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 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.

Effects of adenosine, exercise, and moderate acute hypoxia on energy substrate utilization of human skeletal muscle

2012 ◽  
Vol 302 (3) ◽  
pp. R385-R390 ◽  
Author(s):  
Ilkka Heinonen ◽  
Jukka Kemppainen ◽  
Kimmo Kaskinoro ◽  
Juha E. Peltonen ◽  
Hannu T. Sipilä ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Acute Hypoxia ◽  
Knee Extension ◽  
Substrate Utilization ◽  
Energy Substrate ◽  
Skeletal Muscle Glucose Uptake ◽  
Knee Extension Exercise

Glucose metabolism increases in hypoxia and can be influenced by endogenous adenosine, but the role of adenosine for regulating glucose metabolism at rest or during exercise in hypoxia has not been elucidated in humans. We studied the effects of exogenous adenosine on human skeletal muscle glucose uptake and other blood energy substrates [free fatty acid (FFA) and lactate] by infusing adenosine into the femoral artery in nine healthy young men. The role of endogenous adenosine was studied by intra-arterial adenosine receptor inhibition (aminophylline) during dynamic one-leg knee extension exercise in normoxia and acute hypoxia corresponding to ∼3,400 m of altitude. Extraction and release of energy substrates were studied by arterial-to-venous (A-V) blood samples, and total uptake or release was determined by the product of A-V differences and muscle nutritive perfusion measured by positron emission tomography. The results showed that glucose uptake increased from a baseline value of 0.2 ± 0.2 to 2.0 ± 2.2 μmol·100 g−1·min−1 during adenosine infusion ( P < 0.05) at rest. Although acute hypoxia enhanced arterial FFA levels, it did not affect muscle substrate utilization at rest. During exercise, glucose uptake was higher (195%) during acute hypoxia compared with normoxia ( P = 0.058), and aminophylline had no effect on energy substrate utilization during exercise, despite that arterial FFA levels were increased. In conclusion, exogenous adenosine at rest and acute moderate hypoxia during low-intensity knee-extension exercise increases skeletal muscle glucose uptake, but the increase in hypoxia appears not to be mediated by adenosine.

scholarly journals Microvascular Recruitment Is an Early Insulin Effect That Regulates Skeletal Muscle Glucose Uptake In Vivo

Diabetes ◽  
2004 ◽  
Vol 53 (6) ◽  
pp. 1418-1423 ◽  
Author(s):  
M. A. Vincent ◽  
L. H. Clerk ◽  
J. R. Lindner ◽  
A. L. Klibanov ◽  
M. G. Clark ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Effect ◽  
Skeletal Muscle Glucose Uptake ◽  
Microvascular Recruitment

scholarly journals Postexercise improvement in glucose uptake occurs concomitant with greater γ3-AMPK activation and AS160 phosphorylation in rat skeletal muscle

2018 ◽  
Vol 315 (5) ◽  
pp. E859-E871 ◽  
Author(s):  
Haiyan Wang ◽  
Edward B. Arias ◽  
Mark W. Pataky ◽  
Laurie J. Goodyear ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Contractile Activity ◽  
Exercise Session ◽  
Ampk Activation ◽  
Rat Skeletal Muscle ◽  
Ampk Activity ◽  
Exercise Induced

