Effects of carnitine and taurine on fatty acid metabolism and lipid accumulation in the liver of cats during weight gain and weight loss

Abstract Treatment of epilepsy or bipolar disorder with valproic acid (VPA) induces weight gain and increased serum levels for the satiety hormone, leptin, through an unidentified mechanism. In this study we tested the effects of VPA, a short-chain branched fatty acid (C8:0), on leptin biology and fatty acid metabolism in 3T3-L1 adipocytes. VPA significantly reduced leptin secretion in a dose-dependent manner. Because fatty acid accumulation has been hypothesized to block leptin secretion, we tested the effect of VPA on fatty acid metabolism. Using 14C-radiolabeled VPA, we found that the 14C was mainly incorporated into triacylglycerol. VPA did not alter lipogenesis from acetate, nor did it change the amount of intracellular free fatty acids available for triacylglycerol synthesis. Decreased leptin secretion was accompanied by a reduction in leptin mRNA, even though VPA treatment did not alter the protein levels for known transcription factors affecting leptin transcription including: CCAAT/enhancer binding protein-α, peroxisome proliferator-activated receptor-γ, or steroid regulatory element binding protein 1a. VPA altered levels of leptin mRNA independent of de novo protein synthesis without affecting leptin mRNA degradation. This report demonstrates that VPA decreases leptin secretion and mRNA levels in adipocytes in vitro, suggesting that VPA therapy may be associated with altered leptin homeostasis contributing to weight gain in vivo.

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Comparative Analysis of the Preventive Effects of Canagliflozin, a Sodium-Glucose Co-Transporter-2 Inhibitor, on Body Weight Gain Between Oral Gavage and Dietary Administration by Focusing on Fatty Acid Metabolism

Diabetes Metabolic Syndrome and Obesity Targets and Therapy ◽

10.2147/dmso.s269916 ◽

2020 ◽

Vol Volume 13 ◽

pp. 4353-4359

Author(s):

Satoko Kawarasaki ◽

Honami Sawazaki ◽

Hiroaki Iijima ◽

Su-Ping Ng ◽

Jungin Kwon ◽

...

Keyword(s):

Body Weight ◽

Fatty Acid ◽

Comparative Analysis ◽

Weight Gain ◽

Fatty Acid Metabolism ◽

Acid Metabolism ◽

Body Weight Gain ◽

Oral Gavage ◽

Preventive Effects

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Disorder of fatty acid metabolism in the kidney of PAN-induced nephrotic rats

AJP Renal Physiology ◽

10.1152/ajprenal.00365.2011 ◽

2012 ◽

Vol 303 (7) ◽

pp. F1070-F1079 ◽

Cited By ~ 10

Author(s):

Yoshikazu Muroya ◽

Osamu Ito ◽

Rong Rong ◽

Kenta Takashima ◽

Daisuke Ito ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Metabolism ◽

Lipid Accumulation ◽

Acid Metabolism ◽

Kidney Cortex ◽

Tubular Damage ◽

Sprague Dawley ◽

Puromycin Aminonucleoside ◽

Fatty Acid Binding ◽

Tubulointerstitial Damage

Proteinuria is considered to play an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. Fatty acid-binding albumins are filtered through glomeruli and reabsorbed into proximal tubular epithelial cells (PTECs). However, the role of fatty acid metabolism associated with albuminuria in the development of tubulointerstitial damage remains unclear. Thus, the present study was designed to determine the changes of fatty acid metabolism in the nephrotic kidney. To induce nephrotic syndrome, Sprague-Dawley rats (SDRs) and Nagase analbuminemic rats (NARs) with inherited hypoalbuminemia were treated with a single injection of puromycin aminonucleoside (PAN). In SDRs, PAN treatment induced massive proteinuria and albuminuria and caused tubular damage, apoptosis, and lipid accumulation in PTECs. Among the enzymes of fatty acid metabolism, expressions of medium-chain acyl-CoA dehydrogenase (MCAD) and cytochrome P-450 (CYP)4A significantly decreased in PTECs of PAN-treated SDRs. Expressions of peroxisome proliferator-activated receptor (PPAR)-γ coactivator (PGC)-1α and estrogen-related receptor (ERR)α also significantly decreased, without changes in the expression of PPAR-α. In NARs, PAN treatment induced proteinuria but not albuminuria and did not cause tubular damage, apoptosis, or lipid accumulation. Expressions of MCAD, PGC-1α, or ERRα did not change in the kidney cortex of PAN-treated NARs, but the expression of CYP4A significantly decreased. These results indicate that massive albuminuria causes tubular damage and lipid accumulation with the reduction of MCAD, CYP4A, PGC-1α, and ERRα in PTECs.

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