scholarly journals Effects of Intrabrachial Metacholine Infusion on Muscle Capillary Recruitment and Forearm Glucose Uptake during Physiological Hyperinsulinemia in Obese, Insulin-Resistant Individuals

2008 ◽  
Vol 93 (7) ◽  
pp. 2764-2773 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Mikaela Sjöstrand ◽  
Lena Strindberg ◽  
Soffia Gudbjörnsdóttir ◽  
Lars Lind ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Tolerance Test ◽  
Forearm Blood Flow ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Capillary Recruitment ◽  
Insulin Resistant

Abstract Context: Impairment of insulin-mediated capillary recruitment in skeletal muscle contributes to a hampered glucose uptake in obesity. Objective: The objective of this study was to evaluate whether metacholine (MCh), a nitric oxide vasodilator, potentiates muscle capillary recruitment and forearm glucose uptake (FGU) during physiological hyperinsulinemia. Design: The double-forearm technique [i.e. infused vs. control (Ctrl) forearm] was combined with im microdialysis during an oral glucose tolerance test in 15 nondiabetic, obese subjects divided into a group of insulin-resistant (IR) (n = 7) and insulin-sensitive (n = 8) individuals. Results: After the oral glucose tolerance test, forearm blood flow in the Ctrl forearm was unchanged, whereas it increased about 3-fold (P < 0.0001 vs. baseline) in response to MCh. Capillary permeability surface area product for glucose (PSglu) (capillary recruitment), FGU, and interstitial insulin concentrations increased significantly over time (P < 0.001) in both forearms. Compared with insulin-sensitive, the IR subjects exhibited lower PSglu (P < 0.001) and FGU (P < 0.01) in the Ctrl arm, whereas this difference was insignificant in the MCh arm despite the blunted forearm blood flow increase. Moreover, in IR individuals MCh significantly (P < 0.05) ameliorated the delayed onset of insulin action, i.e. the FGU response to hyperinsulinemia. Finally, we found PSglu to be a strong and independent predictor of FGU response (adjusted R2 0.72; P < 0.0001). Conclusions: MCh-induced vasodilation may improve the microvascular and metabolic responses to physiological hyperinsulinemia in obese, IR individuals. Further studies are required to unravel whether stimulation of nitric oxide production in skeletal muscle may represent an attractive therapeutic approach to bypassing cellular resistance to glucose disposal.

scholarly journals Direct Measurements of the Permeability Surface Area for Insulin and Glucose in Human Skeletal Muscle

2003 ◽  
Vol 88 (10) ◽  
pp. 4559-4564 ◽  
Author(s):  
Soffia Gudbjörnsdóttir ◽  
Mikaela Sjöstrand ◽  
Lena Strindberg ◽  
John Wahren ◽  
Peter Lönnroth
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Permeability Surface ◽  
One Step

Abstract To elucidate mechanisms regulating capillary transport of insulin and glucose, we directly calculated the permeability surface (PS) area product for glucose and insulin in muscle. Intramuscular microdialysis in combination with the forearm model and blood flow measurements was performed in healthy males, studied during an oral glucose tolerance test or during a one-step or two-step euglycemic hyperinsulinemic clamp. PS for glucose increased significantly from 0.29 ± 0.1 to 0.64 ± 0.2 ml/min·100 g after oral glucose tolerance test, and glucose uptake increased from 1.2 ± 0.4 to 2.6 ± 0.6 μmol/min·100 g (P < 0.05). During one-step hyperinsulinemic clamp (plasma insulin, 1.962 pmol/liter), PS for glucose increased from 0.2 ± 0.1 to 2.3 ± 0.9 ml/min·100 g (P < 0.05), and glucose uptake increased from 0.6 ± 0.2 to 5.0 ± 1.4 μmol/min·100 g (P < 0.05). During the two-step clamp (plasma insulin, 1380 ± 408 and 3846 ± 348 pmol/liter), the arterial-interstitial difference and PS for insulin were constant. The PS for glucose tended to increase (P = not significant), whereas skeletal muscle blood flow increased from 4.4 ± 0.7 to 6.2 ± 0.8 ml/min·100 ml (P < 0.05). The present data show that PS for glucose is markedly increased by oral glucose, whereas a further vasodilation exerted by high insulin concentrations may not be physiologically relevant for capillary delivery of either glucose or insulin in resting muscle.

EXERCISE TRAINING AND THE RESPONSE OF NITRIC OXIDE TO AN ORAL GLUCOSE TOLERANCE TEST (OGTT)

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S11
Author(s):  
J A. McKenzie ◽  
E P. Weiss ◽  
J J. Park ◽  
J Y. Park ◽  
O Kulaputana ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Forearm Glucose Uptake During the Oral Glucose Tolerance Test in Normal Subjects

Diabetes ◽  
1973 ◽  
Vol 22 (6) ◽  
pp. 442-458 ◽  
Author(s):  
R. A. Jackson ◽  
N. Peters ◽  
U. Advani ◽  
G. Perry ◽  
J. Rogers ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Uptake ◽  
Glucose Tolerance Test ◽  
Normal Subjects ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Glucose Uptake and Production During the Oral Glucose Tolerance Test

