scholarly journals Intramuscular lipid metabolism, insulin action, and obesity

IUBMB Life ◽  
2009 ◽  
Vol 61 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Leslie A. Consitt ◽  
Jill A. Bell ◽  
Joseph A. Houmard
Keyword(s):  
Lipid Metabolism ◽  
Insulin Action ◽  
Intramuscular Lipid

scholarly journals Altered Intramuscular Lipid Metabolism Relates to Diminished Insulin Action in Men, but Not Women, in Progression to Diabetes

Obesity ◽  
2010 ◽  
Vol 18 (11) ◽  
pp. 2093-2100 ◽  
Author(s):  
Leigh Perreault ◽  
Bryan C. Bergman ◽  
Devon M. Hunerdosse ◽  
Robert H. Eckel
Keyword(s):  
Lipid Metabolism ◽  
Insulin Action ◽  
Intramuscular Lipid

scholarly journals Intramuscular Lipid Metabolism in the Insulin Resistance of Smoking

Diabetes ◽  
2009 ◽  
Vol 58 (10) ◽  
pp. 2220-2227 ◽  
Author(s):  
B. C. Bergman ◽  
L. Perreault ◽  
D. M. Hunerdosse ◽  
M. C. Koehler ◽  
A. M. Samek ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Intramuscular Lipid

Insulin Action on Lipid Metabolism

2005 ◽  
pp. 87-103
Author(s):  
Keith N. Frayn ◽  
Fredrik Karpe
Keyword(s):  
Lipid Metabolism ◽  
Insulin Action

Long-chain acyl-CoA esters as indicators of lipid metabolism and insulin sensitivity in rat and human muscle

2000 ◽  
Vol 279 (3) ◽  
pp. E554-E560 ◽  
Author(s):  
Bronwyn A. Ellis ◽  
Ann Poynten ◽  
Andrew J. Lowy ◽  
Stuart M. Furler ◽  
Donald J. Chisholm ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Insulin Action ◽  
Human Muscle ◽  
Whole Body ◽  
Cellular Processes ◽  
Lipid Species ◽  
Chain Acyl ◽  
Triglyceride Content ◽  
Long Chain

Long-chain acyl-CoAs (LCACoA) are an activated lipid species that are key metabolites in lipid metabolism; they also have a role in the regulation of other cellular processes. However, few studies have linked LCACoA content in rat and human muscle to changes in nutritional status and insulin action. Fasting rats for 18 h significantly elevated the three major LCACoA species in muscle ( P < 0.001), whereas high-fat feeding of rats with a safflower oil (18:2) diet produced insulin resistance and increased total LCACoA content ( P < 0.0001) by specifically increasing 18:2-CoA. The LCACoA content of red muscle from rats (4–8 nmol/g) was 4- to 10-fold higher than adipose tissue (0.4–0.9 nmol/g, P < 0.001), suggesting that any contamination of muscle samples with adipocytes would contribute little to the LCACoA content of muscle. In humans, the LCACoA content of muscle correlated significantly with a measure of whole body insulin action in 17 male subjects ( r 2 = 0.34, P = 0.01), supporting a link between muscle lipid metabolism and insulin action. These results demonstrate that the LCACoA pool reflects lipid metabolism and nutritional state in muscle. We conclude that the LCACoA content of muscle provides a direct index of intracellular lipid metabolism and its links to insulin action, which, unlike triglyceride content, is not subject to contamination by closely associated adipose tissue.

Leptin, skeletal muscle lipids, and lipid-induced insulin resistance

2007 ◽  
Vol 293 (2) ◽  
pp. R642-R650 ◽  
Author(s):  
John J. Dube ◽  
Bankim A. Bhatt ◽  
Nikolas Dedousis ◽  
Arend Bonen ◽  
Robert M. O'Doherty
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Glycogen Synthase ◽  
Acid Oxidation ◽  
Fatty Acid Binding ◽  
Lipid Metabolites

Leptin-induced increases in insulin sensitivity are well established and may be related to the effects of leptin on lipid metabolism. However, the effects of leptin on the levels of lipid metabolites implicated in pathogenesis of insulin resistance and the effects of leptin on lipid-induced insulin resistance are unknown. The current study addressed in rats the effects of hyperleptinemia (HL) on insulin action and markers of skeletal muscle (SkM) lipid metabolism in the absence or presence of acute hyperlipidemia induced by an infusion of a lipid emulsion. Compared with controls (CONT), HL increased insulin sensitivity, as assessed by hyperinsulinemic-euglycemic clamp (∼15%), and increased SkM Akt (∼30%) and glycogen synthase kinase 3α (∼52%) phosphorylation. These improvements in insulin action were associated with decreased SkM triglycerides (TG; ∼61%), elevated ceramides (∼50%), and similar diacylglycerol (DAG) levels in HL compared with CONT. Acute hyperlipidemia in CONT decreased insulin sensitivity (∼25%) and increased SkM DAG (∼33%) and ceramide (∼60%) levels. However, hyperlipidemia did not induce insulin resistance or SkM DAG and ceramide accumulation in HL. SkM total fatty acid transporter CD36, plasma membrane fatty acid binding protein, acetyl Co-A carboxylase phosphorylation, and fatty acid oxidation were similar in HL compared with CONT. However, HL decreased SkM protein kinase Cθ (PKCθ), a kinase implicated in mediating the detrimental effects of lipids on insulin action. We conclude that increases in insulin sensitivity induced by HL are associated with decreased levels of SkM TG and PKCθ and increased SkM insulin signaling, but not with decreases in other lipid metabolites implicated in altering SkM insulin sensitivity (DAG and ceramide). Furthermore, insulin resistance induced by an acute lipid infusion is prevented by HL.

