scholarly journals Comparative timecourse analysis of the skeletal muscle transcriptome from non-diabetic and diabetic rat models administered normal and high fat diets

2016 ◽  
Author(s):  
R Almon
Keyword(s):  
Skeletal Muscle ◽  
Diabetic Rat ◽  
High Fat ◽  
Rat Models ◽  
High Fat Diets ◽  
Fat Diets ◽  
Skeletal Muscle Transcriptome

Development of leptin resistance in rat soleus muscle in response to high-fat diets

2000 ◽  
Vol 279 (6) ◽  
pp. E1374-E1382 ◽  
Author(s):  
Greg R. Steinberg ◽  
David J. Dyck
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Soleus Muscle ◽  
Leptin Resistance ◽  
Safflower Oil ◽  
High Fat ◽  
Muscle Lipid ◽  
High Fat Diets ◽  
Rat Soleus Muscle ◽  
Fat Diets

Direct evidence for leptin resistance in peripheral tissues such as skeletal muscle does not exist. Therefore, we investigated the effects of different high-fat diets on lipid metabolism in isolated rat soleus muscle and specifically explored whether leptin's stimulatory effects on muscle lipid metabolism would be reduced after exposure to high-fat diets. Control (Cont, 12% kcal fat) and high-fat [60% kcal safflower oil (n-6) (HF-Saff); 48% kcal safflower oil plus 12% fish oil (n-3)] diets were fed to rats for 4 wk. After the dietary treatments, muscle lipid turnover and oxidation in the presence and absence of leptin was measured using pulse-chase procedures in incubated resting soleus muscle. In the absence of leptin, phospholipid, diacylglycerol, and triacylglycerol (TG) turnover were unaffected by the high-fat diets, but exogenous palmitate oxidation was significantly increased in the HF-Saff group. In Cont rats, leptin increased exogenous palmitate oxidation (21.4 ± 5.7 vs. 11.9 ± 1.61 nmol/g, P = 0.019) and TG breakdown (39.8 ± 5.6 vs. 27.0 ± 5.2 nmol/g, P = 0.043) and decreased TG esterification (132.5 ± 14.6 vs. 177.7 ± 29.6 nmol/g, P = 0.043). However, in both high-fat groups, the stimulatory effect of leptin on muscle lipid oxidation and hydrolysis was eliminated. Partial substitution of fish oil resulted only in the restoration of leptin's inhibition of TG esterification. Thus we hypothesize that, during the development of obesity, skeletal muscle becomes resistant to the effects of leptin, resulting in the accumulation of intramuscular TG. This may be an important initiating step in the development of insulin resistance common in obesity.

Elevated n-3 fatty acids in a high-fat diet attenuate the increase in PDH kinase activity but not PDH activity in human skeletal muscle

2005 ◽  
Vol 98 (1) ◽  
pp. 350-355 ◽  
Author(s):  
Erin A. Turvey ◽  
George J. F. Heigenhauser ◽  
Michelle Parolin ◽  
Sandra J. Peters
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Pyruvate Dehydrogenase ◽  
High Fat Diet ◽  
Human Skeletal Muscle ◽  
Fat Content ◽  
Pyruvate Dehydrogenase Kinase ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

We tested the hypothesis that a high-fat diet (75% fat; 5% carbohydrates; 20% protein), for which 15% of the fat content was substituted with n-3 fatty acids, would not exhibit the diet-induced increase in pyruvate dehydrogenase kinase (PDK) activity, which is normally observed in human skeletal muscle. The fat content was the same in both the regular high-fat diet (HF) and in the n-3-substituted diet (N3). PDK activity increased after both high-fat diets, but the increase was attenuated after the N3 diet (0.051 ± 0.007 and 0.218 ± 0.047 min−1 for pre- and post-HF, respectively; vs. 0.073 ± 0.016 and 0.133 ± 0.032 min−1 for pre- and post-N3, respectively). However, the active form of pyruvate dehydrogenase (PDHa) activity decreased to a similar extent in both conditions (0.93 ± 0.17 and 0.43 ± 0.09 mmol/kg wet wt pre- and post-HF; vs. 0.87 ± 0.19 and 0.39 ± 0.05 mmol/kg wet wt pre- and post-N3, respectively). This suggested that the difference in PDK activity did not affect PDHa activation in the basal state, and it was regulated by intramitochondrial effectors, primarily muscle pyruvate concentration. Muscle glycogen content was consistent throughout the study, before and after both diet conditions, whereas muscle glucose-6-phosphate, glycerol-3-phosphate, lactate, and pyruvate were decreased after the high-fat diets. Plasma triglycerides decreased after both high-fat diets but decreased to a greater extent after the N3, whereas plasma free fatty acids increased after both diets, but to a lesser extent after the N3. In summary, PDK activity is decreased after a high-fat diet that is rich in n-3 fatty acids, although PDHa activity was unaltered. In addition, our data demonstrated that the hypolipidemic effect of n-3 fatty acids occurs earlier (3 days) than previously reported and is evident even when the diet has 75% of its total energy derived from fat.