Diabetes ◽  
1968 ◽  
Vol 17 (7) ◽  
pp. 415-421 ◽  
Author(s):  
R. Steele ◽  
C. Bjerknes ◽  
I. Rathgeb ◽  
N. Altszuler
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Uptake ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

scholarly journals Reduced Glucose Tolerance and Skeletal Muscle GLUT4 and IRS1 Content in Cyclists Habituated to a Long-Term Low-Carbohydrate, High-Fat Diet

2020 ◽  
Vol 30 (3) ◽  
pp. 210-217
Author(s):  
Christopher C. Webster ◽  
Kathryn M. van Boom ◽  
Nur Armino ◽  
Kate Larmuth ◽  
Timothy D. Noakes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Mixed Diet ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Low Carbohydrate

Very little is known about how long-term (>6 months) adaptation to a low-carbohydrate, high-fat (LCHF) diet affects insulin signaling in healthy, well-trained individuals. This study compared glucose tolerance; skeletal muscle glucose transporter 4 (GLUT4) and insulin receptor substrate 1 (IRS1) content; and muscle enzyme activities representative of the main energy pathways (3-hydroxyacetyl-CoA dehydrogenase, creatine kinase, citrate synthase, lactate dehydrogenase, phosphofructokinase, phosphorylase) in trained cyclists who followed either a long-term LCHF or a mixed-macronutrient (Mixed) diet. On separate days, a 2-hr oral glucose tolerance test was conducted, and muscle samples were obtained from the vastus lateralis of fasted participants. The LCHF group had reduced glucose tolerance compared with the Mixed group, as plasma glucose concentrations were significantly higher throughout the oral glucose tolerance test and serum insulin concentrations peaked later (LCHF, 60 min; Mixed, 30 min). Whole-body insulin sensitivity was not statistically significantly different between groups (Matsuda index: LCHF, 8.7 ± 3.4 vs. Mixed, 12.9 ± 4.6; p = .08). GLUT4 (LCHF: 1.13 ± 0.24; Mixed: 1.44 ± 0.16; p = .026) and IRS1 (LCHF: 0.25 ± 0.13; Mixed: 0.46 ± 0.09; p = .016) protein content was lower in LCHF muscle, but enzyme activities were not different. We conclude that well-trained cyclists habituated to an LCHF diet had reduced glucose tolerance compared with matched controls on a mixed diet. Lower skeletal muscle GLUT4 and IRS1 contents may partially explain this finding. This could possibly reflect an adaptation to reduced habitual glucose availability rather than the development of a pathological insulin resistance.

scholarly journals Normal muscle glucose uptake in mice deficient in muscle GLUT4

2012 ◽  
Vol 214 (3) ◽  
pp. 313-327 ◽  
Author(s):  
Barbara C Fam ◽  
Laura J Rose ◽  
Rebecca Sgambellone ◽  
Zheng Ruan ◽  
Joseph Proietto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Plasma Insulin ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Glucose Disposal ◽  
Glucose Turnover ◽  
Oral Glucose ◽  
Mouse Muscle

Skeletal muscle insulin resistance is a major characteristic underpinning type 2 diabetes. Impairments in the insulin responsiveness of the glucose transporter,Glut4 (Slc2a4), have been suggested to be a contributing factor to this disturbance. We have produced muscle-specificGlut4knockout (KO) mice using Cre/LoxP technology on a C57BL6/J background and shown undetectable levels of GLUT4 in both skeletal muscle and heart. Our aim was to determine whether complete deletion of muscle GLUT4 does in fact lead to perturbations in glucose homoeostasis. Glucose tolerance, glucose turnover and 2-deoxyglucose uptake into muscle and fat under basal and insulin-stimulated conditions were assessed in 12-week-old KO and control mice using the oral glucose tolerance test (OGTT) and hyperinsulinaemic/euglycaemic clamp respectively. KO mice weighed ∼17% less and had significantly heavier hearts compared with control mice. Basally, plasma glucose and plasma insulin were significantly lower in the KO compared with control mice, which conferred normal glucose tolerance. Despite the lack of GLUT4 in the KO mouse muscle, glucose uptake was not impaired in skeletal muscle but was reduced in heart under insulin-stimulated conditions. Neither GLUT1 nor GLUT12 protein levels were altered in the skeletal muscle or heart tissue of our KO mice. High-fat feeding did not alter glucose tolerance in the KO mice but led to elevated plasma insulin levels during the glucose tolerance test. Our study demonstrates that deletion of muscle GLUT4 does not adversely affect glucose disposal and glucose tolerance and that compensation from other transporters may contribute to this unaltered homoeostasis of glucose.

Abstract #873: Association of Patterns in the Oral Glucose Tolerance Test and Different Clinical Features in Patients with Insulinoma

2005 ◽  
Vol 11 ◽  
pp. 28
Author(s):  
Fanny Rodriguez Vallejo ◽  
Juan Manuel Rios Torres ◽  
Francisco J. Gomez-Pérez ◽  
Juan A. Rull Rodrigo ◽  
Bernardo Pérez Enriquez
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Clinical Features ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance
Sign in / Sign up

Export Citation Format

Share Document