scholarly journals Insulin resistance in obese Zucker rat (fa/fa) skeletal muscle is associated with a failure of glucose transporter translocation.

1992 ◽  
Vol 90 (4) ◽  
pp. 1568-1575 ◽  
Author(s):  
P A King ◽  
E D Horton ◽  
M F Hirshman ◽  
E S Horton
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Transporter ◽  
Zucker Rat ◽  
Obese Zucker Rat

Muscle glucose transport, GLUT-4 content, and degree of exercise training in obese Zucker rats

1992 ◽  
Vol 263 (5) ◽  
pp. E1015-E1020 ◽  
Author(s):  
E. A. Banks ◽  
J. T. Brozinick ◽  
B. B. Yaspelkis ◽  
H. Y. Kang ◽  
J. L. Ivy
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Glucose Transporter ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Zucker Rats ◽  
Zucker Rat ◽  
Glut 4 ◽  
Obese Zucker Rat ◽  
Fast Twitch

The effects of high (HI)- and low (LI)-intensity exercise training were examined on insulin-stimulated 3-O-methyl-d-glucose (3-MG) transport and concentration of insulin-regulatable glucose transporter protein (GLUT-4) in the red (fast-twitch oxidative) and white (fast-twitch glycolytic) quadriceps of the obese Zucker rat. Sedentary obese (SED) and lean (LN) Zucker rats were used as controls. 3-MG transport was determined during hindlimb perfusion in the presence of 8 mM 3-MG, 2 mM mannitol, 0.3 mM pyruvate, and 0.5 mU/ml insulin. HI and LI rats displayed greater rates of red quadriceps 3-MG transport and GLUT-4 concentrations than SED rats. No significant differences in rates of 3-MG transport or GLUT-4 concentrations were observed in the red quadriceps of HI and LI rats. There were no differences found in the rates of 3-MG transport in the white quadriceps of HI, LI, and SED rats although the difference between the HI and SED rats approached significance (P < 0.07). The GLUT-4 concentration and citrate synthase activity of HI rats were significantly greater than SED rats. The 3-MG transport rates of LN rats were twofold greater than SED rats regardless of fiber type, but a difference in GLUT-4 content between the LN and SED rats was observed only in the white quadriceps. GLUT-4 content of the obese rats was significantly correlated with citrate synthase activity (r = 0.93) and 3-MG transport (r = 0.82). The results suggest that the improvement in muscle insulin resistance of the obese Zucker rat after exercise training is due in part to an increased GLUT-4 concentration, which is related with the degree to which the muscle is trained. glucose transporter; insulin; insulin resistance; diabetes, muscle fiber type Submitted on May 21, 1992 Accepted on July 31, 1992

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.

Skeletal muscle glucose transport in obese Zucker rats after exercise training

1989 ◽  
Vol 66 (6) ◽  
pp. 2635-2641 ◽  
Author(s):  
J. L. Ivy ◽  
J. T. Brozinick ◽  
C. E. Torgan ◽  
G. M. Kastello
Keyword(s):  
Insulin Resistance ◽  
Glucose Transport ◽  
Transport Process ◽  
Fiber Type ◽  
Zucker Rat ◽  
Muscle Insulin Resistance ◽  
Obese Zucker Rat ◽  
Obese Rats ◽  
Muscle Glucose Transport ◽  
Fast Twitch

Exercise training has been found to reduce the muscle insulin resistance of the obese Zucker rat (fa/fa). The purpose of the present study was to determine whether this reduction in muscle insulin resistance was associated with an improvement in the glucose transport process and if it was fiber-type specific. Rats were randomly assigned to a sedentary or training group. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 days/wk, for 6–8 wk. The rate of muscle glucose transport was assessed in the absence of insulin and in the presence of a physiological (0.15 mU/ml), a submaximal (1.50 mU/ml), and a maximal (15.0 mU/ml) insulin concentration by determining the rate of 3-O-methyl-D-glucose (3-OMG) accumulation during hindlimb perfusion. The average 3-OMG transport rate of the red gastrocnemii (fast-twitch oxidative-glycolytic fibers) was significantly higher in the trained compared with the sedentary obese rats in the absence of insulin and in the presence of the three insulin concentrations. Significant improvements in 3-OMG transport were also observed in the plantarii (mixed fibers) of trained obese rats in the presence of 0, 0.15, and 15.0 mU/ml insulin. Training appeared to have little effect on the insulin-stimulated 3-OMG transport of the soleus (slow-twitch oxidative fibers) or white gastrocnemius (fast-twitch glycolytic fibers). The results suggest that the improvement in the muscle insulin resistance of the obese Zucker rat after moderate endurance training was associated with an improvement in the glucose transport process but that it was fiber-type specific.

