scholarly journals Brief Dietary Restriction Increases Skeletal Muscle Glucose Transport in Old Fischer 344 Rats

1996 ◽  
Vol 51A (3) ◽  
pp. B208-B213 ◽  
Author(s):  
D. J. Dean ◽  
G. D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Dietary Restriction ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Muscle Glucose Transport

Persistent effects of exercise on skeletal muscle glucose transport across the life-span of rats

1993 ◽  
Vol 75 (2) ◽  
pp. 972-978 ◽  
Author(s):  
G. D. Cartee ◽  
C. Briggs-Tung ◽  
E. W. Kietzke
Keyword(s):  
Skeletal Muscle ◽  
Life Span ◽  
Glucose Transport ◽  
Transport Rate ◽  
Brown Norway ◽  
F1 Hybrid ◽  
Fischer 344 ◽  
Glut 4 ◽  
Wide Range ◽  
Muscle Glucose Transport

Very young rats (< 2 mo) have a persistent increase in insulin-stimulated glucose transport rate in skeletal muscle for several hours after completing a bout of exercise. We studied the effect of exercise on the glucose transport activity of isolated epitrochlearis muscles from male Fischer 344/Brown Norway F1 hybrid rats across a wide range of the life-span (at 3.5, 13, and 25 mo). The stimulation of 3-O-methylglucose (3-MG) accumulation by a submaximally effective insulin concentration (100 microU/ml) was enhanced (50–75%) 4 h after exercise, regardless of age. In contrast, the 3-MG transport rate with 20,000 microU/ml insulin was enhanced after exercise only in the youngest rats (35%), and this increased responsiveness occurred despite no changes in muscle total GLUT-4 levels. In addition, epitrochlearis GLUT-4 levels were reduced by 29% between 3.5 and 13 mo of age in sedentary rats but did not decline further between 13 and 25 mo of age. GLUT-4 levels were moderately but significantly (P < 0.05) related (r = 0.554) to epitrochlearis muscle capacity for insulin-stimulated 3-MG transport.

scholarly journals Skeletal Muscle Glucose Transport and Metabolism Are Enhanced in Transgenic Mice Overexpressing the Glut4 Glucose Transporter.

1995 ◽  
Vol 270 (4) ◽  
pp. 1679-1684
Author(s):  
Polly A. Hansen ◽  
Eric A. Gulve ◽  
Bess Adkins Marshall ◽  
Jiaping Gao ◽  
Jeffrey E. Pessin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Muscle Glucose Transport

Isomer-specific actions of conjugated linoleic acid on muscle glucose transport in the obese Zucker rat

2003 ◽  
Vol 285 (1) ◽  
pp. E98-E105 ◽  
Author(s):  
Erik J. Henriksen ◽  
Mary K. Teachey ◽  
Zachary C. Taylor ◽  
Stephan Jacob ◽  
Arne Ptock ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Glucose Transport ◽  
Zucker Rat ◽  
Transport Activity ◽  
Insulin Resistant ◽  
Obese Zucker Rat ◽  
Cla Isomers ◽  
Muscle Glucose Transport

The fatty acid-conjugated linoleic acid (CLA) enhances glucose tolerance and insulin action on skeletal muscle glucose transport in rodent models of insulin resistance. However, no study has directly compared the metabolic effects of the two primary CLA isomers, cis-9, trans-11-CLA (c9,t11-CLA) and trans-10, cis-12-CLA (t10,c12-CLA). Therefore, we assessed the effects of a 50:50 mixture of these two CLA isomers (M-CLA) and of preparations enriched in either c9,t11-CLA (76% enriched) or t10,c12-CLA (90% enriched) on glucose tolerance and insulin-stimulated glucose transport in skeletal muscle of the insulin-resistant obese Zucker ( fa/ fa) rat. Animals were treated daily by gavage with either vehicle (corn oil), M-CLA, c9,t11-CLA, or t10,c12-CLA (all CLA treatments at 1.5 g total CLA/kg body wt) for 21 consecutive days. During an oral glucose tolerance test, glucose responses were reduced ( P < 0.05) by 10 and 16%, respectively, in the M-CLA and t10,c12-CLA animals, respectively, whereas insulin responses were diminished by 21 and 19% in these same groups. There were no significant alterations in these responses in the c9,t11-CLA group. Insulin-mediated glucose transport activity was enhanced by M-CLA treatment in both type I soleus (32%) and type IIb epitrochlearis (58%) muscles and by 36 and 48%, respectively, with t10,c12-CLA. In the soleus, these increases were associated with decreases in protein carbonyls (index of oxidative stress, r = -0.616, P = 0.0038) and intramuscular triglycerides ( r = -0.631, P = 0.0028). Treatment with c9,t11-CLA was without effect on these variables. These results suggest that the ability of CLA treatment to improve glucose tolerance and insulin-stimulated glucose transport activity in insulin-resistant skeletal muscle of the obese Zucker rat are associated with a reduction in oxidative stress and muscle lipid levels and can be specifically ascribed to the actions of the t10,c12 isomer. In the obese Zucker rat, the c9,t11 isomer of CLA is metabolically neutral.

