Insulin-mediated vasodilatation, but not glucose uptake or endothelium-mediated vasodilatation, is enhanced in young females compared with males

2002 ◽  
Vol 102 (2) ◽  
pp. 241-246 ◽  
Author(s):  
Lars LIND ◽  
Andreas FUGMANN ◽  
Jonas MILLGÅRD ◽  
Christian BERNE ◽  
Hans LITHELL
Keyword(s):  
Blood Flow ◽  
Cardiac Index ◽  
Glucose Uptake ◽  
Forearm Blood Flow ◽  
Peripheral Resistance ◽  
Whole Body ◽  
Similar Degree ◽  
Obese Women ◽  
Plasma Insulin Concentration ◽  
Men And Women

In order to evaluate possible differences between men and women with regard to the ability of insulin to induce vasodilatation, promote glucose uptake and enhance endothelium-dependent vasodilatation, 12 young (22-28 years), non-obese women and 15 corresponding males were subjected to 2h of euglycaemic hyperinsulinaemia (insulin infusion rate of 56m-unitsċmin-1ċm-2). Forearm blood flow was measured by venous occlusion plethysmography. Endothelium-dependent vasodilatation was evaluated by the local intra-arterial infusion of methacholine into the brachial artery (2-4μg/min). The cardiac index was measured by thoracic bioimpedance. A 2h period of hyperinsulinaemia increased the plasma insulin concentration to a similar degree in both sexes (females, 84±8.8m-units/l; males, 87±7.5m-units/l), but induced a more marked increase in forearm blood flow in females than in males (+104±67% and +52±30% respectively; P < 0.01; 95% confidence interval for difference 11-94%). Furthermore, a significant decrease in total peripheral resistance (-20±6.9%; P < 0.01) and an increase in cardiac index (+23±13%; P < 0.01) were seen in women only (P < 0.05 compared with men). Blood pressure and heart rate were not altered in either sex. Whole-body insulin-mediated glucose uptake and forearm glucose uptake did not differ between the sexes, and the ability of insulin to enhance endothelium-dependent vasodilatation (+19%; P < 0.01) was similar in men and women. In conclusion, the present study shows that the ability of insulin to cause vasodilatation was greater in non-obese young women compared with men. However, no differences between the sexes were seen with regard to insulin-mediated glucose uptake and the ability of insulin to enhance endothelium-dependent vasodilatation.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

cGMP phosphodiesterase inhibition improves the vascular and metabolic actions of insulin in skeletal muscle

2011 ◽  
Vol 301 (2) ◽  
pp. E342-E350 ◽  
Author(s):  
A. J. Genders ◽  
E. A. Bradley ◽  
S. Rattigan ◽  
S. M. Richards
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Mrna Level ◽  
Microvascular Perfusion ◽  
Microvascular Blood Flow ◽  
Whole Body ◽  
Acute Administration ◽  
Dependent Inhibition ◽  
Promising Avenue

There is considerable support for the concept that insulin-mediated increases in microvascular blood flow to muscle impact significantly on muscle glucose uptake. Since the microvascular blood flow increases with insulin have been shown to be nitric oxide-dependent inhibition of cGMP-degrading phosphodiesterases (cGMP PDEs) is predicted to enhance insulin-mediated increases in microvascular perfusion and muscle glucose uptake. Therefore, we studied the effects of the pan-cGMP PDE inhibitor zaprinast on the metabolic and vascular actions of insulin in muscle. Hyperinsulinemic euglycemic clamps (3 mU·min−1·kg−1) were performed in anesthetized rats and changes in microvascular blood flow assessed from rates of 1-methylxanthine metabolism across the muscle bed by capillary xanthine oxidase in response to insulin and zaprinast. We also characterized cGMP PDE isoform expression in muscle by real-time PCR and immunostaining of frozen muscle sections. Zaprinast enhanced insulin-mediated microvascular perfusion by 29% and muscle glucose uptake by 89%, while whole body glucose infusion rate during insulin infusion was increased by 33% at 2 h. PDE2, -9, and -10 were the major isoforms expressed at the mRNA level in muscle, while PDE1B, -9A, -10A, and -11A proteins were expressed in blood vessels. Acute administration of the cGMP PDE inhibitor zaprinast enhances muscle microvascular blood flow and glucose uptake response to insulin. The expression of a number of cGMP PDE isoforms in skeletal muscle suggests that targeting specific cGMP PDE isoforms may provide a promising avenue for development of a novel class of therapeutics for enhancing muscle insulin sensitivity.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

scholarly journals Mechanisms underlying absent training-induced improvement in insulin action in lean, hyperandrogenic women with polycystic ovary syndrome (PCOS)

