scholarly journals Tlr4-mutant mice are resistant to acute alcohol-induced sterol-regulatory element binding protein activation and hepatic lipid accumulation

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Zhi-Hui Zhang ◽  
Xiao-Qian Liu ◽  
Cheng Zhang ◽  
Wei He ◽  
Hua Wang ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Mutant Mice ◽  
Hepatic Lipid ◽  
Protein Activation ◽  
Hepatic Lipid Accumulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

scholarly journals Curcumin attenuates insulin resistance and hepatic lipid accumulation in a rat model of intra-uterine growth restriction through insulin signalling pathway and sterol regulatory element binding proteins

2019 ◽  
Vol 122 (6) ◽  
pp. 616-624 ◽  
Author(s):  
Yu Niu ◽  
Jintian He ◽  
Hussain Ahmad ◽  
Chao Wang ◽  
Xiang Zhong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Accumulation ◽  
Insulin Signalling ◽  
Regulatory Element ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Uterine Growth ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Intra Uterine Growth Restriction

AbstractThe objective of the present study was to investigate the effect of curcumin on insulin resistance (IR) and hepatic lipid accumulation in intra-uterine growth restriction (IUGR). Rats with a normal birth weight (NBW) or IUGR were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NBW-C and IUGR-C groups) from 6 to 12 weeks. Rats in the IUGR group showed higher levels of glucose and homeostasis model assessment for insulin resistance index (HOMA-IR) (P< 0·05) than in the NBW group. The livers of IUGR rats exhibited higher (P< 0·05) concentration of TAG and lower (P< 0·05) activities of lipolysis enzymes compared with the normal rats. In response to dietary curcumin supplementation, concentrations of serum insulin, glucose and HOMA-IR, pyruvate, TAG, total cholesterol and NEFA in the liver were decreased (P< 0·05). The concentrations of glycogen and activities of lipolysis enzymes in the liver were increased (P< 0·05) in the IUGR-C group compared with the IUGR group. These results were associated with lower (P< 0·05) phosphorylated insulin receptor substrate 1, protein kinase B or Akt, glycogen synthase kinase 3β and expressions of sterol regulatory element binding protein 1 and fatty acid synthase (FASN); decreased expressions forCd36, sterol regulatory element binding protein 1c (Srebf1) andFasn; increased (P< 0·05) expression of PPARα; and expressions forPparaand hormone-sensitive lipase in the liver of IUGR-C rats than the IUGR rats. Maternal malnutrition caused IR and lipid accumulation in the liver. Curcumin supplementation prevented IR by regulating insulin signalling pathways and attenuated hepatic lipid accumulation.

miR-23a/b-3p promotes hepatic lipid accumulation by regulating Srebp-1c and Fas

2021 ◽  
Author(s):  
Linfang Li ◽  
Xiaoyi Zhang ◽  
Hangjiang Ren ◽  
Xiuqing Huang ◽  
Tao Shen ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
Leptin Receptor ◽  
Regulatory Element ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Protein Levels ◽  
Triglyceride Accumulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

miR-23a-3p and miR-23b-3p are members of the miR-23~27~24-2 superfamily. The role of miR-23a/b-3p in regulating hepatic lipid accumulation is still unknown. Here, we found that increased miR-23a-3p and miR-23b-3p levels were accompanied by an increase in the protein levels of the sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS) in the steatotic livers of mice fed a high-fat diet (HFD) and leptin-receptor-deficient type 2 diabetic mice (db/db). Importantly, overexpression of miR-23a/b-3p in Hep1-6 cells elevated the intracellular triglyceride level and upregulated the expression of Srebp-1c and Fas. Taken together, these results suggested that miR-23a/b-3p enhanced mRNA stability by binding the 5'-UTR of Srebp-1c and Fas mRNA, thereby promoting triglyceride accumulation in hepatocytes.

Chronic exercise provides renal-protective effects with upregulation of fatty acid oxidation in the kidney of high fructose-fed rats

2020 ◽  
Vol 318 (3) ◽  
pp. F826-F834
Author(s):  
Gaizun Hu ◽  
Lusi Xu ◽  
Yixuan Ma ◽  
Masahiro Kohzuki ◽  
Osamu Ito
Keyword(s):  
Renal Function ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
Binding Protein ◽  
Regulatory Element ◽  
High Fructose ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Acyl Coa Oxidase ◽  
Renal Expression

Excessive fructose intake causes metabolic syndrome and lipid accumulation in the kidney and leads to renal dysfunction and damage. Exercise (Ex) improves lipids regulation, but the mechanisms are unclarified in the kidney. In the present study, male Sprague-Dawley rats were allocated to groups fed with control or high-fructose (HFr) diet. Part of rats in each group underwent aerobic treadmill Ex for 12 wk. Drug treatment was performed as the fenofibrate gavage during the last 4 wk on HFr diet-fed rats. Renal function, histological changes, and expression of regulators involved in fatty acid (FA) metabolism were assessed. In CON diet-fed groups, Ex did not affect renal function or histology and significantly increased renal expression of FA β-oxidation regulators including acyl-CoA dehydrogenases (CADs), acyl-CoA oxidase, peroxisome proliferator-activated receptor (PPAR)-α, and PPAR-γ coactivator (PGC)-1α and lipogenic factors including acetyl-CoA carboxylase (ACCα), FA synthase (FAS), and sterol regulatory element-binding protein 1c. HFr caused albuminuria, lipid accumulation, and renal pathohistological changes, which were attenuated by Ex but not by fenofibrate. HFr decreased renal expression of medium- and short-chain CADs and PPAR-α and increased renal expression of ACCα, FAS, and sterol regulatory element-binding protein 1c. Ex increased expression of CADs, carnitine palmitoyltransferase type I, acyl-CoA oxidase, PPAR-α, and PGC-1α and decreased renal expression of ACCα and FAS in HFr diet-fed rats. The Ex-induced FA metabolism alteration was similar to that in the fenofibrate-treated group. In conclusion, the present study indicates that Ex enhanced renal FA metabolism, which might protect the kidney in lipid dysregulation diseases.

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