A single exercise session can increase insulin-stimulated glucose uptake (GU) by skeletal muscle, concomitant with greater Akt substrate of 160 kDa (AS160) phosphorylation on Akt-phosphosites (Thr642 and Ser588) that regulate insulin-stimulated GU. Recent research using mouse skeletal muscle suggested that ex vivo 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) or electrically stimulated contractile activity-inducing increased γ3-AMPK activity and AS160 phosphorylation on a consensus AMPK-motif (Ser704) resulted in greater AS160 Thr642 phosphorylation and GU by insulin-stimulated muscle. Our primary goal was to determine whether in vivo exercise that increases insulin-stimulated GU in rat skeletal muscle would also increase γ3-AMPK activity and AS160 site-selective phosphorylation (Ser588, Thr642, and Ser704) immediately postexercise (IPEX) and/or 3 h postexercise (3hPEX). Epitrochlearis muscles isolated from sedentary and exercised (2-h swim exercise; studied IPEX and 3hPEX) rats were incubated with 2-deoxyglucose to determine GU (without insulin at IPEX; without or with insulin at 3hPEX). Muscles were also assessed for γ1-AMPK activity, γ3-AMPK activity, phosphorylated AMPK (pAMPK), and phosphorylated AS160 (pAS160). IPEX versus sedentary had greater γ3-AMPK activity, pAS160 (Ser588, Thr642, Ser704), and GU with unaltered γ1-AMPK activity. 3hPEX versus sedentary had greater γ3-AMPK activity, pAS160 Ser704, and GU with or without insulin; greater pAS160 Thr642 only with insulin; and unaltered γ1-AMPK activity. These results using an in vivo exercise protocol that increased insulin-stimulated GU in rat skeletal muscle are consistent with the hypothesis that in vivo exercise-induced enhancement of γ3-AMPK activation and AS160 Ser704 IPEX and 3hPEX are important for greater pAS160 Thr642 and enhanced insulin-stimulated GU by skeletal muscle.

scholarly journals Constitutively Active CaMKK  Stimulates Skeletal Muscle Glucose Uptake in Insulin-Resistant Mice In Vivo

Diabetes ◽  
2013 ◽  
Vol 63 (1) ◽  
pp. 142-151 ◽  
Author(s):  
J. M. Hinkley ◽  
J. L. Ferey ◽  
J. J. Brault ◽  
C. A. S. Smith ◽  
L. A. A. Gilliam ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Resistant ◽  
Skeletal Muscle Glucose Uptake ◽  
Constitutively Active

scholarly journals Tracing Fasting Glucose Fluxes with Unstressed Catheter Approach in Streptozotocin Induced Diabetic Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7
Author(s):  
Shichun Du ◽  
Hui Wu ◽  
Xiao Xu ◽  
Ying Meng ◽  
Fangzhen Xia ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Glucose Production ◽  
Diabetic Rats ◽  
Endogenous Glucose Production ◽  
Tracer Injection ◽  
Skeletal Muscle Glucose Uptake ◽  
Endogenous Glucose

Objective. Blood glucose concentrations of type 1 diabetic rats are vulnerable, especially to stress and trauma. The present study aimed to investigate the fasting endogenous glucose production and skeletal muscle glucose uptake of Streptozotocin induced type 1 diabetic rats using an unstressed vein and artery implantation of catheters at the tails of the rats as a platform.Research Design and Methods. Streptozotocin (65 mg·kg−1) was administered to induce type 1 diabetic state. The unstressed approach of catheters of vein and artery at the tails of the rats was established before the isotope tracer injection. Dynamic measurement of fasting endogenous glucose production was assessed by continuously infusing stable isotope [6, 6-2H2] glucose, while skeletal muscle glucose uptake by bolus injecting radioactively labeled [1-14C]-2-deoxy-glucose.Results. Streptozotocin induced type 1 diabetic rats displayed polydipsia, polyphagia, and polyuria along with overt hyperglycemia and hypoinsulinemia. They also had enhanced fasting endogenous glucose production and reduced glucose uptake in skeletal muscle compared to nondiabetic rats.Conclusions. The dual catheters implantation at the tails of the rats together with isotope tracers injection is a save time, unstressed, and feasible approach to explore the glucose metabolism in animal models in vivo.

