A 3-Day High-Fat Diet Increases Skeletal Muscle Lipid Oxidation in Lean But Not Obese Individuals

2010 ◽  
Vol 42 ◽  
pp. 83
Author(s):  
Gina Battaglia ◽  
Donghai Zheng ◽  
Timothy P. Gavin ◽  
Joseph A. Houmard
Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1748-P ◽  
Author(s):  
FENGYUAN HUANG ◽  
KEVIN YANG ◽  
KAMALAMMA SAJA ◽  
YICHENG HUANG ◽  
QINGQIANG LONG ◽  
...  

Lipids ◽  
2015 ◽  
Vol 50 (2) ◽  
pp. 205-217 ◽  
Author(s):  
Rebecca E. K. MacPherson ◽  
Laura M. Castelli ◽  
Paula M. Miotto ◽  
Scott Frendo-Cumbo ◽  
Amanda Milburn ◽  
...  

2017 ◽  
Vol 74 (2) ◽  
pp. 195-205 ◽  
Author(s):  
Weiche Wu ◽  
Ziye Xu ◽  
Ling Zhang ◽  
Jiaqi Liu ◽  
Jie Feng ◽  
...  

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Rebecca MacPherson ◽  
Laura Castelli ◽  
Paula Miotto ◽  
Scott Frendo‐Cumbo ◽  
Amanda Milburn ◽  
...  

2011 ◽  
Vol 96 (3) ◽  
pp. 775-781 ◽  
Author(s):  
K. E. Boyle ◽  
J. P. Canham ◽  
L. A. Consitt ◽  
D. Zheng ◽  
T. R. Koves ◽  
...  

Context: In lean individuals, increasing dietary lipid can elicit an increase in whole body lipid oxidation; however, with obesity the capacity to respond to changes in substrate availability appears to be compromised. Objective: To determine whether the responses of genes regulating lipid oxidation in skeletal muscle differed between lean and insulin resistant obese humans upon exposure to a high-fat diet (HFD). Design and Setting: A 5-d prospective study conducted in the research unit of an academic center. Participants: Healthy, lean (n = 12; body mass index = 22.1 ± 0.6 kg/m2), and obese (n=10; body mass index = 39.6 ± 1.7 kg/m2) males and females, between ages 18 and 30. Intervention: Participants were studied before and after a 5-d HFD (65% fat). Main Outcome Measures: Skeletal muscle biopsies (vastus lateralis) were obtained in the fasted and fed states before and after the HFD and mRNA content for genes involved with lipid oxidation determined. Skeletal muscle acylcarnitine content was determined in the fed states before and after the HFD. Results: Peroxisome proliferator activated receptor (PPAR) α mRNA content increased in lean, but not obese, subjects after a single high-fat meal. From Pre- to Post-HFD, mRNA content exhibited a body size × HFD interaction, where the lean individuals increased while the obese individuals decreased mRNA content for pyruvate dehydrogenase kinase 4, uncoupling protein 3, PPARα, and PPARγ coactivator-1α (P ≤ 0.05). In the obese subjects medium-chain acylcarnitine species tended to accumulate, whereas no change or a reduction was evident in the lean individuals. Conclusions: These findings indicate a differential response to a lipid stimulus in the skeletal muscle of lean and insulin resistant obese humans.


2010 ◽  
Vol 42 ◽  
pp. 566
Author(s):  
Gina Battaglia ◽  
Donghai Zheng ◽  
Kristen E. Boyle ◽  
Joseph A. Houmard

2017 ◽  
Vol 76 (3) ◽  
pp. 419-424 ◽  
Author(s):  
Ellen E. Blaak

The obese insulin resistant and/or prediabetic state is characterised by systemic lipid overflow, mainly driven by an impaired lipid buffering capacity of adipose tissue, and an impaired capacity of skeletal muscle to increase fat oxidation upon increased supply. This leads to the accumulation of bioactive lipid metabolites in skeletal muscle interfering with insulin sensitivity via various mechanisms. In this review, the contribution of dietary v. endogenous fatty acids to lipid overflow, their extraction or uptake by skeletal muscle as well as the fractional synthetic rate, content and composition of the muscle lipid pools is discussed in relation to the development or presence of insulin resistance and/or an impaired glucose metabolism. These parameters are studied in vivo in man by combining a dual stable isotope methodology with [2H2]- and [U-13C]-palmitate tracers with the arterio-venous balance technique across forearm muscle and biochemical analyses in muscle biopsies. The insulin-resistant state is characterised by an elevated muscle TAG extraction, despite similar supply, and a reduced skeletal muscle lipid turnover, in particular after intake of a high fat, SFA fat meal, but not after a high fat, PUFA meal. Data are placed in the context of current literature, and underlying mechanisms and implications for long-term nutritional interventions are discussed.


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