Voluntary exercise opposes insulin resistance of skeletal muscle glucose transport during liquid fructose ingestion in rats

2018 ◽  
Vol 74 (3) ◽  
pp. 455-466 ◽  
Author(s):  
Yupaporn Rattanavichit ◽  
Jariya Buniam ◽  
Juthamard Surapongchai ◽  
Vitoon Saengsirisuwan
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Transport ◽  
Voluntary Exercise ◽  
Muscle Glucose Transport

Effect of in vivo injection of cholera and pertussis toxin on glucose transport in rat skeletal muscle

1997 ◽  
Vol 272 (1) ◽  
pp. E7-E17 ◽  
Author(s):  
T. Ploug ◽  
X. Han ◽  
L. N. Petersen ◽  
H. Galbo
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Pertussis Toxin ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Glut 1 ◽  
Glut 4 ◽  
Gastrocnemius Muscles ◽  
Muscle Glucose Transport

Cholera toxin (CTX) and pertussis toxin (PTX) were examined for their ability to inhibit glucose transport in perfused skeletal muscle. Twenty-five hours after an intravenous injection of CTX, basal transport was decreased approximately 30%, and insulin- and contraction-stimulated transport was reduced at least 86 and 49%, respectively, in both the soleus and red and white gastrocnemius muscles. In contrast, PTX treatment was much less efficient. Impairment of glucose transport appeared to develop 10-15 h after CTX administration, which coincided with development of hyperglycemia despite hyperinsulinimia, increased plasma free fatty acid levels, increased adenosine 3',5'-cyclic monophosphate (cAMP) concentrations in muscle, but no difference in plasma catecholamines. Twenty-five hours after CTX treatment, GLUT-4 protein in both soleus and red gastrocnemius muscles was decreased, whereas no change in GLUT-1 protein content was found. In contrast, GLUT-4 mRNA was unchanged, but transcripts for GLUT-1 were increased > or = 150% in all three muscles from CTX-treated rats. The findings suggest that CTX via increased cAMP impairs basal as well as insulin- and contraction-stimulated muscle glucose transport, at least in part from a decrease in intramuscular GLUT-4 protein.

Glucose transport with brief dietary restriction: heterogenous responses in muscles

1994 ◽  
Vol 266 (6) ◽  
pp. E946-E952 ◽  
Author(s):  
G. D. Cartee ◽  
D. J. Dean
Keyword(s):  
Glucose Transport ◽  
Dietary Restriction ◽  
Time Course ◽  
Abdominal Fat ◽  
Transport Activity ◽  
Fischer 344 ◽  
Flexor Digitorum Brevis ◽  
Ad Libitum ◽  
Ad Libitum Intake ◽  
Flexor Digitorum

The time course (1, 5, or 20 days) for the effect of dietary restriction (DR; approximately 25% reduction below ad libitum intake) on epitrochlearis and flexor digitorum brevis (FDB) muscle glucose transport activity was studied in female Fischer 344 rats (8 mo old). Epitrochlearis glucose transport activity with 100 microU/ml insulin was increased by 38% after 5 days of DR (P < 0.05) despite no change in glucose transport activity with 0 or 20,000 microU/ml insulin. The increase with 100 microU/ml insulin was not further enhanced by 20 days of DR. DR did not result in a significant increase in the glucose transport activity of the FDB with 0, 100, or 20,000 microU/ml insulin. Abdominal fat content was significantly (P < 0.01) reduced below ad libitum levels only after 20 days of DR. These results demonstrate that DR-induced improvement in epitrochlearis glucose transport activity with a physiological insulin concentration can occur very rapidly, preceding detectable changes in basal or maximal insulin-stimulated glucose transport activity or abdominal fat pad mass, and the enhancement of insulin action does not occur simultaneously in all muscles.

scholarly journals Glucose-dependent insulinotropic polypeptide directly induces glucose transport in rat skeletal muscle

2015 ◽  
Vol 309 (3) ◽  
pp. R295-R303 ◽  
Author(s):  
Laelie A. Snook ◽  
Emery M. Nelson ◽  
David J. Dyck ◽  
David C. Wright ◽  
Graham P. Holloway
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Soleus Muscle ◽  
Serum Insulin ◽  
Current Data ◽  
Signaling Mechanism ◽  
Akt Phosphorylation ◽  
Glucose Challenge ◽  
Muscle Glucose Transport

Several gastrointestinal proteins have been identified to have insulinotropic effects, including glucose-dependent insulinotropic polypeptide (GIP); however, the direct effects of incretins on skeletal muscle glucose transport remain largely unknown. Therefore, the purpose of the current study was to examine the role of GIP on skeletal muscle glucose transport and insulin signaling in rats. Relative to a glucose challenge, a mixed glucose+lipid oral challenge increased circulating GIP concentrations, skeletal muscle Akt phosphorylation, and improved glucose clearance by ∼35% ( P < 0.05). These responses occurred without alterations in serum insulin concentrations. In an incubated soleus muscle preparation, GIP directly stimulated glucose transport and increased GLUT4 accumulation on the plasma membrane in the absence of insulin. Moreover, the ability of GIP to stimulate glucose transport was mitigated by the addition of the PI 3-kinase (PI3K) inhibitor wortmannin, suggesting that signaling through PI3K is required for these responses. We also provide evidence that the combined stimulatory effects of GIP and insulin on soleus muscle glucose transport are additive. However, the specific GIP receptor antagonist (Pro3)GIP did not attenuate GIP-stimulated glucose transport, suggesting that GIP is not signaling through its classical receptor. Together, the current data provide evidence that GIP regulates skeletal muscle glucose transport; however, the exact signaling mechanism(s) remain unknown.

Rapid impairment of skeletal muscle glucose transport/phosphorylation by free fatty acids in humans

Diabetes ◽  
1999 ◽  
Vol 48 (2) ◽  
pp. 358-364 ◽  
Author(s):  
M. Roden ◽  
M. Krssak ◽  
H. Stingl ◽  
S. Gruber ◽  
A. Hofer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Transport ◽  
Muscle Glucose Transport
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