Plasma Free Fatty Acids Decrease Insulin-Stimulated Skeletal Muscle Glucose Uptake by Suppressing Glycolysis in Conscious Rats

Diabetes ◽  
1996 ◽  
Vol 45 (4) ◽  
pp. 446-453 ◽  
Author(s):  
J. K. Kim ◽  
J. K. Wi ◽  
J. H. Youn
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Plasma Free Fatty Acids ◽  
Conscious Rats ◽  
Skeletal Muscle Glucose Uptake

Net substrates balance across hindlimb in conscious rabbit during late pregnancy

1986 ◽  
Vol 251 (1) ◽  
pp. E42-E47 ◽  
Author(s):  
M. Bouisset ◽  
M. C. Pere ◽  
M. Gilbert
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Ketone Bodies ◽  
Late Pregnancy ◽  
Gravid Uterus ◽  
Minor Importance ◽  
Insulin Effect ◽  
Increase Glucose Uptake

The present work performed in rabbits was designed to investigate whether changes in skeletal muscle metabolism could contribute to glucose homeostasis during late pregnancy a time at which there is a large glucose demand of the gravid uterus. We therefore studied the net substrate balance of glucose, lactate, free fatty acids, and ketone bodies across the hindlimb of pregnant animals (days 24 and 30) and virgin animals. Our data show that on day 24 the basal rate of glucose uptake is similar to that observed in virgin rabbits, but it decreases by approximately 60% on day 30 despite comparable levels of blood glucose and plasma insulin at both gestational ages. A moderate hyperglycemia (20% above basal level) and hyperinsulinemia (2- to 3-fold above basal level) sustained for 80 min failed to increase glucose uptake except in virgin animals. Estimates of the contribution of substrates to oxidative metabolism indicate that free fatty acids could represent the major fuel in all groups, whereas glucose would be of minor importance especially at term. It is concluded that in pregnancy a) under normoglycemia there is a reduced insulin effect on glucose uptake and b) under moderate hyperglycemia and hyperinsulinemia the insulin resistance results from an impaired stimulation of glucose uptake. Sparing glucose from the skeletal muscle, the mother can direct more glucose toward the uterus without marked increase in her production rate.

scholarly journals Mutation yellow in agouti loci prevents age-related increase of skeletal muscle genes regulating free fatty acids oxidation

2018 ◽  
Vol 22 (2) ◽  
pp. 265-272 ◽  
Author(s):  
Y. V. Piskunova ◽  
A. Y. Kazantceva ◽  
A. V. Baklanov ◽  
N. M. Bazhan
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
White Adipose Tissue ◽  
Uncoupling Protein ◽  
Age Related ◽  
Brown Adipose ◽  
Ay Mice

The lethal yellow mutation in agouti loci (Ay mutation) reduces the activity of melanocortin (MC) receptors and causes hyperphagia, obesity and type two diabetes mellitus in aging mice (Ay mice). It is unknown if changes in distinct elements of the metabolic system such as white adipose tissue (WAT) and brown adipose tissue (BAT), and skeletal muscle will manifest before the development of obesity. The aim of this work was to measure the relative gene expression of key proteins that regulate carbohydrate-lipid metabolism in WAT, BAT and skeletal muscle in Ay mice before the development of obesity. C57Bl/6J mice bearing a dominant autosomal mutation Ay (Ay /a mice) and mice of the standard genotype (a/a mice, control) have been studied in three age groups: 10, 15 and 30 weeks. The relative mRNA level of genes was measured by real-time PCR in skeletal muscles (uncoupling protein 3 (Ucp3) and carnitine palmitoyl transferase 1b (Cpt1b) (free fatty acids oxidation), solute carrier family 2 (facilitated glucose transporter), member 4 (Slc2a4) (glucose uptake)), in WAT lipoprotein lipase (Lpl) (triglyceride deposition), hormone-sensitive lipase (Lipe) (lipid mobilization), and Slc2a4 (glucose uptake)), and in BAT: uncoupling protein 1 (Ucp1) (energy expenditure). The expression of Cpt1b was reduced in young Ay mice (10 weeks), there was no transient peak of transcription of Cpt1b, Ucp3 in skeletal muscle tissue and Lipe, Slc2a4 in WAT in early adult Ay mice (15 weeks), which was noted in а/а mice. Reduction of the transcriptional activity of the studied genes in skeletal muscle and white adipose tissue can initiate the development of melanocortin obesity in Ay mice.

