Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise

2006 ◽  
Vol 101 (5) ◽  
pp. 1368-1376 ◽  
Author(s):  
Taku Hamada ◽  
Edward B. Arias ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Genetically Modified ◽  
Extensor Digitorum ◽  
Exercise Protocol ◽  
Mouse Skeletal Muscle ◽  
Prior Exercise

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 μU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation ( P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased ( P < 0.05) ∼85 min after exercise in the epitrochlearis (sedentary: 0.266 ± 0.045 μmol·g−1·15 min−1; exercised: 0.414 ± 0.051) and soleus (sedentary: 0.102 ± 0.049; exercised: 0.347 ± 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.

scholarly journals Exercise training reduces skeletal muscle membrane arachidonate in the obese (fa/fa) Zucker rat

1998 ◽  
Vol 85 (5) ◽  
pp. 1898-1902 ◽  
Author(s):  
Kerry J. Ayre ◽  
Stephen D. Phinney ◽  
Anna B. Tang ◽  
Judith S. Stern
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Zucker Rats ◽  
Muscle Membrane ◽  
Positive Effects ◽  
Fast Twitch ◽  
White Gastrocnemius

Compared with the lean ( Fa/−) genotype, obese ( fa/fa) Zucker rats have a relative deficiency of muscle phospholipid arachidonate, and skeletal muscle arachidonate in humans is positively correlated with insulin sensitivity. To assess the hypothesis that the positive effects of exercise training on insulin sensitivity are mediated by increased muscle arachidonate, we randomized 20 lean and 20 obese weanling male Zucker rats to sedentary or treadmill exercise groups. After 9 wk, fasting serum, three skeletal muscles (white gastrocnemius, soleus, and extensor digitorum longus), and heart were obtained. Fasting insulin was halved by exercise training in the obese rat. In white gastrocnemius and extensor digitorum longus (fast-twitch muscles), but not in soleus (a slow-twitch muscle) or heart, phospholipid arachidonate was lower in obese than in lean rats ( P < 0.001). In all muscles, exercise in the obese rats reduced arachidonate ( P < 0.03, by ANOVA contrast). We conclude that improved insulin sensitivity with exercise in the obese genotype is not mediated by increased muscle arachidonate and that reduced muscle arachidonate in obese Zucker rats is unique to fast-twitch muscles.

scholarly journals Effects of glucose on contractile function, [Ca2+]i, and glycogen in isolated mouse skeletal muscle

2002 ◽  
Vol 282 (6) ◽  
pp. C1306-C1312 ◽  
Author(s):  
Ingrid Helander ◽  
Håkan Westerblad ◽  
Abram Katz
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Contractile Function ◽  
Extensor Digitorum ◽  
Fluorescence Ratio ◽  
Tetanic Force ◽  
Mouse Skeletal Muscle ◽  
Control Value ◽  
Extracellular Glucose ◽  
Initial Force

Extensor digitorum longus muscles were stimulated to contract to fatigue and allowed to recover for 2 h in the absence or presence of 5.5 or 11 mM extracellular glucose. This was followed by a second fatigue run, which ended when the absolute force was the same as at the end of the first run. During the first fatigue run, the fluorescence ratio for indo 1 increased [reflecting an increase in myoplasmic free Ca2+ concentration ([Ca2+]i)] during the initial tetani, peaking at ∼115% of the first tetanic value, followed by a continuous decrease to ∼90% at fatigue. During the first fatigue run, myofibrillar Ca2+ sensitivity was significantly decreased. During the second run, the number of tetani was 57 ± 6% of initial force in muscles that recovered in the absence of glucose and 110 ± 6 and 119 ± 2% of initial force in muscles that recovered in 5.5 and 11 mM glucose, respectively. Fluorescence ratios during the first, peak, and last tetani did not differ significantly between the first and second fatigue runs during any of the three conditions. Glycogen decreased by almost 50% during the first fatigue run and did not change further after recovery in the absence of glucose. After recovery in the presence of 5.5 and 11 mM glucose, glycogen increased 32 and 42% above the nonstimulated control value ( P < 0.01). These data demonstrate that extracellular glucose delays the decrease of tetanic force and [Ca2+]i during fatiguing stimulation and that glycogen supercompensation following contraction can occur in the absence of insulin.

