Perilipin 5 deficiency in mice alters fatty acid metabolism and causes skeletal muscle insulin resistance

2013 ◽  
Vol 7 ◽  
pp. e42-e43
Author(s):  
Rachael Mason ◽  
Ruzaidi Mokhtar ◽  
Maria Matzaris ◽  
Aharthy Selathurai ◽  
Clinton Bruce ◽  
...  
2005 ◽  
Vol 1 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Eun Koh ◽  
Woo Lee ◽  
Min-Seon Kim ◽  
Joong-Yeol Park ◽  
In Lee ◽  
...  

2018 ◽  
Vol 293 (20) ◽  
pp. 7549-7563 ◽  
Author(s):  
Liping Huang ◽  
Surapun Tepaamorndech ◽  
Catherine P. Kirschke ◽  
John W. Newman ◽  
William R. Keyes ◽  
...  

2008 ◽  
Vol 7 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Timothy R. Koves ◽  
John R. Ussher ◽  
Robert C. Noland ◽  
Dorothy Slentz ◽  
Merrie Mosedale ◽  
...  

Diabetologia ◽  
2018 ◽  
Vol 61 (3) ◽  
pp. 688-699 ◽  
Author(s):  
Christophe O. Soulage ◽  
Laura Sardón Puig ◽  
Laurent Soulère ◽  
Bader Zarrouki ◽  
Michel Guichardant ◽  
...  

2008 ◽  
Vol 88 (11) ◽  
pp. 1279-1296 ◽  
Author(s):  
Lorraine P Turcotte ◽  
Jonathan S Fisher

The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. There also is some indication that resistance exercise may be effective in preventing insulin resistance. The information provided is intended to help clinicians understand and explain the roles of exercise in reducing insulin resistance.


1999 ◽  
Vol 277 (6) ◽  
pp. E1130-E1141 ◽  
Author(s):  
David E. Kelley ◽  
Bret Goodpaster ◽  
Rena R. Wing ◽  
Jean-Aime Simoneau

The current study was undertaken to investigate fatty acid metabolism by skeletal muscle to examine potential mechanisms that could lead to increased muscle triglyceride in obesity. Sixteen lean and 40 obese research volunteers had leg balance measurement of glucose and free fatty acid (FFA) uptake (fractional extraction of [9,103H]oleate) and indirect calorimetry across the leg to determine substrate oxidation during fasting and insulin-stimulated conditions. Muscle obtained by percutaneous biopsy had lower carnitine palmitoyl transferase (CPT) activity and oxidative enzyme activity in obesity ( P < 0.05). During fasting conditions, obese subjects had an elevated leg respiratory quotient (RQ, 0.83 ± 0.02 vs. 0.90 ± 0.01; P < 0.01) and reduced fat oxidation but similar FFA uptake across the leg. During insulin infusions, fat oxidation by leg tissues was suppressed in lean but not obese subjects; rates of FFA uptake were similar. Fasting values for leg RQ correlated with insulin sensitivity ( r = −0.57, P < 0.001). Thirty-two of the obese subjects were restudied after weight loss (WL, −14.0 ± 0.9 kg); insulin sensitivity and insulin suppression of fat oxidation improved ( P < 0.01), but fasting leg RQ (0.90 ± 0.02 vs. 0.90 ± 0.02, pre-WL vs. post-WL) and muscle CPT activity did not change. The findings suggest that triglyceride accumulation in skeletal muscle in obesity derives from reduced capacity for fat oxidation and that inflexibility in regulating fat oxidation, more than fatty acid uptake, is related to insulin resistance.


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