scholarly journals The Effect of Chrysin-Loaded Phytosomes on Insulin Resistance and Blood Sugar Control in Type 2 Diabetic db/db Mice

Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5503
Author(s):  
Seong-min Kim ◽  
Jee-Young Imm
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glucose Transporter ◽  
Fasting Blood Glucose ◽  
Normal Diet ◽  
Molar Ratio ◽  
Oral Glucose ◽  
Peroxisome Proliferator ◽  
Model Assessment

Although a variety of beneficial health effects of natural flavonoids, including chrysin, has been suggested, poor solubility and bioavailability limit their practical use. As a promising delivery system, chrysin-loaded phytosomes (CPs) were prepared using egg phospholipid (EPL) at a 1:3 molar ratio and its antidiabetic effects were assessed in db/db diabetic mice. Male C57BLKS/J-db/db mice were fed a normal diet (control), chrysin diet (100 mg chrysin/kg), CP diet (100 mg chrysin equivalent/kg), metformin diet (200 mg/kg) or EPL diet (vehicle, the same amount of EPL used for CP preparation) for 9 weeks. Administration of CP significantly decreased fasting blood glucose and insulin levels in db/db mice compared with the control. An oral glucose tolerance test and homeostatic model assessment for insulin resistance were significantly improved in the CP group (p < 0.05). CP treatment suppressed gluconeogenesis via downregulation of phosphoenolpyruvate carboxykinase while it promoted glucose uptake in the skeletal muscle and liver of db/db mice (p < 0.05). The CP-mediated improved glucose utilization in the muscle was confirmed by upregulation of glucose transporter type 4, hexokinase2 and peroxisome proliferator-activated receptor γ during treatment (p < 0.05). The CP-induced promotion of GLUT4 plasma translocation was confirmed in the skeletal muscle of db/db mice (p < 0.05). Based on the results, CP showed greater antidiabetic performance compared to the control by ameliorating insulin resistance in db/db mice and phytosome can be used as an effective antidiabetic agent.

Oxidative stress impairs insulin signal in skeletal muscle and causes insulin resistance in postinfarct heart failure

2011 ◽  
Vol 300 (5) ◽  
pp. H1637-H1644 ◽  
Author(s):  
Yukihiro Ohta ◽  
Shintaro Kinugawa ◽  
Shouji Matsushima ◽  
Taisuke Ono ◽  
Mochamad A. Sobirin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Serine Phosphorylation ◽  
Glucose Transporter 4

Insulin resistance has been shown to occur as a consequence of heart failure. However, its exact mechanisms in this setting remain unknown. We have previously reported that oxidative stress is enhanced in the skeletal muscle from mice with heart failure after myocardial infarction (MI) ( 30 ). This study is aimed to investigate whether insulin resistance in postinfarct heart failure is due to the impairment of insulin signaling in the skeletal muscle caused by oxidative stress. Mice were divided into four groups: sham operated (sham); sham treated with apocynin, an inhibitor of NAD(P)H oxidase activation (10 mmol/l in drinking water); MI; and MI treated with apocynin. After 4 wk, intraperitoneal insulin tolerance tests were performed, and skeletal muscle samples were obtained for insulin signaling measurements. MI mice showed left ventricular dilation and dysfunction by echocardiography and increased left ventricular end-diastolic pressure and lung weight. The decrease in glucose level after insulin load significantly attenuated in MI compared with sham. Insulin-stimulated serine phosphorylation of Akt and glucose transporter-4 translocation were decreased in MI mice by 61 and 23%, respectively. Apocynin ameliorated the increase in oxidative stress and NAD(P)H oxidase activities measured by the lucigenin assay in the skeletal muscle after MI. It also improved insulin resistance and inhibited the decrease of Akt phosphorylation and glucose transporter-4 translocation. Insulin resistance was induced by the direct impairment of insulin signaling in the skeletal muscle from postinfarct heart failure, which was associated with the enhanced oxidative stress via NAD(P)H oxidase.

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