scholarly journals OR08-02 Do OGTT-based Insulin Secretory Response Measures Approximate 1st Phase Insulin Response in Pregnant Women?

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Camille Elise Powe ◽  
Larraine Huston Gordesky ◽  
Patrick M Catalano
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Late Pregnancy ◽  
Secretory Response ◽  
Oral Glucose ◽  
Glucose Load ◽  
Response Measures ◽  
Insulin Secretory Response ◽  
In Pregnancy

Abstract Background: We previously showed that 1st phase insulin response increases dramatically in pregnancy, independent of changes in insulin sensitivity. Measurement of 1st phase insulin response requires the use of hyperglycemic clamps or intravenous glucose tolerance tests (IVGTTs) which are rarely performed in pregnant women. Oral glucose tolerance test (OGTT)-based measures of insulin secretory response have not been validated in pregnancy. Methods: In a secondary analysis of a longitudinal study of glucose metabolism in pregnancy, we examined Pearson correlations between OGTT-based insulin secretory response measures and 1st phase insulin response. Forty women were studied pre-pregnancy; 36 returned in early and late pregnancy (12–14 and 34–36 weeks gestation). At each time point, after overnight fasts, an IVGTT and an OGTT were performed on separate days. The 1st phase insulin response was calculated as the incremental area under the curve during the 1st 10 minutes after intravenous administration of a 0.5 g/kg glucose load (or 19g/m2 body surface area if weight >120% ideal body weight). Homeostatic Model Assessment (HOMAB), Insulinogenic index (IGI), Corrected insulin response (CIR), Insulin area under the curve/Glucose area under the curve (AUCins/AUCglu), and the Stumvoll 1st Phase Estimate (Stumvoll) were calculated from insulin and glucose levels measured fasting and 30, 60, 90, 120, and 180 minutes after an oral glucose load (75 grams pre-pregnancy, 100 grams in pregnancy). Results: The best OGTT-based measure for estimation of 1st phase insulin response differed across study timepoints. In early and late pregnancy, AUCins/AUCglu had the strongest correlation with 1st phase insulin response (early: R=0.79, P<0.0001; late: R=0.69, P<0.0001), but was not associated with 1st phase insulin response pre-pregnancy (R=0.32, P=0.08). IGI had the strongest correlation with first phase insulin response pre-pregnancy (R=0.50, P=0.005) and was correlated with 1st phase insulin response in late (R=0.68, P=0.0001), but not early (R=0.36, P=0.07) pregnancy. Stumvoll was the only OGTT-based measure that was significantly correlated with 1st phase insulin response at all timepoints (pre: R=0.44, P=0.01; early: R=0.67, P=0.0001; late: R=0.67, P=0.0001). HOMAB was the weakest correlate of 1st phase insulin response, though the correlation was significant in early pregnancy (pre: R=-0.04, P=0.82; early: R=0.33, P=0.05; late: R=0.18, P=0.28). Conclusion: OGTT-based measures of insulin secretion do not have a consistent relationship with 1st phase insulin response across pre-, early, and late pregnancy. Our findings suggest that Stumvoll can be used in OGTT-based longitudinal studies of insulin secretory response that begin prior to pregnancy and span gestation. For cross-sectional studies in pregnancy, AUCins/AUCglu are the best estimates of 1st phase insulin response.

Evidence that the oral glucose-tolerance test does not provide a uniform stimulus to pancreatic islets in pregnancy.

1989 ◽  
Vol 35 (7) ◽  
pp. 1482-1485 ◽  
Author(s):  
E A de Leacy ◽  
D M Cowley
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Pancreatic Islets ◽  
Glucose Tolerance Test ◽  
Insulin Response ◽  
Tolerance Test ◽  
Glucose Absorption ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Glucose Load

Abstract Fifty consecutive pregnant patients referred for a glucose-tolerance test were classified on the basis of increasing (n = 20) or decreasing (n = 28) hematocrit after an oral 75-g glucose load. (The hematocrit did not change in the other two patients.) Patients with increasing hematocrit, a response previously seen in patients with the dumping syndrome, showed significantly flatter increases in glucose concentrations in plasma after the load. The mean decrease in the concentration of phosphate in plasma, measured as an index of glucose uptake by cells, was significantly less (P less than 0.05) 2 h after the load in the group with flatter glucose responses, suggesting that the flat response is ascribable to poor glucose absorption rather than to an exaggerated insulin response. These results indicate that the oral glucose-tolerance test stresses the pancreatic islets differently in different pregnant subjects, owing to individual variations in the gastrointestinal handling of the glucose load. Consequently, patients may give a "normal" result who might otherwise become hyperglycemic after normal meals. We suggest that alternative screening procedures be investigated to assess pregnant patients postprandially.

