scholarly journals Sparstolonin B suppresses free fatty acid palmitate‐induced chondrocyte inflammation and mitigates post‐traumatic arthritis in obese mice

2021 ◽  
Author(s):  
Haiwei Ma ◽  
Chenglong Xie ◽  
Gaolu He ◽  
Zhengtai Chen ◽  
Hongwei Lu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Obese Mice ◽  
Sparstolonin B ◽  
Post Traumatic ◽  
Traumatic Arthritis

scholarly journals High Fat Diet Stimulates Beta-Oxidation, Alters Electrical Properties and Induces Adipogenicity of Atria in Obese Mice

2020 ◽  
Author(s):  
Nadine Suffee ◽  
Elodie Baptista ◽  
Jérôme Piquereau ◽  
Maharajah Ponnaiah ◽  
Nicolas Doisne ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
High Fat Diet ◽  
Potassium Current ◽  
Obese Mice ◽  
High Fat ◽  
Beta Oxidation ◽  
Long Chain

SUMMARYMetabolic disorders such as obesity are risk factors of atrial fibrillation, not only by sharing comorbidities but likely through their direct impact on atria, notably its adipogenicity. Here, we submitted mice that lack cardiac adipose tissue to a high fat diet and first studied the atrial metabolomic and lipidomic phenotypes using liquid chromatography-mass spectrometry. We found an increased consumption of free fatty acid by the beta-oxidation and an accumulation of long-chain lipids in atria of obese mice. Free fatty acid was the main substrate of mitochondrial respiration studied in the saponin-permeabilized atrial muscle. Conducted action potential recorded in atrial trabeculae was short, and ATP-sensitive potassium current was increased in perforated patch-clamp atrial myocytes of obese mice. There was histological and phenotypical evidence for an accumulation of adipose tissue in obese mice atria. Thus, an obesogenic diet transforms the energy metabolism, causes fat accumulation and induces electrical remodeling of atria myocardium.HIGHLIGHTS- Untargeted metabolomic and lipidomic analysis revealed that a high fat diet induces profound transformation of atrial energy metabolism with beta-oxidation activation and long-chain lipid accumulation.- Mitochondria respiration studied in atrial myocardial trabecula preferentially used Palmitoyl-CoA as energy substrate in obese mice.- Atria of obese mice become vulnerable to atrial fibrillation and show short action potential due to the activation of K-ATP dependent potassium current.- Adipocytes and fat molecular markers were detected in atria of obese mice together with an inflammatory profile consistence with a myocardial accumulation of fat.

scholarly journals Acute administration of IL-6 improves indices of hepatic glucose and insulin homeostasis in lean and obese mice

2019 ◽  
Vol 316 (1) ◽  
pp. G166-G178 ◽  
Author(s):  
Willem T. Peppler ◽  
Logan K. Townsend ◽  
Grace M. Meers ◽  
Matthew R. Panasevich ◽  
Rebecca E. K. MacPherson ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Lipid Accumulation ◽  
Acute Administration ◽  
Obese Mice ◽  
Hepatic Lipid Accumulation ◽  
Hepatic Glucose ◽  
Insulin Homeostasis

Obesity can lead to impairments in hepatic glucose and insulin homeostasis, and although exercise is an effective treatment, the molecular targets remain incompletely understood. As IL-6 is an exercise-inducible cytokine, we aimed to identify whether IL-6 itself influences hepatic glucose and insulin homeostasis and whether this response differs during obesity. In vivo, male mice were fed a low-fat diet (LFD; 10% kcal) or a high-fat diet (HFD; 60% kcal) for 7 wk, which induced obesity and hepatic lipid accumulation. LFD- and HFD-fed mice were injected with IL-6 (400 ng, 75 min) or PBS and then with insulin (1 U/kg; ~15 min) or saline, at which point livers were collected. In both LFD- and HFD-fed mice, IL-6 decreased blood glucose and mRNA expression of gluconeogenic genes alongside increased phosphorylation of AKT in comparison to PBS controls, and this occurred without changes in circulating insulin. To determine whether this effect of IL-6 was directly on the liver, we completed in vitro isolated primary hepatocyte experiments from chow-fed mice and cultured with or without exposure to free fatty acid (250 μm palmitate and 250 μm oleate, 24 h) to induce lipid accumulation. In both control and free fatty acid-treated hepatocytes, IL-6 (20 ng/ml, 75 min) slightly attenuated insulin-stimulated (10 nM; ~15 min) AKT phosphorylation. Together, these data suggest that IL-6 may lead to improvements in indices of hepatic glucose and insulin homeostasis in vivo; however, this is likely due to an indirect effect on the hepatocyte. NEW & NOTEWORTHY In this study, we used lean and obese mice and found that a single injection of IL-6 improved glucose tolerance, decreased hepatic gluconeogenic gene expression, and increased hepatic phosphorylation of AKT. In primary hepatocytes cultured under control and lipid-laden conditions, IL-6 had a mild, but deleterious, effect on phosphorylation of AKT. Our results show that the beneficial effects of IL-6 on glucose and insulin homeostasis, in vivo, are maintained in obesity.

Measurement of plasma glucose, free fatty acid, lactate, and insulin for 24 h in patients with NIDDM

Diabetes ◽  
1988 ◽  
Vol 37 (8) ◽  
pp. 1020-1024 ◽  
Author(s):  
G. M. Reaven ◽  
C. Hollenbeck ◽  
C. Y. Jeng ◽  
M. S. Wu ◽  
Y. D. Chen
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Glucose

Free fatty acid as a link in the regulation of hepatic glucose output by peripheral insulin

Diabetes ◽  
1995 ◽  
Vol 44 (9) ◽  
pp. 1038-1045 ◽  
Author(s):  
K. Rebrin ◽  
G. M. Steil ◽  
L. Getty ◽  
R. N. Bergman
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output
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