GLUCOSE METABOLISM IN TRAUMATIC BRAIN INJURY

1974 ◽  
Vol 77 (1) ◽  
pp. 103-110 ◽  
Author(s):  
V. Keymolen-Jardini ◽  
E. Mouawad ◽  
P. Claeys-De Clercq ◽  
E. Van Laer ◽  
S. Levin ◽  
...  
Keyword(s):  
Amino Nitrogen ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Plasma Growth Hormone ◽  
Intravenous Glucose ◽  
Brain Contusion ◽  
Male Patients ◽  
Low K ◽  
Normal Controls

ABSTRACT The present study was designed to evaluate some key metabolic parameters in patients suffering from a traumatic brain contusion with coma. This evaluation was carried out before and during an intravenous glucose tolerance test (iv – GTT) in 6 male patients paired with normal controls Four patients presented a fasting hyperglycaemia and a low K rate of glucose disappearance but the basal level of insulin was normal or high and the insulin response to the glucose load was not significantly impaired. The basal level of plasma growth hormone (HGH) was usually normal but it increased paradoxically during the iv – GTT; 2 patients had a striking hyper-response. Plasma cortisol levels were always elevated. On the other hand no gross or systematic anomaly in the regulation of plasma free fatty acids, acetoacetate and amino nitrogen was detected. The paradoxical HGH response was the only finding which could be specifically attributed to the central neural lesions.

Hyperinsulinemic Compensation For Insulin Resistance Occurs Independent Of Elevated Glycemia In Male Dogs

Endocrinology ◽  
2021 ◽  
Author(s):  
Marilyn Ader ◽  
Richard N Bergman
Keyword(s):  
Insulin Resistance ◽  
Subcutaneous Fat ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Intravenous Glucose ◽  
Primary Element ◽  
Subcutaneous Adiposity ◽  
Hyperinsulinemic Compensation

Abstract Insulin resistance (IR) engenders a compensatory increase in plasma insulin. Inadequate compensation is a primary element in the pathogenesis of Type 2 diabetes. The signal which heralds developing IR and initiates hyperinsulinemic compensation is not known. It has often been assumed to be increased glucose. We tested this assumption by determining whether development of fasting and/or glucose-stimulated hyperinsulinemia with diet-induced insulin resistance occurs because of concomitant elevation of glycemia. Male dogs (n=58) were fed a hypercaloric, fat-supplemented diet for 6 wks. Dogs underwent MRI to quantify total and regional (visceral, subcutaneous) adiposity as well as euglycemic hyperinsulinemic clamps. A subset of animals also underwent an insulin-modified intravenous glucose tolerance test (IVGTT) to assess insulin sensitivity, acute insulin response (AIRg), and glucose effectiveness. Fat feeding caused modest weight gain, increased visceral and subcutaneous fat, and IR at both peripheral and hepatic levels. Hyperinsulinemic compensation was observed in fasting levels as well as increased AIRg. However, we observed absolutely no increase in carefully measured fasting, evening (6-8 pm) or nocturnal glycemia (2-4 am). IR and hyperinsulinemia occurred despite no elevation in 24-hour glucose. Compensatory development of hyperinsulinemia during diet-induced insulin resistance occurs without elevated fasting or 24-hour glycemia. These data refute the idea that glucose itself is a requisite signal for β-cell upregulation. Alternative feedback mechanisms need to be identified.

Modified protocols improve insulin sensitivity estimation using the minimal model

1987 ◽  
Vol 253 (6) ◽  
pp. E595-E602 ◽  
Author(s):  
Y. J. Yang ◽  
J. H. Youn ◽  
R. N. Bergman
Keyword(s):  
Standard Deviation ◽  
Insulin Sensitivity ◽  
Minimal Model ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Improve Insulin Sensitivity ◽  
Intravenous Glucose ◽  
Sensitivity Estimation ◽  
Model Technique

We attempted to improve the precision of the estimation of insulin sensitivity (S1) from the minimal model technique by modifying insulin dynamics during a frequently sampled intravenous glucose tolerance test (FSIGT). Tolbutamide and somatostatin (SRIF) were used to change the insulin dynamics without directly affecting insulin sensitivity. Injection of tolbutamide (100 mg) at t = 20 min provoked an immediate secondary peak in insulin response, resulting in a greater integrated incremental insulin than the standard FSIGT. SRIF, injected at t = -1 min, delayed insulin secretion in proportion to the dose without any change in magnitude. Computer simulation was used to assess the precision of S1 estimation. Insulin dynamics from both standard and modified protocols were adjusted in magnitude, with the shape unchanged and analyzed to determine the effect of the magnitude of insulin response. Fractional standard deviation was reduced from 73% with the standard insulin profile to 23% with tolbutamide and 18% with the highest dose of SRIF. In addition, the fractional standard deviation of S1 estimates decreased exponentially with increasing magnitude of insulin response. Modified FSIGTs require a smaller insulin response than the standard protocol to achieve the same precision.

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.

