Glucose Tolerance and Insulin and Gastric Inhibitory Polypeptide Responses following Intraduodenal Glucose Loading in Dogs with Obstructive Jaundice

1987 ◽  
Vol 4 (2) ◽  
pp. 76-81
Author(s):  
Kenichi Yoshiya ◽  
Takehira Yamamura ◽  
Yoshio Ishikawa ◽  
Joji Utsunomiya ◽  
Jiro Takemura ◽  
...  
Keyword(s):  
Obstructive Jaundice ◽  
Glucose Tolerance ◽  
Gastric Inhibitory Polypeptide ◽  
Glucose Loading

Predictive value of glucose tolerance test

1982 ◽  
Vol 63 (1) ◽  
pp. 18-19
Author(s):  
V. G. Baranov
Keyword(s):  
Glucose Tolerance ◽  
Tolerance Test ◽  
Normal Glucose Tolerance ◽  
Time Intervals ◽  
Glucose Content ◽  
Glucose Loading ◽  
Normal Glucose ◽  
Risk Zones ◽  
Long Term Observation

Abstract. A retrospective analysis of the long-term observation of the dynamics of normal glucose tolerance in 564 women was carried out. Re-examination revealed violations of tolerance in 33.8% (of doubtful type in 25.7% and of diabetic type in 8.1%). An unfavorable prognostic value of the blood glucose content after glucose loading was established after 1 hour - from 7.8 mmol / L and more and after 2 hours - from 6.1 mmol / L or more. It is proposed to consider these levels as the limit of normoglycemia at the indicated time intervals when conducting a test for glucose tolerance. Glycemia from 7.8 to 9.9 mmol / L 1 hour after glucose loading and from 6.1 to 7.2 mmol / L after 2 hours are regarded by the authors as risk zones for diabetes mellitus.

scholarly journals The effect of soluble- and insoluble-fibre supplementation on post-prandial glucose tolerance, insulin and gastric inhibitory polypeptide secretion in healthy subjects

1990 ◽  
Vol 64 (1) ◽  
pp. 103-110 ◽  
Author(s):  
L. M. Morgan ◽  
J. A. Tredger ◽  
J. Wright ◽  
V. Marks
Keyword(s):  
Gastric Emptying ◽  
Glucose Tolerance ◽  
Sugar Beet ◽  
Guar Gum ◽  
Venous Blood ◽  
Gastric Inhibitory Polypeptide ◽  
Soya Bean ◽  
Blood Samples ◽  
Insulin Levels ◽  
Prandial Insulin

Six healthy non-obese male subjects were given three test meals containing 100 g carbohydrate and 1.5 g soluble paracetamol, supplemented on one occasion with 10 g guar gum and on another with 10 g sugarbeet fibre. A further six subjects were given the same test meal supplemented on one occasion with 10 g soya-bean-cotyledon fibre and on another, 5 g glucomannan. Venous blood samples were taken before, and at intervals for 180 min following the meal, and analysed for insulin, gastric inhibitory polypeptide (GIP) and paracetamol (as an index of gastric emptying). Arterialized blood samples were taken and analysed for glucose. Meal supplementation with both guar gum and sugar-beet fibre improved glucose tolerance, but circulating glucose levels were unaffected by the addition of either soya-bean-cotyledon fibre or glucomannan to the meals. Supplementation with guar gum and glucomannan lowered post-prandial insulin levels. Insulin levels were enhanced by addition of soya-bean-cotyledon fibre to the meal and unaffected by sugar-beet fibre. Post-prandial GIP levels were lowered in the guar–gum–supplemented meal and augmented with sugar-beet fibre supplementation. Addition of glucomannan and soya-bean-cotyledon fibre did not affect circulating GIP levels. The study failed to confirm previous reports of improved glucose tolerance following glucomannan and soya-bean-cotyledon fibre supplementation. The failure of sugar-beet fibre to reduce post-prandial insulin secretion despite improved glucose tolerance may be due to the observed increased secretion of GIP. The increased insulin levels seen following soya-bean-cotyledon fibre supplementation cannot be attributed either to changes in glucose tolerance, GIP secretion or gastric emptying.

Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms

2009 ◽  
Vol 297 (2) ◽  
pp. E532-E537 ◽  
Author(s):  
Sandra Bonuccelli ◽  
Elza Muscelli ◽  
Amalia Gastaldelli ◽  
Elisabetta Barsotti ◽  
Brenno D. Astiarraga ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Cell Function ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Fat Free Mass ◽  
Oral Glucose ◽  
Glucose Response ◽  
Glucose Loading ◽  
Endogenous Glucose

Improved glucose tolerance to sequential glucose loading (Staub-Traugott effect) is an important determinant of day-to-day glycemic exposure. Its mechanisms have not been clearly established. We recruited 17 healthy volunteers to receive two sequential oral glucose tolerance tests (OGTTs), at time 0 min and 180 min ( Study I). The protocol was repeated on a separate day ( Study II) except that plasma glucose was clamped at 8.3 mmol/l between 60 and 180 min. β-Cell function was analyzed by mathematical modeling of C-peptide concentrations. In a subgroup, glucose kinetics were measured by a triple-tracer technique (infusion of [6,6-2H2]glucose and labeling of the 2 glucose loads with [1-2H]glucose and [U-13C]glucose). In both Studies I and II, the plasma glucose response to the second OGTT equaled 84 ± 2% ( P = 0.003) of the response to the first OGTT. Absolute insulin secretion was lower (37.8 ± 4.3 vs. 42.8 ± 5.1 nmol/m2, P = 0.02), but glucose potentiation (i.e., higher secretion at the same glycemia) was stronger (1.08 ± 0.02- vs. 0.92 ± 0.02-fold, P = 0.006), the increment being higher in Study II (+36 ± 5%) than Study I (+19 ± 6%, P < 0.05). In pooled data, a higher glucose area during the first OGTT was associated with a higher potentiation during the second OGTT (rho=0.60, P = 0.002). Neither insulin clearance nor glucose clearance differed between loads, and appearance of glucose over 3 h totalled 60 ± 6 g for the first load and 52 ± 5 g for the second load ( P = not significant). Fasting endogenous glucose production [13.3 ± 0.6 μmol·min−1·kg fat-free mass (FFM)−1] averaged 6.0 ± 3.8 μmol·min−1·kg FFM−1 between 0 and 180 min and 1.7 ± 2.6 between 180 and 360 min ( P < 0.03). Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect.

