scholarly journals Glucose Tolerance and Insulin Response to Intravenous Glucose Load in Sheep Fed on Germinated Sorghum Grain

2007 ◽  
Vol 20 (10) ◽  
pp. 1575-1579 ◽  
Author(s):  
Joelal Achmadi ◽  
Eko Pangestu ◽  
Fajar Wahyono
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Sorghum Grain ◽  
Intravenous Glucose Load

Low Vitamin K Intake Effects on Glucose Tolerance in Rats

1999 ◽  
Vol 69 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Sakamoto ◽  
Wakabayashi ◽  
Sakamoto
Keyword(s):  
Glucose Tolerance ◽  
Vitamin K ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Glucose Tolerance Tests ◽  
Early Insulin Response ◽  
Intravenous Glucose Tolerance Tests

To investigate the effects of vitamin K (VK) on pancreatic function, intravenous glucose tolerance tests were performed in rats fed with and without low VK diet (inclucing less than 20% required vitamin K1). Plasma glucose and immuno-reactive insulin (IRI) were determined. It was found that at 0 min., plasma glucose and IRI levels in low VK group were slightly less than in the control (glucose, 204.5 ± 21.7 vs. 229 ± 19.6 mg/dl, IRI, 6.6 ± 1.3 vs. 9.3 ± 1.8 ng/ml mean ± SEM). At 3 min. after glucose administration, plasma glucose was higher (391.8 ± 25.6 vs. 371.8 ± 18.7 mg/dl) and IRI, lower (11.8 ± 2.1 vs. 18.2 ± 3.6 ng/ml) in the low VK group. The disappearance rate of plasma glucose in the low VK group at 5–10 min. was significantly less than in the control (6.7 ± 2.2 vs. 11.9 ± 1.8 mg/ dl/min.). Incremental IRI area at 0 to 5 min. in the low VK group is less than in the control (15.2 ± 4.4 vs. 25.0 ± 9.1 ng/ml/min.), but at 5–60 min. and 0–60 min., it was found to be significantly higher compared to the control (210.3 ± 55.2 vs. 32.5 ± 47.1 ng/ml/min. at 5–60 min.). Dietary low VK intake would thus appear to induce a tendency of poor early insulin response, and late hyperinsulinemia to the glucose load in rats.

Interactions of cold exposure and starvation on glucose tolerance and insulin response

1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki
Keyword(s):  
Glucose Tolerance ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
Intravenous Glucose ◽  
Peripheral Tissues ◽  
Insulin Levels ◽  
Plasma Insulin Levels

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.

scholarly journals Overestimation of minimal model glucose effectiveness in presence of insulin response is due to undermodeling

1998 ◽  
Vol 275 (6) ◽  
pp. E1031-E1036 ◽  
Author(s):  
Claudio Cobelli ◽  
Francesca Bettini ◽  
Andrea Caumo ◽  
Michael J. Quon
Keyword(s):  
Glucose Tolerance ◽  
Minimal Model ◽  
Insulin Response ◽  
Model Analysis ◽  
Published Data ◽  
Glucose Kinetics ◽  
Model Estimate ◽  
Intravenous Glucose ◽  
Glucose Effectiveness ◽  
Model Independent

Glucose effectiveness is an important determinant of glucose tolerance that can be derived from minimal model analysis of an intravenous glucose tolerance test (IVGTT). However, recent evidence suggests that glucose effectiveness is overestimated by minimal model analysis. Here we compare a new model-independent estimate of glucose effectiveness with the minimal model estimate by reanalyzing published data in which insulin-dependent diabetic subjects were each given IVGTTs under two conditions (Quon, M. J., C. Cochran, S. I. Taylor, and R. C. Eastman. Diabetes 43: 890–896, 1994). In one case, a basal insulin level was maintained (BI-IVGTT). In the second case, a dynamic insulin response was recreated (DI-IVGTT). Our results show that minimal model glucose effectiveness is very similar to the model-independent measurement during a BI-IVGTT but is three times higher during a DI-IVGTT. To investigate the causes of minimal model overestimation in the presence of a dynamic insulin response, Monte Carlo simulation studies on a two-compartment model of glucose kinetics with various insulin response patterns were performed. Results suggest that minimal model overestimation is due to single-compartment representation of glucose kinetics that results in a critical oversimplification in the presence of increasingly dynamic insulin secretion patterns.

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.

Glucose effectiveness is the major determinant of intravenous glucose tolerance in the rat

1999 ◽  
Vol 276 (4) ◽  
pp. E739-E746 ◽  
Author(s):  
M. Dawn McArthur ◽  
Dan You ◽  
Kim Klapstein ◽  
Diane T. Finegood
Keyword(s):  
Glucose Tolerance ◽  
Bolus Injection ◽  
Insulin Response ◽  
Tolerance Test ◽  
Physiological Effect ◽  
Intravenous Glucose Tolerance Test ◽  
Glucose Disposal ◽  
Disappearance Rate ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance

To determine the importance of insulin for glucose disposal during an intravenous glucose tolerance test in rats, experiments were performed in four cohorts of conscious unrestrained rats fasted overnight. In cohorts 1- 3, a bolus of tracer ([3-3H]glucose, 50 μCi) was given alone, with glucose (0.3 g/kg) to induce an endogenous insulin response (∼1,100 pmol/l), or with exogenous insulin to give physiological (1,700 pmol/l) or supraphysiological (12,000 pmol/l) plasma levels. Raising plasma insulin within the physiological range had no effect ( P > 0.05), but supraphysiological levels induced hypoglycemia (7.3 ± 0.2 to 3.6 ± 0.2 mmol/l) and increased [3H]glucose disappearance rate ( P < 0.001). In cohort 4, a primed, continuous tracer infusion was started 120 min before saline or glucose bolus injection. [3H]glucose levels fell 15–20%, and the disappearance rate rose 36% ( P < 0.05) after glucose injection. These results indicate that in fasted rats a tracer bolus injection protocol is not sufficiently sensitive to measure the physiological effect of insulin released in response to a bolus of glucose because this effect of insulin is small. Glucose itself is the predominant mediator of glucose disposal after a bolus of glucose in the fasted rat.

992 IMPACT OF INTRAVENOUS GLUCOSE LOAD ON BILE SALT TRANSPORTERS IN CRITICALLY ILL RABBITS

2010 ◽  
Vol 52 ◽  
pp. S383
Author(s):  
Y.-M. Vanwijngaerden ◽  
S. Derde ◽  
A. Keereman ◽  
L. Langouche ◽  
L. Mebis ◽  
...  
Keyword(s):  
Bile Salt ◽  
Critically Ill ◽  
Glucose Load ◽  
Intravenous Glucose ◽  
Bile Salt Transporters ◽  
Intravenous Glucose Load
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