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

A Systematic Review of Low-Carbohydrate High-Fat Diets: Does the Research Evidence Support Practice?

2018 ◽  
Vol 118 (10) ◽  
pp. A126
Author(s):  
L. Ross ◽  
J. Musial ◽  
R. Hay ◽  
A. Cawte ◽  
D. McDermid ◽  
...  
Keyword(s):  
Systematic Review ◽  
Research Evidence ◽  
High Fat ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Fat Diets

An Understanding of Low-Carbohydrate, High-Fat Diets and Cancer

2006 ◽  
Vol 2 (3) ◽  
pp. 136-140
Author(s):  
Vasundara Venkateswaran ◽  
Ahmed Q. Haddad ◽  
Laurence H. Klotz ◽  
Rob Nam ◽  
Neil E. Fleshner
Keyword(s):  
High Fat ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Fat Diets

scholarly journals Very low-carbohydrate high-fat diets are superior to low-fat diets in improving cardiovascular markers: meta-analysis of large, long-term randomised controlled trials

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Teuta Gjuladin-Hellon ◽  
Ian Davies ◽  
Jackie Fealey ◽  
Alexander Montasem ◽  
Katie Lane
Keyword(s):  
Total Cholesterol ◽  
Randomised Controlled Trials ◽  
Fasting Glucose ◽  
Meta Analysis ◽  
High Fat ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Randomised Controlled ◽  
Fat Diets

AbstractOur recent study (1) showed that the amount of dietary carbohydrates in obesity interventions has differential effects on cardiovascular risk markers (CVM) and effects magnitude depends on intervention duration. Very-low carbohydrate high-fat diets (VLCD) were superior in ameliorating lipid markers compared to high-carbohydrate low-fat diets (LFD).We updated our systematic review and meta-analysis to include long-term effects of VLCD (< 50 g /day) on weight, glucose, total cholesterol, insulin and blood pressure (BP) among overweight/obese adults in comparison to LFD.Medline, PubMed, Cochrane Central, and CINAHLPlus were searched to identify large (n > 100) randomised controlled trials (RCT) with duration ≥ 6 months. Risk of bias, a random effects model and subgroup analyses based on duration of follow-up were performed using Review Manager. Results were reported according to PRISMA.Four open label RCT (n = 723; 362 VLCD; 361 LFD) with some form of behavioral intervention and duration 6–24 months were identified. VLCD showed more favorable effects on diastolic BP at 6 months (-1.96; 95%CI, -2.99 to 00.93; P = 0.0002) and 24 months (-2.69; 95%CI, -4.87 to -0.51; P = 0.001), near significant level at 12 months (-1.79; 95%CI, -3.56 to 0.04; P = 0.05) and an overall total favourable effect (-1.98; 95%CI, -2.73 to -1.22). The decrease in systolic BP was greater among VLCD for the whole period and the overall total effect reached the level of significance (-1.76; 95%CI, -3.56 to 0.04; P = 0.05). VLCD showed beneficial effect on total cholesterol level at 6 and 12 months (-0.01 mmol/L; 95%CI, -0.01 to –0.00; P = 0.002 and -0.01 mmol/L; 95%CI, -0.01 to –0.00; P = 0.005, respectively). The mean changes in weight, and fasting glucose and insulin levels revealed non-significant differences between both diets at any measured time, although these parameters decreased within both groups compared to baseline.VLCD led to significant total weighted mean decrease of diastolic BP and near significant decrease of systolic BP independent of changes in body weight, fasting glucose or insulin levels. The present data on decreased levels of diastolic BP and total cholesterol, combined with our recently published results on increased HDL-cholesterol, decreased triglycerides and no significant effect on LDL-cholesterol (1) provide evidence that VLCD are superior to LFD in improving traditional CVM in longer term.

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.

Adipose tissue metabolism of obese mice on standard and high-fat diets

1961 ◽  
Vol 201 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Serene Lochaya ◽  
Nicole Leboeuf ◽  
Jean Mayer ◽  
Bernard Leboeuf
Keyword(s):  
Adipose Tissue ◽  
Obese Mice ◽  
High Fat ◽  
Carbon Incorporation ◽  
Adipose Tissue Metabolism ◽  
Glucose Carbon ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Fat Diets ◽  
Fat Feeding

Adipose tissue metabolism in vitro was studied, after substitution for several weeks of synthetic low-carbohydrate, high-fat (saturated or unsaturated) diets for the standard chow diet, in obese hyperglycemic mice and in their nonobese littermates. In tissue from nonobese mice fed the high-fat diets, glucose metabolism to CO2 and to fatty acids was diminished in the absence of added hormone, while glucose carbon incorporation to glyceride-glycerol was increased. Under insulin (0.1 unit/ml) stimulation, total glucose uptake was relatively decreased by the diets, as was glucose metabolism to CO2, to fatty acids, and to glycogen; however, glucose carbon incorporation to glyceride-glycerol was unaltered. Under epinephrine stimulation, the sum of glucose carbon recovery was less after high-fat feeding. No effect of high-fat feeding was detected on base-line rates of free fatty acid release nor on the effects of insulin or epinephrine on this process. No differences were found between the effects of saturated- or unsaturated-fat diets on any parameters. The metabolism of adipose tissue from obese mice was slightly, if at all, affected by high-fat feeding. These results are discussed in reference to the normal adaptation to low-carbohydrate, high-fat diets and to the metabolic abnormalities present in obese hyperglycemic mice.

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.

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