scholarly journals The B2 Receptor of Bradykinin Is Not Essential for the Post-Exercise Increase in Glucose Uptake by Insulin-Stimulated Mouse Skeletal Muscle

2011 ◽  
pp. 511-519 ◽  
Author(s):  
G. G. SCHWEITZER ◽  
C. M. CASTORENA ◽  
T. HAMADA ◽  
K. FUNAI ◽  
E. B. ARIAS ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Treadmill Exercise ◽  
Post Exercise ◽  
Skeletal Muscle Glucose Uptake ◽  
Glucose Plasma ◽  
Exercise Induced

Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both bradykinin production and muscle insulin sensitivity, but bradykinin’s relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post-exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [3H]-2-deoxyglucose ±insulin (60 or 100 μU/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 μU/ml insulin (P=0.166) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 μU/ml insulin (P=0.063) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exercise-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle.

IL-6 is not essential for exercise-induced increases in glucose uptake

2013 ◽  
Vol 114 (9) ◽  
pp. 1151-1157 ◽  
Author(s):  
Hayley M. O'Neill ◽  
Rengasamy Palanivel ◽  
David C. Wright ◽  
Tara MacDonald ◽  
James S. Lally ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Glucose Uptake ◽  
Substrate Utilization ◽  
Treadmill Running ◽  
Glucose Clearance ◽  
Skeletal Muscle Glucose Uptake ◽  
Exercise Induced ◽  
Similar Body

Interleukin-6 (IL-6) increases glucose uptake in resting skeletal muscle. IL-6 is released from skeletal muscle during exercise; however; it is not known whether this IL-6 response is important for exercise-induced increases in skeletal muscle glucose uptake. We report that IL-6 knockout (KO) mice, 4 mo of age, have similar body weight to wild-type (WT), and, under resting conditions, oxygen consumption, food intake, substrate utilization, glucose tolerance, and insulin sensitivity are not different. Maximal exercise capacity is also similar to WT. We investigated substrate utilization and glucose clearance in vivo during steady-state treadmill running at 70% of maximal running speed and found that WT and IL-6 KO mice had similar rates of substrate utilization, muscle glucose clearance, and phosphorylation of AMP-activated protein kinase T172. These data provide evidence that IL-6 does not play a major role in regulating substrate utilization or skeletal muscle glucose uptake during steady-state endurance exercise.

scholarly journals Insulin action on heart and skeletal muscle glucose uptake in essential hypertension.

1995 ◽  
Vol 96 (2) ◽  
pp. 1003-1009 ◽  
Author(s):  
P Nuutila ◽  
M Mäki ◽  
H Laine ◽  
M J Knuuti ◽  
U Ruotsalainen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Essential Hypertension ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Skeletal Muscle Glucose Uptake

Endurance training fails to inhibit skeletal muscle glucose uptake during exercise

1994 ◽  
Vol 76 (5) ◽  
pp. 1876-1881 ◽  
Author(s):  
K. D. Sumida ◽  
C. M. Donovan
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Endurance Training ◽  
Plasma Glucose ◽  
Tibialis Anterior ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Glycogen Depletion ◽  
Post Exercise ◽  
Skeletal Muscle Glucose Uptake

The effects of endurance training (running 30 m/min, 10% grade for 90 min, 5 days/wk for 12 wk) on skeletal muscle glucose uptake during steady-state exercise (running 20 m/min) were studied in fed rats. A bolus injection of 2-[1,2–3H]deoxyglucose was administered to assess the glucose metabolic index (R′g), an indicator of glucose uptake, in individual tissues of the animal. After 55 min of rest or moderate exercise, various tissues were analyzed for accumulation of phosphorylated 2-[1,2–3H]-deoxyglucose and/or glycogen content. No differences were observed between groups in the resting glycogen content for any of the muscle samples examined. Resting plasma glucose concentrations were not significantly different between groups. Furthermore, no significant differences were observed in R′g between groups for any of the muscle examined (tibialis anterior, extensor digitorum longus, soleus, white gastrocnemius, red gastrocnemius). During exercise, plasma glucose concentrations were not significantly different between groups. Exercise significantly elevated R′g above resting values in the tibialis anterior (5-fold), soleus (3-fold), and red gastrocnemius (7.5-fold). Despite an elevated R′g for specific muscles during exercise, no significant differences were observed in glucose uptake between groups for any tissue examined. Concomitantly, trained animals exhibited significantly less muscle glycogen depletion during exercise compared with control animals. Liver glycogen levels were also significantly higher post-exercise in trained vs. control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Simvastatin Impairs Glucose Homeostasis in Mice Depending on PGC-1α Skeletal Muscle Expression