2020 ◽  
Author(s):  
Ada Admin ◽  
Solvejg L. Hansen ◽  
Kirstine N. Bojsen-Møller ◽  
Anne-Marie Lundsgaard ◽  
Frederikke L. Hendrich ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Polycystic Ovary Syndrome ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Polycystic Ovary ◽  
Whole Body ◽  
Ovary Syndrome ◽  
Leg Blood Flow

Women with polycystic ovary syndrome (PCOS) have been shown to be less insulin sensitive compared with control women, independent of BMI. Training is associated with molecular adaptations in skeletal muscle improving glucose uptake and metabolism in both healthy and type 2 diabetic individuals. In the present study, lean, hyperandrogenic women with PCOS (n=9) and healthy controls (CON, n=9) completed 14 weeks of controlled and supervised exercise training. In CON, the training intervention increased whole body insulin action by 26% and insulin-stimulated leg glucose uptake by 53%, together with increased insulin-stimulated leg blood flow and a more oxidative muscle fiber type distribution. In PCOS, no such changes were found, despite similar training intensity and improvements in maximal oxygen uptake. In skeletal muscle of CON, but not PCOS, training increased GLUT4 and HKII mRNA and protein expressions. These data suggest that the impaired increase in whole body insulin action in women with PCOS with training is caused by an impaired ability to upregulate key glucose handling proteins for insulin-stimulated glucose uptake in skeletal muscle, and insulin-stimulated leg blood flow. Still, other important benefits of exercise training appeared in women with PCOS, including an improvement of the hyperandrogenic state.

Interactions between local and reflex influences on human forearm skin blood flow

1976 ◽  
Vol 41 (6) ◽  
pp. 826-831 ◽  
Author(s):  
J. M. Johnson ◽  
G. L. Brengelmann ◽  
L. B. Rowell
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Vasoconstrictor Response ◽  
Human Forearm ◽  
Forearm Skin ◽  
Forearm Muscle

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.

Effect of local sympathetic blockade on forearm blood flow and glucose uptake during hypoglycemia

Metabolism ◽  
1999 ◽  
Vol 48 (12) ◽  
pp. 1575-1583 ◽  
Author(s):  
Robert P. Hoffman ◽  
Christine A. Sinkey ◽  
Eva Tsalikian
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Forearm Blood Flow ◽  
Sympathetic Blockade

scholarly journals Diminished Insulin-Mediated Forearm Blood Flow and Muscle Glucose Uptake in Young Men with Low Birth Weight

2010 ◽  
Vol 47 (2) ◽  
pp. 139-147 ◽  
Author(s):  
M.P. Sonne ◽  
L. H&oslash;jbjerre ◽  
A.C. Alibegovic ◽  
A. Vaag ◽  
B. Stallknecht ◽  
...  
Keyword(s):  
Blood Flow ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Glucose Uptake ◽  
Forearm Blood Flow ◽  
Young Men

Influence of endurance exercise training status and gender on postexercise hypotension

2002 ◽  
Vol 92 (6) ◽  
pp. 2368-2374 ◽  
Author(s):  
Annette N. Senitko ◽  
Nisha Charkoudian ◽  
John R. Halliwill
Keyword(s):  
Cardiac Output ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Peripheral Resistance ◽  
Peak Oxygen Consumption ◽  
Similar Degree ◽  
Men And Women ◽  
Endurance Exercise Training ◽  
Before And After ◽  
Postexercise Hypotension