scholarly journals Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet

1988 ◽  
Vol 59 (3) ◽  
pp. 373-380 ◽  
Author(s):  
L. M. Morgan ◽  
S. M. Hampton ◽  
J. A. Tredger ◽  
R. Cramb ◽  
V. Marks
Keyword(s):  
Glucose Tolerance ◽  
Energy Intake ◽  
Plasma Glucose ◽  
High Fat Diet ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Fat Intake ◽  
High Fat ◽  
C Peptide ◽  
Glucose Levels

1. Five healthy volunteers (usual fat intake 103) (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose.2. Subjects increased their fat intake by 68 (SE 9·6) % for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)).3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured.4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0–180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P < 0·05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P < 0·01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0–180 min, following oral glucose 6·7 (SE 0·3) mmol/l.h for control and 4·2 (SE 0·6) mmol/l.h for HFD; P < 0·01).5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance.6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine.

Reduced gastric inhibitory polypeptide but normal glucagon-like peptide 1 response to oral glucose in postmenopausal women with impaired glucose tolerance

1997 ◽  
pp. 127-131 ◽  
Author(s):  
B Ahren ◽  
H Larsson ◽  
JJ Holst
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Postmenopausal Women ◽  
Plasma Levels ◽  
Insulin Response ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

OBJECTIVE: The gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are both released from the gut after oral glucose ingestion and stimulate insulin secretion. This study examined the release of these hormones in subjects with impaired glucose tolerance (IGT), which precedes the development of non-insulin-dependent diabetes. DESIGN AND METHODS: Six postmenopausal women with IGT, aged 59 years, underwent a 75 g oral glucose tolerance test and plasma levels of GIP and GLP-1 were determined regularly during the following 2 h. The results were compared with those in seven age- and weight-matched women with normal glucose tolerance (NGT). RESULTS: Basal plasma levels of GIP and GLP-1 were not different between the groups. In response to the oral glucose ingestion, plasma levels of both GIP and GLP-1 increased in both groups. The plasma GIP increase after glucose ingestion was, however, reduced in women with IGT. Thus, the GIP response as determined as the area under the curve for the 60 min after oral glucose was 34.8 +/- 3.2 pmol/l per min in women with IGT versus 56.4 +/- 7.8 pmol/l per min in those with NGT (P = 0.021). In contrast, the GLP-1 response to oral glucose was not different between the groups. By definition, the glucose response to oral glucose was markedly increased in women with IGT, and the insulin response during the second hour after glucose ingestion was exaggerated. CONCLUSIONS: The GIP response to oral glucose is impaired in postmenopausal women with IGT, whereas the plasma GLP-1 response is not affected.

Effects of an oral glucose tolerance test on the myogenic response in healthy individuals

2007 ◽  
Vol 292 (1) ◽  
pp. H304-H310 ◽  
Author(s):  
Mary E. J. Lott ◽  
Cynthia Hogeman ◽  
Michael Herr ◽  
Robert Gabbay ◽  
Lawrence I. Sinoway
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Transmural Pressure ◽  
Oral Glucose ◽  
Myogenic Response ◽  
Oral Glucose Tolerance ◽  
Healthy Individuals ◽  
Glucose Loading

The myogenic response, the inherent ability of blood vessels to rapidly respond to changes in transmural pressure, is involved in local blood flow autoregulation. Animal studies suggest that both acute hyperglycemia and hyperinsulinemia may impair myogenic vasoconstriction. The purpose of this study was to examine the effects of an oral glucose load on brachial mean blood velocity (MBV) during increases in forearm transmural pressure in humans. Eight healthy men and women (38 ± 5 yr) underwent an oral glucose tolerance test (OGTT). MBV (in cm/s; Doppler ultrasound) responses to a rise in forearm transmural pressure (arm tank suction, −50 mmHg) were studied before and every 30 min for 120 min during the OGTT. Before the start of the OGTT, MBV was lower than baseline values 30 and 60 s after the application of negative pressure. This suggests that myogenic constriction was present. During the OGTT, blood glucose rose from 88 ± 2 to 120 ± 6 mg/dl ( P < 0.05) and insulin rose from 14 ± 1 to 101 ± 32 μU/ml ( P < 0.05). Glucose loading attenuated the reduction in MBV with arm suction (Δ−0.73 ± 0.14 vs. Δ−1.67 ± 0.43 cm/s and Δ−1.07 ± 0.14 vs. Δ−2.38 ± 0.54 cm/s, respectively, during 30 and 60 s of suction postglucose compared with preglucose values; all P < 0.05). We observed no such time effect for myogenic responses during a sham OGTT. In an additional 5 subjects, glucose loading had no effect on brachial diameters with the application of negative pressure. Oral glucose loading leads to attenuated myogenic vasoconstriction in healthy individuals. The role that this diminished postglucose reactivity plays in mediating postprandial hypotension and/or orthostasis needs to be further explored.

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