Effect of acute exercise and prolonged training on insulin response to intravenous glucose in vivo in rat

1983 ◽  
Vol 55 (6) ◽  
pp. 1660-1664 ◽  
Author(s):  
D. E. James ◽  
K. M. Burleigh ◽  
E. W. Kraegen ◽  
D. J. Chisholm
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Physical Training ◽  
Acute Exercise ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Intensive Training ◽  
Single Bout ◽  
Intravenous Glucose Tolerance Tests

Physical training causes hypoinsulinemia and enhanced insulin sensitivity. Insulin sensitivity is also enhanced by a single bout of exercise. However, changes in beta-cell responsiveness with acute exercise are ill defined. To clarify these relationships intravenous glucose tolerance tests were performed in 1) physically trained rats (3 different levels), 48 h after the last bout of exercise; 2) untrained rats, 0.5, 4, and 24 h after a single bout of exercise; or 3) sedentary control rats. The total area under the glucose-stimulated insulin response curve (GSIR) was negatively correlated with total distance run during training (r = -0.45, P less than 0.05), whereas glucose tolerance was improved (P less than 0.005 vs. controls) with intensive training. GSIR was suppressed by 38% (P less than 0.01 vs. controls) 0.5 h after a single bout of exercise. This effect persisted for 4 h but was not present after 24 h. These results indicate that a single bout of exercise induces suppression of GSIR which lasts less than 24 h. In contrast, physical training induces prolonged suppression (for at least 48 h) of GSIR, proportional to the intensity of training, and improved glucose tolerance.

scholarly journals Glucose tolerance and insulin sensitivity in malnourished children

1972 ◽  
Vol 27 (3) ◽  
pp. 585-592 ◽  
Author(s):  
G. A. O. Alleyne ◽  
P. M. Trust ◽  
H. Flores ◽  
H. Robinson
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Malnourished Child ◽  
Normal Children ◽  
Intravenous Glucose ◽  
Malnourished Children ◽  
Isocaloric Diets ◽  
Blood Glucose Concentrations

1. In malnourished, compared with recovered children, fasting blood glucose concentrations were low and there was impaired peripheral glycolysis as shown by a failure of blood lactate to rise after glucose was injected intravenously.2. Homogenates of muscle biopsies from malnourished and recovered children produced equal amounts of lactate when incubated anaerobically with various substrates, but when compared with homogenates of biopsies from normal children the pattern suggested an impairment of glycolysis.3. The rate of glucose disappearance after intravenous glucose was slow in the malnourished child and there was possibly diminished sensitivity to exogenous insulin.4. Isocaloric diets relatively high or low in fat were fed to children who had recovered from malnutrition. Glucose tolerance, insulin sensitivity, fasting plasma insulin and insulin response to intravenous glucose were all the same in children on either diet.

scholarly journals PACAP stimulates insulin secretion but inhibits insulin sensitivity in mice

1998 ◽  
Vol 274 (5) ◽  
pp. E834-E842 ◽  
Author(s):  
Karin Filipsson ◽  
Giovanni Pacini ◽  
Anton J. W. Scheurink ◽  
Bo Ahrén
Keyword(s):  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Elimination Rate ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Glucose Disposal ◽  
Sensitivity Index ◽  
Maximal Effect ◽  
Intravenous Glucose

Although pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates insulin secretion, its net influence on glucose homeostasis in vivo has not been established. We therefore examined the action of PACAP-27 and PACAP-38 on insulin secretion, insulin sensitivity, and glucose disposal as derived from the minimal model of glucose disappearance during an intravenous glucose tolerance test in anesthetized mice. PACAP-27 and PACAP-38 markedly and equipotently potentiated glucose-stimulated insulin secretion, with a half-maximal effect at 33 pmol/kg. After PACAP-27 or PACAP-38 (1.3 nmol/kg), the acute (1–5 min) insulin response was 3.8 ± 0.4 nmol/l (PACAP-27) and 3.3 ± 0.3 nmol/l (PACAP-38), respectively, vs. 1.4 ± 0.1 nmol/l after glucose alone ( P < 0.001), and the total area under the curve for insulin (AUCinsulin) was potentiated by 60% ( P < 0.001). In contrast, PACAP-27 and PACAP-38 reduced the insulin sensitivity index (SI) [0.23 ± 0.04 10−4min−1/(pmol/l) for PACAP-27 and 0.29 ± 0.06 10−4min−1/(pmol/l) for PACAP-38 vs. 0.46 ± 0.02 10−4min−1/(pmol/l) for controls ( P < 0.01)]. Furthermore, PACAP-27 or PACAP-38 did not affect glucose elimination determined as glucose half-time or the glucose elimination rate after glucose injection or the area under the curve for glucose. Moreover, glucose effectiveness and the global disposition index (AUCinsulin times SI) were not affected by PACAP-27 or PACAP-38. Finally, when given together with glucose, PACAP-27 did not alter plasma glucagon or norepinephrine levels but significantly increased plasma epinephrine levels. We conclude that PACAP, besides its marked stimulation of insulin secretion, also inhibits insulin sensitivity in mice, the latter possibly explained by increased epinephrine. This complex action explains why the peptide does not enhance glucose disposal.