Involvement of capsaicin-sensitive nerves in regulation of insulin secretion and glucose tolerance in conscious mice

1994 ◽  
Vol 267 (4) ◽  
pp. R1071-R1077 ◽  
Author(s):  
S. Karlsson ◽  
A. J. Scheurink ◽  
A. B. Steffens ◽  
B. Ahren
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Response ◽  
Secretory Response ◽  
Sensory Nerves ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Intravenous Glucose ◽  
The Impact ◽  
Insulin Secretory Response

The impact of sensory nerves in glucose-stimulated insulin secretion and glucose tolerance was investigated in conscious mice treated neonatally with either capsaicin (Cap) or vehicle (Veh). At 10-12 wk after Cap, both the early (1 min) insulin secretory response to intravenous glucose (2.8 mmol/kg) (by 67%) and glucose elimination were potentiated (P < 0.05). In contrast, basal insulin, glucagon, and glucose were not affected by Cap. Plasma norepinephrine and epinephrine levels did not differ between Cap- and Veh-treated animals, whereas the increase in plasma insulin levels normally induced by alpha-adrenoceptor blockade by phentolamine was absent after Cap treatment. In isolated islets, the insulin secretory response to glucose (20 mmol/l), carbachol (0.1 mmol/l), or phentolamine (0.5 mmol/l) was not affected after Cap. It is concluded that sensory denervation by Cap results in increased glucose tolerance, which is in part because of a potentiated early insulin response to glucose. This potentiation does not seem secondary to altered plasma catecholamine levels or to altered islet secretory capacity. The results suggest rather that Cap-sensitive nerves, by a local effector function and/or as the afferent loop of a neural reflex, exert inhibitory influences on insulin secretion.

Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity

1983 ◽  
Vol 55 (2) ◽  
pp. 512-517 ◽  
Author(s):  
G. W. Heath ◽  
J. R. Gavin ◽  
J. M. Hinderliter ◽  
J. M. Hagberg ◽  
S. A. Bloomfield ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Insulin Binding ◽  
Normal Glucose Tolerance ◽  
Residual Effects ◽  
Oral Glucose ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Normal Glucose ◽  
Blood Glucose Concentrations

Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations to training which correlate with maximal oxygen uptake (VO2max) and reduced adiposity. Our study was undertaken to test the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon. Eight well-trained subjects stopped training for 10 days. There were no significant changes in VO2max (58.6 +/- 2.2 vs. 57.6 +/- 2.1 ml/kg), estimated percent body fat (12.5 +/- 0.7 vs. 12.5 +/- 0.8%), or body weight. The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Despite the increased insulin levels, blood glucose concentrations were higher after 10 days without exercise. Insulin binding to monocytes also decreased with physical inactivity. One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial “trained” value. These results support our hypothesis.

scholarly journals Interesting insulin response to oral glucose load in young Japanese subjects with impaired glucose tolerance

Diabetes Care ◽  
2000 ◽  
Vol 23 (5) ◽  
pp. 710-712 ◽  
Author(s):  
Y. Tanaka ◽  
Y. Atsumi ◽  
K. Matsuoka ◽  
T. Onuma ◽  
R. Kawamori
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Insulin Response ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Japanese Subjects

Effect of an enkephalin-analogue (FK 33-824) on glucose tolerance in man

1983 ◽  
Vol 104 (1) ◽  
pp. 85-90 ◽  
Author(s):  
X. Jeanrenaud ◽  
E. Maeder ◽  
E. Del Pozo ◽  
J. P. Felber
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Normal Subjects ◽  
Glucose Absorption ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Oral Test ◽  
Insulin Response To Glucose ◽  
Glucose Curve

