Rosmarinic acid improves hypertension and skeletal muscle glucose transport in angiotensin II-treated rats

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.

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Direct inhibition by angiotensin II of insulin‐dependent glucose transport activity in mammalian skeletal muscle involves a ROS‐dependent mechanism

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.783.10 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Maggie Keck Diamond‐Stanic ◽

Erik J. Henriksen

Keyword(s):

Skeletal Muscle ◽

Angiotensin Ii ◽

Glucose Transport ◽

Mammalian Skeletal Muscle ◽

Transport Activity ◽

Direct Inhibition ◽

Insulin Dependent ◽

Dependent Mechanism

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

Journal of Physiology and Biochemistry ◽

10.1007/s13105-018-0639-8 ◽

2018 ◽

Vol 74 (3) ◽

pp. 455-466 ◽

Cited By ~ 1

Author(s):

Yupaporn Rattanavichit ◽

Jariya Buniam ◽

Juthamard Surapongchai ◽

Vitoon Saengsirisuwan

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Glucose Transport ◽

Voluntary Exercise ◽

Muscle Glucose Transport

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1997.272.1.e7 ◽

1997 ◽

Vol 272 (1) ◽

pp. E7-E17 ◽

Cited By ~ 1

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.

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00003.2015 ◽

2015 ◽

Vol 309 (3) ◽

pp. R295-R303 ◽

Cited By ~ 5

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.

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