scholarly journals Dietary Conjugated Linoleic Acid and Hepatic Steatosis: Species-Specific Effects on Liver and Adipose Lipid Metabolism and Gene Expression

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Diwakar Vyas ◽  
Anil Kumar G. Kadegowda ◽  
Richard A. Erdman

Objective. To summarize the recent studies on effect of conjugated linoleic acid (CLA) on hepatic steatosis and hepatic and adipose lipid metabolism highlighting the potential regulatory mechanisms.Methods. Sixty-four published experiments were summarized in whichtrans-10,cis-12 CLA was fed either alone or in combination with other CLA isomers to mice, rats, hamsters, and humans were compared.Summary and Conclusions. Dietarytrans-10,cis-12 CLA induces a severe hepatic steatosis in mice with a more muted response in other species. Regardless of species, when hepatic steatosis was present, a concurrent decrease in body adiposity was observed, suggesting that hepatic lipid accumulation is a result of uptake of mobilized fatty acids (FA) from adipose tissue and the liver's inability to sufficiently increase FA oxidation and export of synthesized triglycerides. The potential role of liver FA composition, insulin secretion and sensitivity, adipokine, and inflammatory responses are discussed as potential mechanisms behind CLA-induced hepatic steatosis.

Lipids ◽  
2006 ◽  
Vol 41 (2) ◽  
pp. 179-188 ◽  
Author(s):  
Amy Noto ◽  
Peter Zahradka ◽  
Natalia Yurkova ◽  
Xueping Xie ◽  
Evan Nitschmann ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Hao-Yu Liu ◽  
Haotian Gu ◽  
Yanwei Li ◽  
Ping Hu ◽  
Yatian Yang ◽  
...  

Scope: Disruptions of circadian rhythm cause metabolic disorders and are closely related to dietary factors. In this study, we investigated the interplays between the dietary conjugated linoleic acid (CLA)-induced hepatic steatosis and the circadian clock regulation, in association with lipid homeostasis.Methods and Results: Exposure of mice to 1.5% dietary CLA for 28 days caused insulin resistance, enlarged livers, caused hepatic steatosis, and increased triglyceride levels. Transcriptional profiling showed that hepatic circadian clock genes were significantly downregulated with increased expression of the negative transcription factor, REV-ERBα. We uncovered that the nuclear receptor (NR) PPARα, as a major target of dietary CLA, drives REV-ERBα expression via its binding to key genes of the circadian clock, including Cry1 and Clock, and the recruitment of histone marks and cofactors. The PPARα or REV-ERBα inhibition blocked the physical connection of this NR pair, reduced the cobinding of PPARα and REV-ERBα to the genomic DNA response element, and abolished histone modifications in the CLA-hepatocytes. In addition, we demonstrated that CLA promotes PPARα driving REV-ERBα transcriptional activity by directly binding to the PPAR response element (PPRE) at the Nr1d1 gene.Conclusions: Our results add a layer to the understanding of the peripheral clock feedback loop, which involves the PPARα-REV-ERBα, and provide guidance for nutrients optimization in circadian physiology.


2018 ◽  
Vol 24 (6) ◽  
pp. 1752-1768 ◽  
Author(s):  
Qi Zou ◽  
Yan‐ou Yang ◽  
Bang‐Hong Wei ◽  
Deng‐hang Yu ◽  
Lu Chen ◽  
...  

Lipids ◽  
2002 ◽  
Vol 37 (8) ◽  
pp. 741-750 ◽  
Author(s):  
E. A. Emken ◽  
R. O. Adlof ◽  
S. Duval ◽  
G. Nelson ◽  
P. Benito

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