In sedentary individuals, postexercise hypotension after a single bout of aerobic exercise is due to a peripheral vasodilation. Endurance exercise training has the potential to modify this response and perhaps reduce the degree of postexercise hypotension. We tested the hypothesis that endurance exercise-trained men and women would have blunted postexercise hypotension compared with sedentary subjects but that the mechanism of hypotension would be similar (i.e., vasodilation). We studied 16 endurance-trained and 16 sedentary men and women. Arterial pressure, cardiac output, and total peripheral resistance were determined before and after a single 60-min bout of exercise at 60% peak oxygen consumption. All groups exhibited a similar degree of postexercise hypotension (∼4–5 mmHg; P < 0.05 vs. preexercise). In sedentary men and women, hypotension was the result of vasodilation (Δresistance: −8.9 ± 2.2%). In endurance-trained women, hypotension was also the result of vasodilation (−8.1 ± 4.1%). However, in endurance-trained men, hypotension was the result of a reduced cardiac output (−5.2 ± 2.4%; P < 0.05 vs. all others) and vasodilation was absent (−0.7 ± 3.3%; P < 0.05 vs. all others). Thus we conclude the magnitude of postexercise hypotension is similar in sedentary and endurance-trained men and women but that endurance-trained men and women achieve this fall in pressure via different mechanisms.

Laser-Doppler measurement of skin blood flow: comparison with plethysmography

1984 ◽  
Vol 56 (3) ◽  
pp. 798-803 ◽  
Author(s):  
J. M. Johnson ◽  
W. F. Taylor ◽  
A. P. Shepherd ◽  
M. K. Park
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Laser Doppler Velocimetry ◽  
Response Pattern ◽  
Small Volume ◽  
Forearm Blood Flow ◽  
Laser Doppler ◽  
Whole Body ◽  
Doppler Measurement ◽  
The Relationship

We compared laser-Doppler velocimetry with plethysmographically determined changes in skin blood flow (SkBF) in five studies on four men. Increments in SkBF were induced by raising whole-body skin temperature to 39 degrees C for 50–70 min. We found laser-Doppler blood flow (LDF) to correlate well with total forearm blood flow (FBF) within each study (r = 0.94–0.98), but the relationship varied among studies. Thus the slopes for the LDF vs. FBF relationship varied from 40 to 122 mV X ml-1 X 100 ml X min. The value for LDF at zero FBF, extrapolated from the regression relationships, ranged from 246 to 599 mV above the value for LDF set with the probe on a stationary object. The value for LDF when blood flow to the arm was mechanically occluded ranged from 110 to 230 mV. In a second series, we measured the LDF values from six sites on forearms of each of four normothermic men. There was marked regional variation, with 1.8- to 5.7-fold ranges in LDF within a given subject. Values for LDF during occlusion of the forearm were more consistent within and between subjects. Thus LDF appears to provide a good indicator of the response pattern of SkBF from the region of illuminated skin. However, variability in the relationship to total SkBF (probably arising from variation in the number of perfused capillaries in the small volume of tissue) and uncertainties in the value of LDF at zero SkBF make quantitative use difficult.

Influence of muscular development, obesity, and age on the fat-free mass of adults

1976 ◽  
Vol 41 (2) ◽  
pp. 223-229 ◽  
Author(s):  
J. Womersley ◽  
J. V. Durnin ◽  
K. Boddy ◽  
M. Mahaffy
Keyword(s):  
Body Fat ◽  
The Body ◽  
Fat Free Mass ◽  
Potassium Content ◽  
Whole Body ◽  
Obese Women ◽  
Men And Women ◽  
Muscular Development ◽  
Total Body ◽  
Water Measurement

Body fat and the fat-free mass (FFM) were estimated in 36 men and 43 women deliberately chosen to represent a variety of physical types; these were 1) young sedentary, 2) “muscular,” 3) younger obese, 4) older obese, and 5) older nonobese individuals of both sexes. The body fat and the FFM were estimated from measurements of body density (by total immersion in water, measurement being made of the residual volume of air present in the lungs at immersion) and from measurements of total body potassium (using a whole-body monitor to assess the natural 40K isotope present in the body). The muscular men and women and the younger obese men and women had a considerably greater FFM and thus had greater quantities of potassium than the corresponding sedentary groups. There were significantly different estimates of the FFM calculated from density and from total body K in three groups, the sedentary young men, the muscular, and the younger obese women. The density and the potassium content of the FFM appear to decline with obesity and aging. Muscular development is associated with a decrease in the density but an increase in the potassium content of the FFM.

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