Limitations to basal and insulin-stimulated skeletal muscle glucose uptake in the high-fat-fed rat

2000 ◽  
Vol 279 (5) ◽  
pp. E1064-E1071 ◽  
Author(s):  
Amy E. Halseth ◽  
Deanna P. Bracy ◽  
David H. Wasserman
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Steady State ◽  
Glucose Uptake ◽  
Glucose Concentration ◽  
High Fat Diet ◽  
High Fat ◽  
Skeletal Muscle Glucose Uptake ◽  
Fast Twitch ◽  
Total Muscle

Rats fed a high-fat diet display blunted insulin-stimulated skeletal muscle glucose uptake. It is not clear whether this is due solely to a defect in glucose transport, or if glucose delivery and phosphorylation are also impaired. To determine this, rats were fed standard chow (control rats) or a high-fat diet (HF rats) for 4 wk. Experiments were then performed on conscious rats under basal conditions or during hyperinsulinemic euglycemic clamps. Rats received primed constant infusions of 3- O-methyl-[3H]glucose (3- O-MG) and [1-14C]mannitol. Total muscle glucose concentration and the steady-state ratio of intracellular to extracellular 3- O-MG concentration [which distributes based on the transsarcolemmal glucose gradient (TSGG)] were used to calculate glucose concentrations at the inner and outer sarcolemmal surfaces ([G]imand [G]om, respectively) in soleus. Total muscle glucose was also measured in two fast-twitch muscles. Muscle glucose uptake was markedly decreased in HF rats. In control rats, hyperinsulinemia resulted in a decrease in soleus TSGG compared with basal, due to increased [G]im. In HF rats during hyperinsulinemia, [G]imalso exceeded zero. Hyperinsulinemia also decreased muscle glucose in HF rats, implicating impaired glucose delivery. In conclusion, defects in extracellular and intracellular components of muscle glucose uptake are of major functional significance in this model of insulin resistance.

scholarly journals Rates and tissue sites of non-insulin- and insulin-mediated glucose uptake in humans

1988 ◽  
Vol 255 (6) ◽  
pp. E769-E774 ◽  
Author(s):  
A. D. Baron ◽  
G. Brechtel ◽  
P. Wallace ◽  
S. V. Edelman
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Serum Glucose ◽  
Whole Body ◽  
Healthy Men ◽  
Catheter Technique ◽  
Muscle Tissues ◽  
Skeletal Muscle Glucose Uptake ◽  
The Difference

In vivo glucose uptake can occur via two mechanisms, namely, insulin-mediated glucose uptake (IMGU) and non-insulin-mediated glucose uptake (NIMGU). Although the principal tissue sites for IMGU are skeletal muscle, the tissue sites for NIMGU at a given serum glucose concentration are not known. To examine this issue, rates of whole body glucose uptake (Rd) were measured at basal and during glucose clamp studies performed at euglycemia (approximately 90 mg/dl) and hyperglycemia (approximately 220 mg/dl) in six lean healthy men. Studies were performed during hyperinsulinemia (approximately 70 microU/ml) and during somatostatin-induced insulinopenia to measure IMGU and NIMGU, respectively. During each study, leg glucose balance (arteriovenous catheter technique) was also measured. With this approach, rates of whole body skeletal muscle IMGU and NIMGU can be estimated, and the difference between overall Rd and skeletal muscle glucose uptake represents non-skeletal muscle Rd. The results indicate that approximately 20% of basal Rd is into skeletal muscle. During insulinopenia approximately 86% of body NIMGU occurs in non-skeletal muscle tissues at euglycemia. When hyperglycemia was created, whole body NIMGU increased from 128 +/- 6 to 213 +/- 18 mg/min (P less than 0.01); NIMGU into non-skeletal muscle tissues was 134 +/- 11 and 111 +/- 6 mg/min at hyperglycemia and euglycemia, respectively, P = NS. Therefore, virtually all the hyperglycemia induced increment in NIMGU occurred in skeletal muscle. During hyperinsulinemia, IMGU in skeletal muscle represented 75 and 95% of body Rd, at euglycemia and hyperglycemia, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin 1–7 improves insulin sensitivity by increasing skeletal muscle glucose uptake in vivo

Peptides ◽  
2014 ◽  
Vol 51 ◽  
pp. 26-30 ◽  
Author(s):  
Omar Echeverría-Rodríguez ◽  
Leonardo Del Valle-Mondragón ◽  
Enrique Hong
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Skeletal Muscle Glucose Uptake
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