Abstract. The purpose of the present work was to study the effect of a methionine-enkephalin analogue (FK 33-824) on glucose tolerance in man. Groups of 5 to 8 normal subjects were given a 0.5 mg im injection of the drug or placebo just before a 100 g oral glucose load or a 0.5 g/kg iv glucose load. In the enkephalin analogue treated subjects, diminished insulin response to glucose was observed following the oral glucose load, with insulin values significantly lower than in the controls from time 10 to 90 min, but no corresponding change in the glucose curve. This effect was not observed when glucose was given iv in another group of 5 subjects in whom the significant blunting of the insulin response was accompanied by a significant decrease in glucose tolerance. These observations demonstrate that in man, enkephalin produces a decrease in insulin secretion in response to both oral and iv glucose loads. The absence of any marked impairment in glucose tolerance in the oral test in spite of the decreased insulin response suggests that enkephalin might have an additional effect in delaying glucose absorption.

A NEW PRINCIPLE FOR THE COMPARISON OF INSULIN SECRETORY RESPONSES

1973 ◽  
Vol 74 (3) ◽  
pp. 524-541 ◽  
Author(s):  
Klaus Johansen
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Beta Cells ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Secretory Response ◽  
Obese People ◽  
Intravenous Glucose ◽  
Large Groups ◽  
Insulin Secretory Response

ABSTRACT In an attempt to circumvent the difficulties inherent in the use of insulin/glucose ratios a new principle for the comparison of insulin secretory resonses has been developed. From large groups of obese and non-obese people subjects are selected so that the subgroups ultimately formed are comparable with regard to age and to their degree of glucose tolerance. This means that the blood glucose curves of the two groups are merging and that the beta cells are subjected to identical glycaemic stimuli. The study shows that obese young non-diabetics and obese young and old diabetics exhibit an augmented insulin response to stimulation with oral and intravenous glucose and to intravenous tolbutamide. No increase in plasma insulin secretory response is, however, demonstrable in obese, old non-diabetics.

Endocrine pancreatic function in women with gestational diabetes

1986 ◽  
Vol 113 (3_Suppl) ◽  
pp. S19-S23 ◽  
Author(s):  
Claus Kühl ◽  
Peter J. Hornnes
Keyword(s):  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Pregnant Women ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Insulin Degradation ◽  
Insulinogenic Index ◽  
Insulin Responses ◽  
In Pregnancy

Abstract. Glucose tolerance deteriorates in normal human pregnancy but 99% of all pregnant women retain normal glucose tolerance whereas the remaining 1% develop abnormal glucose tolerance and are designated gestational diabetics. The possibility that glucose tolerance deteriorates in pregnancy because of diabetes-like changes in the secretory function of the endocrine pancreas has been investigated in gestational diabetics and healthy controls. Even though the insulin responses to oral glucose and mixed meals are equally large in gestational diabetics and normal pregnant women, the insulin responses of the gestational diabetics differ in two pertinent ways from those of the normals. First, a delayed insulin response is frequently seen, and second, the insulin response per unit of glycaemic stimulus (the 'insulinogenic index') is normally significantly lower than that of the normal pregnant women. Diabetes-like changes in the secretion of glucagon are not seen in neither group. Insulin degradation is unaffected by pregnancy and the proinsulin share of the total plasma insulin immunoreactivity does not increase in pregnancy. It is therefore likely that the main reason for the diabetogenicity of pregnancy is insulin resistance. Most pregnant women are able to increase their insulin secretion and thus overcome the resistance. Some pregnant women do, however, seem to have a more limited insulin secretory capacity which eventually may lead to the development of gestational diabetes.

scholarly journals Acute Postexercise Effects of Concentric and Eccentric Exercise on Glucose Tolerance

2015 ◽  
Vol 25 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Matthew David Cook ◽  
Stephen David Myers ◽  
John Stephen Michael Kelly ◽  
Mark Elisabeth Theodorus Willems
Keyword(s):  
Glucose Tolerance ◽  
Eccentric Exercise ◽  
Glucose Control ◽  
Isometric Force ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Acute Effect ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Downhill Running