GLUCOSE TOLERANCE AND INSULIN RESPONSE DURING DAILY CONTINUOUS LOW-DOSE ORAL CONTRACEPTIVE TREATMENT

1969 ◽  
Vol 62 (2) ◽  
pp. 242-250 ◽  
Author(s):  
U. Larsson-Cohn ◽  
B. Tengström ◽  
L. Wide
Keyword(s):  
Glucose Tolerance ◽  
Blood Glucose Concentration ◽  
Fasting Blood Glucose ◽  
Insulin Response ◽  
Continuous Treatment ◽  
Intravenous Glucose ◽  
Dose Oral ◽  
Glucose Tolerance Tests ◽  
Insulin Response To Glucose ◽  
Intravenous Glucose Tolerance Tests

ABSTRACT Intravenous glucose tolerance tests and insulin determinations were performed on 37 women at different stages of the menstrual cycle and after one, three and twelve months of daily continuous treatment with 0.5 mg of norethindrone or 0.5 mg of chlormadinone acetate. The fasting blood glucose concentration, the k-values (percentage disappearance rate of glucose per minute) and the insulin response to glucose administration were compared. No statistically significant differences were found between the values obtained on two occasions before treatment, and during treatment.

scholarly journals Adiposity and Insulin Sensitivity Derived from Intravenous Glucose Tolerance Tests in Antipsychotic-Treated Patients

2007 ◽  
Vol 32 (12) ◽  
pp. 2561-2569 ◽  
Author(s):  
Dan W Haupt ◽  
Peter A Fahnestock ◽  
Karen A Flavin ◽  
Julie A Schweiger ◽  
Angela Stevens ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
Glucose Tolerance Tests ◽  
Intravenous Glucose Tolerance Tests

Contribution to glucose tolerance of insulin-independent vs. insulin-dependent mechanisms in mice

2001 ◽  
Vol 281 (4) ◽  
pp. E693-E703 ◽  
Author(s):  
Giovanni Pacini ◽  
Karl Thomaseth ◽  
Bo Ahrén
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Area Under The Curve ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance ◽  
High Insulin ◽  
Insulin Dependent ◽  
Per Se

To study the contributions of insulin-dependent vs. insulin-independent mechanisms to intravenous glucose tolerance (KG), 475 experiments in mice were performed. An intravenous glucose bolus was given either alone or with exogenous insulin or with substances modulating insulin secretion and sensitivity. Seven samples were taken over 50 min. Insulin [suprabasal area under the curve (ΔAUCins)] ranged from 0 to 100 mU · ml−1 · 50 min. After validation against the euglycemic hyperinsulinemic clamp, the minimal model of net glucose disappearance was exploited to analyze glucose and insulin concentrations to measure the action of glucose per se independent of dynamic insulin (SG) and the combined effect of insulin sensitivity (SI) and secretion. Sensitivity analysis showed that insulin [through disposition index (DI)] contributed to glucose tolerance by 29 ± 4% in normal conditions. In conditions of elevated hyperinsulinemia, contribution by insulin increased on average to 69%. KG correlated with DI but was saturated for ΔAUCins above 15 mU · ml−1 · 50 min. Insulin sensitivity related to ΔAUCins in a hyperbolic manner, whereas SG did not correlate with the insulin peak in the physiological range. Thus glucose tolerance in vivo is largely mediated by mechanisms unrelated to dynamic insulin and saturates with high insulin.