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 351
Author(s):  
Miljenko Valentin Panajatovic ◽  
François Singh ◽  
Stephan Krähenbühl ◽  
Jamal Bouitbir
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Homeostasis ◽  
Simvastatin Treatment ◽  
Skeletal Muscle Glucose Uptake ◽  
Skeletal Muscle Insulin Sensitivity ◽  
Glycogen Stores

Several studies showed an increased risk for diabetes with statin treatment. PGC-1α is an important regulator of muscle energy metabolism and mitochondrial biogenesis. Since statins impair skeletal muscle PGC-1α expression and reduced PGC-1α expression has been observed in diabetic patients, we investigated the possibility that skeletal muscle PGC1α expression influences the effect of simvastatin on muscle glucose metabolism. Mice with muscle PGC-1α knockout (KO) or PGC-1α overexpression (OE), and wild-type (WT) mice were investigated. Mice were treated orally for 3 weeks with simvastatin (5 mg/kg/day) and investigated by intraperitoneal glucose tolerance (iGTT), in vivo skeletal muscle glucose uptake, muscle glycogen content, and Glut4 and hexokinase mRNA and protein expression. Simvastatin impaired glucose metabolism in WT mice, as manifested by increased glucose blood concentrations during the iGTT, decreased skeletal muscle glucose uptake and glycogen stores. KO mice showed impaired glucose homeostasis with increased blood glucose concentrations during the iGTT already without simvastatin treatment and simvastatin induced a decrease in skeletal muscle glucose uptake. In OE mice, simvastatin treatment increased blood glucose and insulin concentrations during the iGTT, and increased skeletal muscle glucose uptake, glycogen stores, and Glut4 and hexokinase protein expression. In conclusion, simvastatin impaired skeletal muscle insulin sensitivity in WT mice, while KO mice exhibited impaired skeletal muscle insulin sensitivity already in the absence of simvastatin. In OE mice, simvastatin augmented muscular glucose uptake but impaired whole-body insulin sensitivity. Thus, simvastatin affected glucose homeostasis depending on PGC-1α expression.

An amino acid mixture improves glucose tolerance and insulin signaling in Sprague-Dawley rats

2011 ◽  
Vol 300 (4) ◽  
pp. E752-E760 ◽  
Author(s):  
Jeffrey R. Bernard ◽  
Yi-Hung Liao ◽  
Daisuke Hara ◽  
Zhenping Ding ◽  
Chung-Yu Chen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Amino Acid ◽  
Glucose Uptake ◽  
White Muscle ◽  
Amino Acid Mixture ◽  
Acid Mixture ◽  
Glucose Response ◽  
Skeletal Muscle Glucose Uptake ◽  
Fast Twitch

The aims of this investigation were to evaluate the effect of an amino acid supplement on the glucose response to an oral glucose challenge ( experiment 1) and to evaluate whether differences in blood glucose response were associated with increased skeletal muscle glucose uptake ( experimental 2). Experiment 1 rats were gavaged with either glucose (CHO), glucose plus an amino acid mixture (CHO-AA-1), glucose plus an amino acid mixture with increased leucine concentration (CHO-AA-2), or water (PLA). CHO-AA-1 and CHO-AA-2 had reduced blood glucose responses compared with CHO, with no difference in insulin among these treatments. Experiment 2 rats were gavaged with either CHO or CHO-AA-1. Fifteen minutes after gavage, a bolus containing 2-[3H]deoxyglucose and [U-14C]mannitol was infused via a tail vein. Blood glucose was significantly lower in CHO-AA-1 than in CHO, whereas insulin responses were similar. Muscle glucose uptake was higher in CHO-AA-1 compared with CHO in both fast-twitch red (8.36 ± 1.3 vs. 5.27 ± 0.7 μmol·g−1·h−1) and white muscle (1.85 ± 0.3 vs. 1.11 ± 0.2 μmol·g−1·h−1). There was no difference in Akt/PKB phosphorylation between treatment groups; however, the amino acid treatment resulted in increased AS160 phosphorylation in both muscle fiber types. Glycogen synthase phosphorylation was reduced in fast-twitch red muscle of CHO-AA-1 compared with CHO, whereas mTOR phosphorylation was increased. These differences were not noted in fast-twitch white muscle. These findings suggest that amino acid supplementation can improve glucose tolerance by increasing skeletal muscle glucose uptake and intracellular disposal through enhanced intracellular signaling.

