scholarly journals Cardiomyocyte‐specific miR‐100 overexpression preserves heart function under pressure overload in mice and diminishes fatty acid uptake as well as ROS production by direct suppression of Nox4 and CD36

2021 ◽  
Vol 35 (11) ◽  
Author(s):  
Christian Smolka ◽  
Delia Schlösser ◽  
Christoph Koentges ◽  
Aleksandre Tarkhnishvili ◽  
Oliver Gorka ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Heart Function ◽  
Pressure Overload ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Ros Production ◽  
Direct Suppression

scholarly journals Male-Specific Cardiac Dysfunction in CTP:Phosphoethanolamine Cytidylyltransferase (Pcyt2)-Deficient Mice

2015 ◽  
Vol 35 (15) ◽  
pp. 2641-2657 ◽  
Author(s):  
Poulami Basu ◽  
Faisal J. Alibhai ◽  
Elena V. Tsimakouridze ◽  
Ratnesh K. Singh ◽  
Sabina Paglialunga ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Cardiac Dysfunction ◽  
Heart Function ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Ros Production ◽  
Altered Expression ◽  
Gender Specific Differences ◽  
Male Specific

Phosphatidylethanolamine (PE) is the most abundant inner membrane phospholipid. PE synthesis from ethanolamine and diacylglycerol is regulated primarily by CTP:phosphoethanolamine cytidylyltransferase (Pcyt2).Pcyt2+/−mice have reduced PE synthesis and, as a consequence, perturbed glucose and fatty acid metabolism, which gradually leads to the development of hyperlipidemia, obesity, and insulin resistance. Glucose and fatty acid uptake and the corresponding transporters Glut4 and Cd36 are similarly impaired in male and femalePcyt2+/−hearts. These mice also have similarly reduced phosphatidylinositol 3-kinase (PI3K)/Akt1 signaling and increased reactive oxygen species (ROS) production in the heart. However, onlyPcyt2+/−males develop hypertension and cardiac hypertrophy.Pcyt2+/−males have upregulated heart AceI expression, heart phospholipids enriched in arachidonic acid and other n-6 polyunsaturated fatty acids, and dramatically increased ROS production in the aorta. In contrast,Pcyt2+/−females have unmodified heart phospholipids but have reduced heart triglyceride levels and altered expression of the structural genesActa(low) andMyh7(high). These changes together protectPcyt2+/−females from cardiac dysfunction under conditions of reduced glucose and fatty acid uptake and heart insulin resistance. Our data identify Pcyt2 and membrane PE biogenesis as important determinants of gender-specific differences in cardiac lipids and heart function.

scholarly journals Endothelial Lipase Modulates Pressure Overload–Induced Heart Failure Through Alternative Pathway for Fatty Acid Uptake

Hypertension ◽  
2013 ◽  
Vol 61 (5) ◽  
pp. 1002-1007 ◽  
Author(s):  
Hideto Nakajima ◽  
Tatsuro Ishida ◽  
Seimi Satomi-Kobayashi ◽  
Kenta Mori ◽  
Tetsuya Hara ◽  
...  
Keyword(s):  
Heart Failure ◽  
Fatty Acid ◽  
Alternative Pathway ◽  
Pressure Overload ◽  
Fatty Acid Uptake ◽  
Endothelial Lipase ◽  
Acid Uptake

Unaltered Fatty Acid Uptake, Utilization, and Mitochondrial Respiration in Right Atrial Appendage of Type 2 Diabetic Human Heart

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 335-OR
Author(s):  
NANDINI RJ ◽  
SR RAJI ◽  
VIVEK V. PILLAI ◽  
JAYAKUMAR K. ◽  
SRINIVAS GOPALA
Keyword(s):  
Fatty Acid ◽  
Mitochondrial Respiration ◽  
Human Heart ◽  
Fatty Acid Uptake ◽  
Atrial Appendage ◽  
Right Atrial ◽  
Acid Uptake ◽  
Right Atrial Appendage ◽  
Type 2 Diabetic

scholarly journals Lipid Accumulation and Chronic Kidney Disease

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 722 ◽  
Author(s):  
Zhibo Gai ◽  
Tianqi Wang ◽  
Michele Visentin ◽  
Gerd Kullak-Ublick ◽  
Xianjun Fu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Kidney Disease ◽  
Lipid Accumulation ◽  
Scavenger Receptor ◽  
Fatty Acid Uptake ◽  
Lipid Lowering ◽  
Fatty Acid Transport ◽  
Acid Uptake

Obesity and hyperlipidemia are the most prevalent independent risk factors of chronic kidney disease (CKD), suggesting that lipid accumulation in the renal parenchyma is detrimental to renal function. Non-esterified fatty acids (also known as free fatty acids, FFA) are especially harmful to the kidneys. A concerted, increased FFA uptake due to high fat diets, overexpression of fatty acid uptake systems such as the CD36 scavenger receptor and the fatty acid transport proteins, and a reduced β-oxidation rate underlie the intracellular lipid accumulation in non-adipose tissues. FFAs in excess can damage podocytes, proximal tubular epithelial cells and the tubulointerstitial tissue through various mechanisms, in particular by boosting the production of reactive oxygen species (ROS) and lipid peroxidation, promoting mitochondrial damage and tissue inflammation, which result in glomerular and tubular lesions. Not all lipids are bad for the kidneys: polyunsaturated fatty acids (PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) seem to help lag the progression of chronic kidney disease (CKD). Lifestyle interventions, especially dietary adjustments, and lipid-lowering drugs can contribute to improve the clinical outcome of patients with CKD.

Effect of insulin on free fatty acid uptake by hepatocytes in the duck

1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Free Fatty Acids ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Low Doses ◽  
Higher Doses

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386

Sign in / Sign up

Export Citation Format

Share Document