Insulin sensitivity of rat skeletal muscle: effects of starvation and aging.

1979 ◽  
Vol 236 (5) ◽  
pp. E519 ◽  
Author(s):  
M N Goodman ◽  
N B Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Extensor Digitorum Longus ◽  
Glucose Utilization ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Low Concentrations ◽  
Longus Muscle ◽  
Relative Differences

The effects of starvation and of aging on the sensitivity of skeletal muscle to insulin were studied in the isolated perfused rat hindquarter preparation. As we have shown previously, starvation for 48 h had no effect on glucose uptake in hindquarters perfused with high levels of insulin (5 and 20 mU/ml). On the other hand, in the presence of physiological concentrations of insulin (50--200 muU/ml), glucose utilization was substantially greater in starved rats. Low concentrations of insulin had a greater effect on glucose uptake in fed young (100-g) than in fed older (350-g) rats. Starvation for 48 h enhanced glucose uptake in both young and older rats; however, the relative differences persisted. Starvation had similar effects on glucose utilization by the incubated soleus and extensor digitorum longus muscle. In addition, it augmented the stimulation by insulin of alpha-aminoisobutyric acid transport into the incubated extensor digitorum longus muscle. These results suggest that the in vitro sensitivity of skeletal muscle to physiological concentrations of insulin is enhanced during starvation. The basis for these findings and their physiological implications remain to be determined.

scholarly journals AS160 Regulates Insulin- and Contraction-stimulated Glucose Uptake in Mouse Skeletal Muscle*

2006 ◽  
Vol 281 (42) ◽  
pp. 31478-31485
Author(s):  
Henning F. Kramer ◽  
Carol A. Witczak ◽  
Eric B. Taylor ◽  
Nobuharu Fujii ◽  
Michael F. Hirshman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Mouse Skeletal Muscle

Exercise-induced enhancement of insulin sensitivity is associated with accumulation of M2-polarized macrophages in mouse skeletal muscle

2013 ◽  
Vol 441 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Shin-ichi Ikeda ◽  
Yoshifumi Tamura ◽  
Saori Kakehi ◽  
Kageumi Takeno ◽  
Minako Kawaguchi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Mouse Skeletal Muscle ◽  
Exercise Induced

Human growth hormone treatment of hypophysectomized rats increases the proportion of type-1 fibres in skeletal muscle

1989 ◽  
Vol 123 (3) ◽  
pp. 429-NP ◽  
Author(s):  
C. M. Ayling ◽  
B. H. Moreland ◽  
J. M. Zanelli ◽  
D. Schulster
Keyword(s):  
Skeletal Muscle ◽  
Fibre Type ◽  
Extensor Digitorum Longus ◽  
Human Growth ◽  
Hormone Treatment ◽  
Pituitary Hormones ◽  
Extensor Digitorum ◽  
Replacement Treatment ◽  
Hypophysectomized Rats

ABSTRACT The studies describe alterations after hypophysectomy in the proportion of the type-1 and type-2 fibres in rat skeletal muscles, and the effects of replacement treatment with pituitary human (h) GH. Cytochemical analysis of myosin ATPase, succinate dehydrogenase and lactate dehydrogenase activities in sections of rat hind limb muscles were used as markers of fibre type and revealed that hypophysectomy reduced the proportion of type-1 fibres by 50% in soleus and in extensor digitorum longus muscles. This reduction in the proportion of type-1 fibres was accompanied by the appearance of transitional fibres (type 2C/1B). Following seven daily injections of hGH (60 mIU/day) to hypophysectomized rats, the proportion of type-1 fibres in both soleus and in extensor digitorum longus was increased with a concomitant reduction in the number of transitional fibres. After 11 days of treatment, all these transitional fibres had reverted back to type-1 fibres. Only hGH was observed to elicit this effect; injections of other pituitary hormones had no effect on the proportions of these transitional fibres. These alterations in fibre type occurred more rapidly than the changes reported after prolonged electrical stimulation of muscle or following extended exercise. These findings suggest that hypophysectomy and GH injection can result in a rapid alteration in the fibre composition of skeletal muscle, which may have important implications in terms of the resistance to fatigue and speed of contraction of the muscle. Journal of Endocrinology (1989) 123, 429–435

scholarly journals Identification in skeletal muscle of a distinct extracellular pool of amino acids, and its role in protein synthesis