Impaired glucose tolerance was shown to be present 48 hr following muscle-damaging eccentric exercise. We examined the acute effect of concentric and muscle-damaging eccentric exercise, matched for intensity, on the responses to a 2-hr 75-g oral glucose tolerance test (OGTT). Ten men (27 ± 9 years, 178 ± 7 cm, 75 ± 11 kg, VO2max: 52.3 ± 7.3 ml·kg-1·min-1) underwent three OGTTs after an overnight 12 hr fast: rest (control), 40-min (5 × 8-min with 2-min interbout rest) of concentric (level running, 0%, CON) or eccentric exercise (downhill running, –12%, ECC). Running intensity was matched at 60% of maximal metabolic equivalent. Maximal isometric force of m. quadriceps femoris of both legs was measured before and after the running protocols. Downhill running speed was higher (level: 9.7 ± 2.1, downhill: 13.8 ± 3.2 km·hr-1, p < .01). Running protocols had similar VO2max (p = .59), heart rates (p = .20) and respiratory exchange ratio values (p = .74) indicating matched intensity and metabolic demands. Downhill running resulted in higher isometric force deficits (level: 3.0 ± 6.7, downhill: 17.1 ± 7.3%, p < .01). During OGTTs, area-under-the-curve for plasma glucose (control: 724 ± 97, CON: 710 ± 77, ECC: 726 ± 72 mmol·L-1·120 min, p = .86) and insulin (control: 24995 ± 11229, CON: 23319 ± 10417, ECC: 21842 ± 10171 pmol·L-1·120 min, p = .48), peak glucose (control: 8.1 ± 1.3, CON: 7.7 ± 1.2, ECC: 7.7 ± 1.1 mmol·L-1, p = .63) and peak insulin levels (control: 361 ± 188, CON: 322 ± 179, ECC: 299 ± 152 pmol·L-1, p = .30) were similar. It was concluded that glucose tolerance and the insulin response to an OGTT were not changed immediately by muscle-damaging eccentric exercise.

scholarly journals P007 Eating in alignment with the circadian clock: A strategy to reduce the metabolic impact of nightwork

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A23-A24
Author(s):  
S Centofanti ◽  
L Heilbronn ◽  
G Wittert ◽  
A Coates ◽  
J Dorrian ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Mixed Model ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Metabolic Effects ◽  
Energy Requirements ◽  
Oral Glucose ◽  
Recovery Sleep ◽  
The Impact

Abstract Nightwork disrupts circadian rhythms and impairs glucose metabolism, increasing the risk for type 2 diabetes. We investigated eliminating or reducing the amount of food consumed during simulated nightwork as a countermeasure to reduce the impact of circadian disruption on glucose metabolism. N=52 healthy, non-shiftworking participants (24.4±4.9 years; 26 Females; BMI 23.8±2.5kg/m2) underwent a 7-day laboratory protocol with an 8h TIB baseline sleep, followed by 4 simulated nightshifts with 7h TIB daytime sleep and an 8h TIB recovery sleep in groups of 4 participants. Each group was randomly assigned to a meal-at-midnight (n=17, 30% energy requirements), snack-at-midnight (n=16, 10% energy requirements) or no-eating-at-midnight (n=19) condition. Total 24h energy and macronutrient intake were constant across conditions. Standard oral glucose tolerance tests (OGTT) were conducted on day2 (baseline), and day7 (recovery). Plasma was sampled at -15, 0, 15, 30, 60, 90, 120, 150 mins, assayed for glucose and insulin. Area under the curve (AUC) was the calculated. Mixed model analyses of glucose AUC found a condition-by-day interaction (p&lt;0.001). Glucose responses to OGTT did not change with nightwork in the no-eating-at-midnight condition (p=0.219) but worsened in the meal-at-midnight (p&lt;0.001) and snack-at-midnight (p=0.022) conditions. Insulin AUC was different by condition (p=0.047). Insulin was highest after nightwork in the no-eating-at-midnight compared to meal-at-midnight (p=0.014) but not snack-at-midnight (p=0.345). Glucose tolerance was impaired by eating-at-midnight, associated with a lower than expected insulin response. Further work is required to determine the effect of meal or snack composition as a strategy to mitigate adverse metabolic effects of nightwork.

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