Endurance training partially reverses dietary-induced leptin resistance in rodent skeletal muscle

2004 ◽  
Vol 286 (1) ◽  
pp. E57-E63 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Angela C. Smith ◽  
Sam Wormald ◽  
Patrick Malenfant ◽  
Cheryl Collier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Training ◽  
Exercise Intervention ◽  
Leptin Resistance ◽  
Cytokine Signaling ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets ◽  
Socs3 Mrna

Leptin acutely stimulates skeletal muscle fatty acid (FA) metabolism in lean rodents and humans. This stimulatory effect is eliminated following the feeding of high-fat diets in rodents as well as in obese humans. The mechanism(s) responsible for the development of skeletal muscle leptin resistance is unknown; however, a role for increased suppressor of cytokine signaling-3 (SOCS3) inhibition of the leptin receptor has been demonstrated in other rodent tissues. Furthermore, whether exercise intervention is an effective strategy to prevent or attenuate the development of skeletal muscle leptin resistance has not been investigated. Toward this end, 48 Sprague-Dawley rats (175-190 g; ∼2-3 mo of age) were fed control or high-fat (60% kcal) diets for 4 wk and either remained sedentary or were treadmill trained. In control diet-fed animals that remained sedentary (CS) or were endurance trained (CT), leptin stimulated FA oxidation (CS +32 ± 15%, CT +30 ± 17%; P < 0.05), suppressed triacylglycerol (TAG) esterification (CS -17 ± 7%, CT -24 ± 8%; P < 0.05), and reduced the esterification-to-oxidation ratio (CS -19 ± 13%, CT -29 ± 10%; P < 0.001) in soleus muscle. High-fat feeding induced leptin resistance in the soleus of sedentary rats (FS), whereas endurance exercise training (FT) restored the ability of leptin to suppress TAG esterification (-19 ± 9%, P = 0.038). Training did not completely restore the ability of leptin to stimulate FA oxidation. High-fat diets stimulated SOCS3 mRNA expression irrespective of training status (FS +451 ± 120%, P = 0.024; FT +381 ± 141%, P = 0.023). Thus the development of skeletal muscle leptin resistance appears to involve an increase in SOCS3 mRNA expression. Endurance training was generally effective in preventing the development of leptin resistance, although this did not appear to require a decrease in SOCS3 expression. Future studies should examine changes in the actual protein content of SOCS3 in muscle and establish whether aerobic exercise is also effective in treating leptin resistance in humans.

scholarly journals Effects of Low-Carbohydrate, High-Fat Diets on Body and Skeletal Muscle Weights in Mice

2020 ◽  
Vol 67 (4) ◽  
pp. 128-133
Author(s):  
Kanako Oshita ◽  
Yurie Hara ◽  
Nakamichi Watanabe
Keyword(s):  
Skeletal Muscle ◽  
High Fat ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals The role of CD36-Fabp4-PPARγ in skeletal muscle involves insulin resistance in intrauterine growth retardation mice with catch-up growth

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Jing Liu ◽  
Hang Zhao ◽  
Linlin Yang ◽  
Xing Wang ◽  
Linquan Yang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Dna Methylation ◽  
Birth Weight ◽  
High Fat Diet ◽  
Dietary Intervention ◽  
Normal Diet ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

Abstract Background Studies have shown that the high incidence of type 2 diabetes in China is associated with low birth weight and excessive nutrition in adulthood, which occurred during the famine years of the 1950s and 1960s, though the specific molecular mechanisms are unclear. In this study, we proposed a severe maternal caloric restriction during late pregnancy, followed by a post weaning high-fat diet in mice. After weaning, normal and high-fat diets were provided to mice to simulate the dietary pattern of modern society. Methods The pregnant mice were divided into two groups: normal birth weight (NBW) group and low birth weight (LBW) group. After 3 weeks for weaning, the male offspring mice in the NBW and LBW groups were then randomly divided into four subgroups: NC, NH, LC and LC groups. The offspring mice in the NC, NH, LC and LC groups were respectively fed with normal diet, normal diet, high-fat diet and high-fat diet for 18 weeks. After 18 weeks of dietary intervention, detailed analyses of mRNA and protein expression patterns, signaling pathway activities, and promoter methylation states were conducted for all relevant genes. Results After dietary intervention for 18 weeks, the expressions of CD36, Fabp4, PPARγ, FAS, and ACC1 in the skeletal muscle tissue of the LH group were significantly increased compared with the LC and NH groups (P < 0.05). The level of p-AMPK/AMPK in the skeletal muscle tissue of the LH group was significantly decreased compared with the LC and NH groups (P < 0.05). CPT1 and PGC-1α protein expressions were up-regulated in the LH group (P < 0.05) compared to the LC group. Additionally, the DNA methylation levels of the PGC-1α and GLUT4 gene promoters in the skeletal muscle of the LH groups were higher than those of the LC and NH groups (P < 0.05). However, PPARγ DNA methylation level in the LH group was lower than those of the LC and NH groups (P < 0.05). Conclusions LBW combined with high-fat diets may increase insulin resistance and diabetes through regulating the CD36-related Fabp4-PPARγ and AMPK/ACC signaling pathways.

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