Control Subjects ◽  
Free Tryptophan

1. The metabolic responses to an oral glucose tolerance test (100 g) and an intravenous insulin provocation test (0·1 i.u./kg) were studied in nine control subjects and nine patients with Huntington's chorea. 2. Plasma glucose responses to these stimuli were identical in both groups. 3. High fasting concentrations of non-esterified fatty acid (NEFA) were recorded in the choreic patients when compared with control subjects. This difference was maintained under hypoglycaemic conditions. However, during hyperglycaemia the differences in NEFA concentrations between the groups was abolished. 4. Total plasma tryptophan concentrations were equal in the two groups. Free plasma tryptophan, however, was markedly reduced in the choreic group, and this appeared to be a result of a disturbed relationship between free tryptophan and NEFA concentrations. The abnormalities in free tryptophan values were sensitive to plasma glucose concentrations, as hyperglycaemic conditions markedly reduced the differences between the choreic and control group. 5. Patients with Huntington's chorea showed reduced fasting plasma concentrations of leucine, isoleucine and valine.

scholarly journals Mechanisms Underlying the Pathogenesis of Isolated Impaired Glucose Tolerance in Humans

2016 ◽  
Vol 101 (12) ◽  
pp. 4816-4824 ◽  
Author(s):  
Ron T. Varghese ◽  
Chiara Dalla Man ◽  
Anu Sharma ◽  
Ivan Viegas ◽  
Cristina Barosa ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Fasting Glucose ◽  
Glucose Production ◽  
Tolerance Test ◽  
Endogenous Glucose Production ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Endogenous Glucose

Context: Prediabetes is a heterogeneous disorder classified on the basis of fasting glucose concentrations and 2-hour glucose tolerance. Objective: We sought to determine the relative contributions of insulin secretion and action to the pathogenesis of isolated impaired glucose tolerance (IGT). Design: The study consisted of an oral glucose tolerance test and a euglycemic clamp performed in two cohorts matched for anthropometric characteristics and fasting glucose but discordant for glucose tolerance. Setting: An inpatient clinical research unit at an academic medical center. Patients or Other Participants: Twenty-five subjects who had normal fasting glucose (NFG) and normal glucose tolerance (NGT) and 19 NFG/IGT subjects participated in this study. Intervention(s): Subjects underwent a seven-sample oral glucose tolerance test and a 4-hour euglycemic, hyperinsulinemic clamp on separate occasions. Glucose turnover during the clamp was measured using tracers, and endogenous hormone secretion was inhibited by somatostatin. Main Outcome Measures: We sought to determine whether hepatic glucose metabolism, specifically the contribution of gluconeogenesis to endogenous glucose production, differed between subjects with NFG/NGT and those with NFG/IGT. Results: Endogenous glucose production did not differ between groups before or during the clamp. Insulin-stimulated glucose disappearance was lower in NFG/IGT (24.6 ± 2.2 vs 35.0 ± 3.6 μmol/kg/min; P = .03). The disposition index was decreased in NFG/IGT (681 ± 102 vs 2231 ± 413 × 10−14 dL/kg/min2 per pmol/L; P &lt; .001). Conclusions: We conclude that innate defects in the regulation of glycogenolysis and gluconeogenesis do not contribute to NFG/IGT. However, insulin-stimulated glucose disposal is impaired, exacerbating defects in β-cell function.

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