scholarly journals Rat amylin-(8—37) enhances insulin action and alters lipid metabolism in normal and insulin-resistant rats

1997 ◽  
Vol 273 (5) ◽  
pp. E859-E867 ◽  
Author(s):  
M. Hettiarachchi ◽  
S. Chalkley ◽  
S. M. Furler ◽  
Y.-S. Choong ◽  
M. Heller ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Glycogen Synthesis ◽  
Human Growth ◽  
Whole Body ◽  
Nonesterified Fatty Acids ◽  
Insulin Resistant

To clarify roles of amylin, we investigated metabolic responses to rat amylin-(8—37), a specific amylin antagonist, in normal and insulin-resistant, human growth hormone (hGH)-infused rats. Fasting conscious rats were infused with saline or hGH, each with and without amylin-(8—37) (0.125 μmol/h), over 5.75 h. At 3.75 h, a hyperinsulinemic (100 mU/l) clamp with bolus 2-deoxy-d-[3H]glucose and [14C]glucose was started. hGH infusion led to prompt (2- to 3-fold) basal hyperamylinemia ( P < 0.02) and hyperinsulinemia. Amylin-(8—37) reduced plasma insulin ( P < 0.001) and enhanced several measures of whole body and muscle insulin sensitivity ( P < 0.05) in both saline- and hGH-infused rats. Amylin-(8—37) corrected hGH-induced liver insulin resistance, increased basal plasma triglycerides and lowered plasma nonesterified fatty acids in both groups, and reduced muscle triglyceride and total long-chain acyl-CoA content in saline-treated rats ( P < 0.05). In isolated soleus muscle, amylin-(8—37) blocked amylin-induced inhibition of glycogen synthesis but had no effect in the absence of amylin. Thus 1) hyperamylinemia accompanies insulin resistance induced by hGH infusion; 2) amylin-(8—37) increases whole body and muscle insulin sensitivity and consistently reduces basal insulin levels in normal and hGH-induced insulin-resistant rats; and 3) amylin-(8—37) elicits a significant alteration of in vivo lipid metabolism. These findings support a role of amylin in modulating insulin action and suggest that this could be mediated by effects on lipid metabolism.

The forkhead box O family in insulin action and lipid metabolism

2020 ◽  
pp. 247-272
Author(s):  
Sojin Lee ◽  
Cuiling Zhu ◽  
Jun Yamauchi ◽  
Ping Zhu ◽  
Xiaoyun Feng ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Insulin Action ◽  
Forkhead Box

Weight Loss and Exercise: Implications for Muscle Lipid Metabolism and Insulin Action

2004 ◽  
Vol 36 (7) ◽  
pp. 1191-1195 ◽  
Author(s):  
JASON R. BERGGREN ◽  
MATTHEW W. HULVER ◽  
G. LYNIS DOHM ◽  
JOSEPH A. HOUMARD
Keyword(s):  
Weight Loss ◽  
Lipid Metabolism ◽  
Insulin Action ◽  
Muscle Lipid

scholarly journals Increased intramuscular lipid synthesis and low saturation relate to insulin sensitivity in endurance-trained athletes

2010 ◽  
Vol 108 (5) ◽  
pp. 1134-1141 ◽  
Author(s):  
Bryan C. Bergman ◽  
Leigh Perreault ◽  
Devon M. Hunerdosse ◽  
Mary C. Koehler ◽  
Ali M. Samek ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Action ◽  
Lipid Synthesis ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Synthesis Rate ◽  
Dietary Control ◽  
Intravenous Glucose ◽  
Intramuscular Lipid

Intramuscular triglyceride (IMTG) has received considerable attention as a potential mechanism promoting insulin resistance. Endurance-trained athletes have high amounts of IMTG but are insulin sensitive, suggesting IMTG content alone does not change insulin action. Recent data suggest increased muscle lipid synthesis protects against fat-induced insulin resistance. We hypothesized that rates of IMTG synthesis at rest would be increased in athletes compared with controls. Eleven sedentary men and 11 endurance-trained male cyclists participated in this study. An intravenous glucose tolerance test was performed to assess insulin action. After 3 days of dietary control and an overnight fast, [13C16]palmitate was infused at 0.0174 μmol·kg−1·min−1 for 4 h, followed by a muscle biopsy to measure isotope incorporation into IMTG and diacylglycerol. Compared with controls, athletes were twice as insulin sensitive ( P = 0.004) and had a significantly greater resting IMTG concentration (athletes: 20.4 ± 1.6 μg IMTG/mg dry wt, controls: 14.5 ± 1.8 μg IMTG/mg dry wt, P = 0.04) and IMTG fractional synthesis rate (athletes: 1.56 ± 0.37%/h, controls: 0.61 ± 0.15%/h, P = 0.03). Stearoyl-CoA desaturase 1 mRNA expression ( P = 0.02) and protein content ( P = 0.03) were also significantly greater in athletes. Diacylglycerol, but not IMTG, saturation was significantly less in athletes compared with controls ( P = 0.002). These data indicate endurance-trained athletes have increased synthesis rates of skeletal muscle IMTG and decreased saturation of skeletal muscle diacylglycerol. Increased synthesis rates are not due to recovery from exercise and are likely adaptations to chronic endurance exercise training.

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