THE OCCURRENCE OF ABNORMAL INSULIN AND GROWTH HORMONE (HGH) RESPONSES TO SUSTAINED HYPERCLYCAEMIA IN A DISEASE WITH SEX CHROMOSOME ABERRATIONS (TURNER'S SYNDROME)

1967 ◽  
Vol 56 (1) ◽  
pp. 107-131 ◽  
Author(s):  
J. Lindsten ◽  
E. Cerasi ◽  
R. Luft ◽  
G. Hultquist
Keyword(s):  
Growth Hormone ◽  
Sex Chromosome ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Turner's Syndrome ◽  
Turner’S Syndrome ◽  
Intravenous Glucose ◽  
Islet Tissue ◽  
Plasma Insulin Response

ABSTRACT The plasma insulin response to prolonged glucose infusion was studied in 14 patients with Turner's syndrome having a normal intravenous glucose tolerance test. The insulin response was in most instances delayed and diminished in spite of a higher than normal blood glucose level. The fasting plasma growth hormone (HGH) level was elevated, and hyperglycaemia induced a paradoxical increase in plasma HGH in most of the patients. The HGH response to hypoglycaemia was normal. Oestrogen replacement accentuated the paradoxical HGH reaction to hyperglycaemia while the insulin response diminished further. In contrast to earlier studies no increase in the frequency of diabetes was found among the relatives of the Turner patients. In one subject there was a definite hyperplasia of the islet tissue of the pancreas with signs of decreased activity of the β-cells, in a second one the amount of islet tissue was fairly high. Possible relationships between the above findings are discussed.

Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes

1993 ◽  
Vol 264 (1) ◽  
pp. E60-E67 ◽  
Author(s):  
P. M. Catalano ◽  
E. D. Tyzbir ◽  
R. R. Wolfe ◽  
J. Calles ◽  
N. M. Roman ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Carbohydrate Metabolism ◽  
Insulin Response ◽  
Glucose Production ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Endogenous Glucose Production ◽  
Fat Free Mass ◽  
Late Gestation ◽  
Intravenous Glucose

The purpose of this study was to characterize carbohydrate metabolism associated with the development of gestational diabetes. Six control (Ctl) and ten women with gestational diabetes mellitus (GDM) were evaluated using an intravenous glucose tolerance test and hyperinsulinemic-euglycemic clamp with [6,6-2H2]glucose prior to conception (P) and at 12-14 (E), and 34-36 wk of gestation (L). There was an increase (P = 0.0001) in first-phase insulin response in Ctl (P 174 +/- 133, E 388 +/- 120, and L 587 +/- 303 microU/ml) and GDM (P 197 +/- 94, E 267 +/- 77, and L 376 +/- 162 microU/ml) but a significant (P = 0.02) lag in change in GDM with advancing gestation. Basal endogenous glucose production increased during gestation [Ctl: P 2.74 +/- 0.23, E 2.62 +/- 0.38, and L 3.14 +/- 0.36; GDM: P 2.68 +/- 0.51, E 2.78 +/- 0.45, and L 2.98 +/- 0.48 mg.kg fat-free mass (FFM)-1 x min-1; P = 0.02], but there was resistance to suppression by insulin infusion (P = 0.03) in late gestation (GDM: 0.61 +/- 0.44 vs. Ctl: 0.16 +/- 0.17 mg.kg FFM-1 x min-1). Insulin sensitivity decreased during gestation (Ctl: P 10.78 +/- 2.78, E 8.34 +/- 2.36, and L 4.75 +/- 1.22; GDM: P 7.49 +/- 2.13, E 7.40 +/- 1.45, and L 4.21 +/- 1.01 mg.kg FFM-1 x min-1; P = 0.0001) and was primarily decreased (P = 0.04) in GDM compared with Ctl from P through E. These findings closely resemble those of non-insulin-dependent, predominantly insulin-resistant diabetes, which is often a sequel of GDM.

Exercise-induced changes in insulin action are associated with ACE gene polymorphisms in older adults

2002 ◽  
Vol 11 (2) ◽  
pp. 73-80 ◽  
Author(s):  
Donald R. Dengel ◽  
Michael D. Brown ◽  
Robert E. Ferrell ◽  
Thomas H. Reynolds ◽  
Mark A. Supiano
Keyword(s):  
Insulin Action ◽  
Insulin Response ◽  
Exercise Program ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Sensitivity Index ◽  
Intravenous Glucose ◽  
Before And After ◽  
Ace Genotype ◽  
Exercise Induced

We evaluated the association between insulin resistance and the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) gene polymorphism in a group of older hypertensive subjects (63 ± 1 yr, n = 35) before and after a 6-mo aerobic exercise program (AEX). Insulin sensitivity index (SI), assessed by the frequently sampled intravenous glucose tolerance test, was significantly ( P = 0.0001) increased following AEX. In addition, there was a significant ( P = 0.001) interaction between AEX and ACE genotype. SI increased significantly ( P < 0.05) more in those with the II (2.5 ± 0.8 μU × 10−4 · min−1 · ml−1) ACE genotype compared with both the DD and ID (0.7 ± 0.1 and 0.7 ± 0.2 μU × 10−4 · min−1 · ml−1, respectively) ACE genotypes. Similarly, there was a significant ( P = 0.036) decrease in the acute insulin response to glucose (AIRG) and a significant ( P = 0.05) interaction between AEX and ACE genotype. AIRG decreased significantly ( P < 0.05) more in those with the II (−17.6 ± 5.6 mU/ml) ACE genotype compared with both the DD and ID (−1.4 ± 6.2 and −3.6 ± 2.5 mU/ml) ACE genotypes. In conclusion, we demonstrated that those older hypertensives with the ACE II genotype have the greatest improvement in insulin action following AEX.

scholarly journals Ablation of capsaicin-sensitive afferent nerves affects insulin response during an intravenous glucose tolerance test

Life Sciences ◽  
2005 ◽  
Vol 77 (11) ◽  
pp. 1283-1292 ◽  
Author(s):  
Esther H.E.M. van de Wall ◽  
Dorte X. Gram ◽  
Jan H. Strubbe ◽  
Anton J.W. Scheurink ◽  
Jaap M. Koolhaas
Keyword(s):  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Intravenous Glucose ◽  
Afferent Nerves ◽  
Intravenous Glucose Tolerance
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