scholarly journals Effect of Lactate on Insulin Action in Rats

2008 ◽  
Vol 8 (2) ◽  
pp. 131-134 ◽  
Author(s):  
Muhidin Hamamdžić ◽  
Boris Hrabač ◽  
Amer Alić ◽  
Eva Pašić-Juhas ◽  
Aida Hodžić
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Wistar Rats ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Treated Group ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Previous Part

The aim of the study was to explore the effect of lactate on insulin-stimulated glucose uptake in rats. Thirty Wistar rats, weighing 250 - 300 g. were arbitrarily divided into one of three groups (n =10): insulin (1 IU/kg) treated group, lactate (80 mg/kg), and insulin plus lactate treated groups. Blood glucose levels were measured in venous samples collected from the tail vein over 3 hour period after insulin or/and lactate administration in 30-minute intervals.To estimate the influence of lactate on insulin blood level, a total of 20 rats were divided into 4 groups (n = 5): saline, insulin, lactate, and insulin plus lactate treated group, respectively.Sixty minutes after the appropriate application of the same doses of insulin, lactate, and lactate plus insulin, as in the previous part of the experiment, plasma insulin and blood glucose levels were determined in blood samples drawn from the abdominal aorta. Lactate in combination with insulin, in comparison to insulin application alone, caused a dramatic increase in plasma insulin level (p<0,001) and more profound hypoglicaemia (p<0,001). The results of this investigation indicate that lactate application significantly increases the rate of glucose uptake from peripheral blood caused by exogenous insulin action. The possible involvement of lactate in the mechanism of enhanced glucose uptake due to insulin action after physical exercise is discussed.

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.

scholarly journals Effects of Oral Resveratrol Supplementation on Glycogen Replenishment and Mitochondria Biogenesis in Exercised Human Skeletal Muscle

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3721
Author(s):  
Chun-Ching Huang ◽  
Chia-Chen Liu ◽  
Jung-Piao Tsao ◽  
Chin-Lin Hsu ◽  
I-Shiung Cheng
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Young Male ◽  
Gene Expressions ◽  
Plasma Parameters ◽  
Post Exercise ◽  
Glycogen Resynthesis ◽  
Mitochondria Biogenesis

The present study aimed to investigate the effect of oral resveratrol supplementation on the key molecular gene expressions involved in mitochondria biogenesis and glycogen resynthesis in human skeletal muscle. Nine young male athletes participated in the single-blind and crossover designed study. All subjects completed a 4-day resveratrol and placebo supplement in a randomized order while performing a single bout of cycling exercise. Immediately after the exercise challenge, the subjects consumed a carbohydrate (CHO) meal (2 g CHO/Kg body mass) with either resveratrol or placebo capsules. Biopsied muscle samples, blood samples and expired gas samples were obtained at 0 h and 3 h after exercise. The muscle samples were measured for gene transcription factor expression by real-time PCR for glucose uptake and mitochondria biogenesis. Plasma glucose, insulin, glycerol, non-esterified fatty acid concentrations and respiratory exchange ratio were analyzed during post-exercise recovery periods. The results showed that the muscle glycogen concentrations were higher at 3 h than at 0 h; however, there were no difference between resveratrol trial and placebo trial. There were no significantly different concentrations in plasma parameters between the two trials. Similarly, no measured gene expressions were significant between the two trials. The evidence concluded that the 4-day oral resveratrol supplementation did not improve post-exercise muscle glycogen resynthesis and related glucose uptake and mitochondrial biosynthesis gene expression in men.

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

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