1971 ◽  
Vol 121 (5) ◽  
pp. 817-827 ◽  
Author(s):  
R. C. Hider ◽  
E. B. Fern ◽  
D. R. London
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Incubation Medium ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Longus Muscle ◽  
Kinetics Of

1. The kinetics of radioactive labelling of extra- and intra-cellular amino acid pools and protein of the extensor digitorum longus muscle were studied after incubations with radioactive amino acids in vitro. 2. The results indicated that an extracellular pool could be defined, the contents of which were different from those of the incubation medium. 3. It was concluded that amino acids from the extracellular pool, as defined in this study, were incorporated directly into protein.

scholarly journals Prep1 Deficiency Induces Protection from Diabetes and Increased Insulin Sensitivity through a p160-Mediated Mechanism

2008 ◽  
Vol 28 (18) ◽  
pp. 5634-5645 ◽  
Author(s):  
Francesco Oriente ◽  
Luis Cesar Fernandez Diaz ◽  
Claudia Miele ◽  
Salvatore Iovino ◽  
Silvia Mori ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Normal Glucose Tolerance ◽  
Glucose Disposal ◽  
Protein Levels ◽  
Normal Glucose ◽  
Enhanced Expression ◽  
The Stability

ABSTRACT We have examined glucose homeostasis in mice hypomorphic for the homeotic transcription factor gene Prep1. Prep1-hypomorphic (Prep1 i / i ) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance. In addition, these mice exhibit protection from streptozotocin-induced diabetes and enhanced insulin sensitivity with improved glucose uptake and insulin-dependent glucose disposal by skeletal muscle. This muscle phenotype does not depend on reduced expression of the known Prep1 transcription partner, Pbx1. Instead, in Prep1 i / i muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160. Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1α, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle. Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1. In vivo skeletal muscle delivery of p160 cDNA in Prep1 i / i mice also reverses the molecular phenotype. Finally, we show that Prep1 controls the stability of the p160 protein. We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.

ALY688 elicits adiponectin-mimetic signaling and improves insulin action in skeletal muscle cells

2021 ◽  
Author(s):  
Hye Kyoung Sung ◽  
Patricia L. Mitchell ◽  
Sean Gross ◽  
Andre Marette ◽  
Gary Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Muscle Cells ◽  
Temporal Analysis ◽  
Skeletal Muscle Cells ◽  
Adiponectin Receptor ◽  
Metabolic Effects

Adiponectin is well established to mediate many beneficial metabolic effects, and this has stimulated great interest in development and validation of adiponectin receptor agonists as pharmaceutical tools. This study investigated the effects of ALY688, a peptide-based adiponectin receptor agonist, in rat L6 skeletal muscle cells. ALY688 significantly increased phosphorylation of several adiponectin downstream effectors, including AMPK, ACC and p38MAPK, assessed by immunoblotting and immunofluorescence microscopy. Temporal analysis using cells expressing an Akt biosensor demonstrated that ALY688 enhanced insulin sensitivity. This effect was associated with increased insulin-stimulated Akt and IRS-1 phosphorylation. The functional metabolic significance of these signaling effects was examined by measuring glucose uptake in myoblasts stably overexpressing the glucose transporter GLUT4. ALY688 treatment both increased glucose uptake itself and enhanced insulin-stimulated glucose uptake. In the model of high glucose/high insulin (HGHI)-induced insulin resistant cells, both temporal studies using the Akt biosensor as well as immunoblotting assessing Akt and IRS-1 phosphorylation indicated that ALY688 significantly reduced insulin resistance. Importantly, we observed that ALY688 administration to high-fat high sucrose fed mice also improve glucose handling, validating its efficacy in vivo. In summary, these data indicate that ALY688 activates adiponectin signaling pathways in skeletal muscle, leading to improved insulin sensitivity and beneficial metabolic effects.

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