Acute elevation of free fatty acids impairs hepatic glucose uptake in conscious rats

2004 ◽  
Vol 66 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Itsuro Nakahara ◽  
Munehide Matsuhisa ◽  
Yuichi Shiba ◽  
Akio Kuroda ◽  
Yoshihisa Nakatani ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Conscious Rats ◽  
Hepatic Glucose ◽  
Acute Elevation ◽  
Hepatic Glucose Uptake

Peripheral Glucose Uptake and Skeletal Muscle GLUT4 Content in Man: Effect of Insulin and Free Fatty Acids

1992 ◽  
Vol 9 (7) ◽  
pp. 605-610 ◽  
Author(s):  
Aa. Handberg ◽  
A. Vaag ◽  
H. Beck-Nielsen ◽  
J. Vinten
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake

PPAR-α activation required for decreased glucose uptake and increased susceptibility to injury during ischemia

2005 ◽  
Vol 288 (6) ◽  
pp. H2677-H2683 ◽  
Author(s):  
Marcello Panagia ◽  
Geoffrey F. Gibbons ◽  
George K. Radda ◽  
Kieran Clarke
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Null Mouse ◽  
Elevated Plasma ◽  
Wild Type ◽  
Plasma Free Fatty Acids ◽  
Protein Levels ◽  
Glut 4 ◽  
Metabolic States

The transcription of key metabolic regulatory enzymes in the heart is altered in the diabetic state, yet little is known of the underlying mechanisms. The aim of this study was to investigate the role of peroxisome proliferator-activated receptor-α (PPAR-α) in modulating cardiac insulin-sensitive glucose transporter (GLUT-4) protein levels in altered metabolic states and to determine the functional consequences by assessing cardiac ischemic tolerance. Wild-type and PPAR-α-null mouse hearts were isolated and perfused 6 wk after streptozotocin administration or after 14 mo on a high-fat diet or after a 24-h fast. Myocardial d-[2-3H]glucose uptake was measured during low-flow ischemia, and differences in GLUT-4 protein levels were quantified using Western blotting. In wild-type mice in all three metabolic states, elevated plasma free fatty acids were associated with lower total cardiac GLUT-4 protein levels and decreased glucose uptake during ischemia, resulting in poor postischemic functional recovery. Although PPAR-α-null mice also had elevated plasma free fatty acids, they had neither decreased cardiac GLUT-4 levels nor decreased glucose uptake during ischemia and, consequently, did not have poor recovery during reperfusion. We conclude that elevated plasma free fatty acids are associated with increased injury during ischemia due to decreased cardiac glucose uptake resulting from lower cardiac GLUT-4 protein levels, the levels of GLUT-4 being regulated, probably indirectly, through PPAR-α activation.

Effect of high FFA on glycogenolysis in oxidative rat hindlimb muscles during twitch stimulation

1996 ◽  
Vol 270 (4) ◽  
pp. R766-R776 ◽  
Author(s):  
D. J. Dyck ◽  
S. J. Peters ◽  
P. S. Wendling ◽  
L. L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Rat Skeletal Muscle ◽  
Acetyl Coa ◽  
Hindlimb Muscles ◽  
Rest Perfusion ◽  
Wide Range ◽  
Glycogen Sparing

The effect of elevated free fatty acids (FFA) on carbohydrate (CHO) utilization in the oxidative muscles of the isolated hindlimb was determined using twitch contraction paradigms evoking a wide range of O2 uptakes and glycogenolysis. The hindlimb was perfused with either 0 or 1.8 mM FFA for 10 min at rest and then subjected to 20 min of stimulation at 0.4, 0.7, 1, 2, 3, or 4 Hz. Soleus (Sol), plantaris (Pl), and red gastrocnemius (RG) were sampled after rest perfusion or stimulation. FFA had little effect on glycogenolysis during stimulation, although glycogen sparing occurred with one of the lesser intensity protocols in each muscle (Sol, 0.4 Hz; RG, 0.7 Hz; Pl, 1 Hz). Muscle citrate and acetyl-CoA were elevated in Sol during several stimulation protocols with high FFA, but this effect was inconsistent in Pl and RG. The sparing of glycogen, when it did occur, was generally unrelated to increases in either citrate or acetyl-CoA content. Furthermore, protocols in which citrate or acetyl-CoA were elevated in the presence of elevated FFA did not demonstrate glycogen sparing. Hindlimb lactate efflux at rest was reduced with FFA but unaffected during stimulation. Glucose uptake was unaffected by FFA at rest and during stimulation protocols, except 3 Hz. The present study does not support the classically proposed roles of citrate and acetyl-CoA in the FFA-induced downregulation of CHO utilization in electrically stimulated rat skeletal muscle.

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