scholarly journals Protective Effects of Voluntary Exercise on Hepatic Fat Accumulation Induced by Dietary Restriction in Zucker Fatty Rats

2021 ◽  
Vol 22 (4) ◽  
pp. 2014
Author(s):  
Yuka Kurosaka ◽  
Shuichi Machida ◽  
Yoko Shiroya ◽  
Hideki Yamauchi ◽  
Kumiko Minato
Keyword(s):  
Fatty Acid ◽  
Dietary Restriction ◽  
Voluntary Exercise ◽  
Protective Effects ◽  
Strong Negative Correlation ◽  
Fatty Acid Binding ◽  
Fat Accumulation ◽  
Expression Levels ◽  
Hepatic Fatty Acid ◽  
Hepatic Fat

Weight control based on dietary restriction (DR) alone can cause lipid metabolic failure and progression to fatty liver. This study aimed to investigate the effect of exercise on preventing DR-induced hepatic fat accumulation in Zucker fatty (ZF) rats by focusing on the relationship between adipose tissue lipolysis and hepatic fat uptake. Six-week-old male ZF rats were randomly assigned to obese, DR, or DR with exercise (DR + Ex) groups. The DR and DR + Ex groups were fed a restricted diet, with the latter also undergoing voluntary exercise. After 6 weeks, hepatic fat accumulation was observed in the DR group, whereas intrahepatic fat was markedly reduced in the DR + Ex group. Compared with the obese (Ob) group, the DR group exhibited 2.09-fold expression of hepatic fatty acid translocase (FAT)/CD36 proteins (p < 0.01) and 0.14-fold expression of hepatic fatty acid-binding protein (FABP)1 (p < 0.01). There were no significant differences between the DR + Ex group and the Ob group. FAT/CD36 and hepatic triglyceride (TG) expression levels were strongly positively correlated (r = 0.81, p < 0.001), whereas there was a strong negative correlation between FABP1 and hepatic TG expression levels (r = −0.65, p < 0.001). Our results suggest that hepatic fat accumulation induced by DR in ZF rats might be prevented through exercise-induced modifications in FAT/CD36 and FABP1 expression.

scholarly journals Studies on fatty acid-binding proteins. Changes in the concentration of hepatic fatty acid-binding protein during development in the rat

1987 ◽  
Vol 242 (3) ◽  
pp. 919-922 ◽  
Author(s):  
M Sheridan ◽  
T C I Wilkinson ◽  
D C Wilton
Keyword(s):  
Fatty Acid ◽  
Binding Proteins ◽  
Fatty Acid Binding Protein ◽  
Fluorescence Enhancement ◽  
Binding Protein ◽  
Fold Increase ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Hepatic Fatty Acid

The concentration of hepatic fatty acid-binding protein was determined in the livers of rats at various stages of development from foetus to young adult. Fatty acid-binding protein concentrations were determined by quantifying the fluorescence enhancement on the binding of the fluorescent probe 11-(dansylamino)-undecanoic acid. A 20-fold increase in the concentration of the protein was observed between the foetus and adult, and this increase was confirmed by immuno-blotting. No other protein in the 14,000-Mr range was observed in the foetus. Possible alternative fatty acid-binding proteins could not be detected in h.p.l.c.-fractionated foetal cytosol by the fluorescence-enhancement method.

scholarly journals RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary study

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8529
Author(s):  
Dong Qu ◽  
Kaikai Zhang ◽  
Lijian Chen ◽  
Qi Wang ◽  
Huijun Wang
Keyword(s):  
Fatty Acid ◽  
Rna Sequencing ◽  
Biochemical Analysis ◽  
Fatty Acid Synthase ◽  
Sequencing Analysis ◽  
Protective Effects ◽  
Rna Seq ◽  
Oral Gavage ◽  
Fatty Acid Binding ◽  
Preliminary Study

In this study, RNA-sequencing (RNA-seq) was utilized to investigate the effects of luteolin on hepatotoxicity caused by methamphetamine (METH). The rats in METH group were administrated with METH (15 mg/kg, two times per day) via intraperitoneal (i.p.) injections for four consecutive days. The rats in luteolin + METH group were firstly administrated with luteolin (100 mg/kg, once a day) by oral gavage for 3 days before METH treatment. Lueolin attenuated the hepatotoxicity induced by METH via histopathological and biochemical analysis. The results of RNA-seq showed that luteolin could regulate 497 differentially expressed genes (DEGs), and the selected DEGs were mainly enriched in eight pathways, according to KEGG analysis. Furthermore, qRT-PCR was utilized to verify the results of RNA-seq. Six genes were selected as follows: liver enriched antimicrobial peptide 2 (Leap2), fatty acid synthase (Fasn), fatty acid binding protein 5 (Fabp5), patatin like phospholipase domain containing 3 (Pnpla3), myelin basic protein (Mbp) and calmodulin 3 (Calm3). Though because of the design flaws, the luteolin group has not been included, this study demonstrated that luteolin might exert hepato-protective effects from METH via modulation of oxidative phosphorylation, cytochrome P450 and certain signaling pathways.

Role of Fatty Acid Binding Protein 4 (FABP4) in Kidney Disease

2020 ◽  
Vol 27 (22) ◽  
pp. 3657-3664 ◽  
Author(s):  
Min Shi ◽  
Liang Ma ◽  
Ping Fu
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Current Knowledge ◽  
Kidney Diseases ◽  
Binding Protein ◽  
Experimental Studies ◽  
Protective Effects ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

Accumulating evidences indicated that obesity and metabolic syndrome were independent risk factors for the development and progression of kidney diseases. Apart from inflammation, lipotoxicity, and hemodynamic factors, adipokines have been proposed to play crucial roles in the relationship between kidney diseases and metabolic disorders. As one of the key adipokines, fatty acid binding protein 4 (FABP4), which is mainly expressed in adipocytes and macrophages, has recently been shown to be associated with renal dysfunction and kidney damage. Both clinical and experimental studies have proposed circulating FABP4 as a novel predictor for renal injuries, and it might also be a predictor for cardiovascular events in patients with end stage renal disease (ESRD). FABP4 has also been detected in the glomerular cells and epithelial tubular cells in mouse and human kidneys, and the expression of FABP4 in these cells has been involved in the pathogenesis of kidney diseases. In addition, experimental studies suggested that inhibition of FABP4 had protective effects on renal damage. Here, we reviewed current knowledge regarding the role of FABP4 in pathophysiological insights as well as its potential function as a predictor and therapeutic target for kidney diseases.

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