THE INSULINOGENIC RESPONSE TO INTRAVENOUS GLUCOSE IN DOGS FED DIETS OF DIFFERENT PROTEIN VALUE

1969 ◽  
Vol 45 (3) ◽  
pp. 375-386 ◽  
Author(s):  
C. R. C. HEARD ◽  
PAMELA A. J. HENRY
Keyword(s):  
Glucose Tolerance ◽  
Insulin Response ◽  
High Protein Diet ◽  
Intravenous Glucose ◽  
Low Protein ◽  
Intravenous Glucose Tolerance ◽  
Plasma Insulin Levels ◽  
Glucose Tolerance Tests ◽  
Loss Of Appetite ◽  
Intravenous Glucose Tolerance Tests

SUMMARY Dogs were fed diets of high, suboptimal or low protein value (NDpCal% = 10, 7 or 5) from weaning at approximately 6 weeks of age. Immunoreactive plasma insulin levels were measured during intravenous glucose tolerance tests at 8, 13 and 20 weeks of age. In the dogs fed on diets of suboptimal or low protein value, the assimilation coefficient (K) increased within the first 2 weeks on diet, without any corresponding increase in insulin output. Later, as glucose tolerance tended to become impaired, the insulin output increased significantly. A significant increase in insulin response also occurred in dogs fed the high protein diet, at approximately 6 months of age, when the growth rate had slowed down. The increase in insulin response to i.v. glucose, observed in dogs fed the diets of low protein value, did not occur in animals which became marasmic through loss of appetite. Such animals had a very feeble insulin response. The findings are discussed in relation to human protein-calorie deficiency syndromes (kwashiorkor and marasmus).

Effect of physical training on insulin response to intravenous glucose in male peripubertal rats

1992 ◽  
Vol 73 (4) ◽  
pp. 1227-1231 ◽  
Author(s):  
J. Bongbele ◽  
A. Gutierrez ◽  
S. Cardin ◽  
J. M. Lavoie
Keyword(s):  
Glucose Tolerance ◽  
Body Weight Gain ◽  
Insulin Response ◽  
Exercise Bout ◽  
Male Rats ◽  
Sprague Dawley ◽  
Intravenous Glucose ◽  
Sprague Dawley Rats ◽  
Body Weights ◽  
Intravenous Glucose Tolerance Tests

This study was undertaken to evaluate the effects of regular endurance-type exercise (i.e., swimming) on glucose tolerance and glucose-stimulated insulin response (GSIR) in 55- and 90-day-old peripubertal male rats. Intravenous glucose tolerance tests (0.5 g/kg) were done in four groups of male Sprague-Dawley rats: two groups of trained (TR; 55- and 90-day-old) and two groups of age- and weight-matched untrained (UNTR) rats. The UNTR rats were subjected to a continuous food restriction to maintain body weights equal to those of the TR rats. Rats were received in our laboratory after weaning at 21 days of age and were evaluated 48 h after the last exercise bout. No significant differences in body weights were found between TR and UNTR rats, at the age of either 55 or 90 days. A significant (P < 0.01) decrease in the mean integrated area under the glucose and insulin curves was observed in TR compared with UNTR groups in 55- as well as 90-day-old rats. These results indicate that exercise training in male rats improves the glucose tolerance and GSIR before and during puberty (21–90 days) independently of a reduction in body weight gain.

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.

Muscarinic stimulation maintains in vivo insulin secretion in response to glucose after prolonged hyperglycemia

1995 ◽  
Vol 268 (2) ◽  
pp. R475-R479 ◽  
Author(s):  
B. Balkan ◽  
B. E. Dunning
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
General Mechanism ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance

Prolonged hyperglycemia impairs the in vitro insulin release by islets of Langerhans in response to glucose but exaggerates the in vivo insulin response. We hypothesized that this discrepancy results from increased vagal stimulation of the islets. Conscious chronically cannulated rats were infused with glucose (15 mg/min) or saline for 48 h. Three hours thereafter, an intravenous glucose tolerance test was performed with or without prior injection of atropine (0.2 mg). Atropine markedly (> 70%) reduced the insulin response in glucose-infused, but not in saline-infused, rats. Glucose-infused rats displayed basal hypoglycemia but normal glucose excursions during an intravenous glucose tolerance test. It is concluded that prolonged hyperglycemia produces exaggerated muscarinic activation of the beta-cells that will persist > or = 3 h after the termination of the glucose infusion and normalizes in vivo insulin secretion. It is possible that increased parasympathetic activation of the pancreas might constitute a general mechanism to maintain insulin output when the demand for insulin exceeds the inherent beta-cell responsiveness.

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