Abstract
ScopeConjugated linoleic acids are linoleic acid isomers found in the diet that can also be produced through bacterial metabolism of polyunsaturated fatty acids. Our objective was to evaluate the contribution of fatty acid metabolites produced from polyunsaturated fatty acids by the gut microbiota in vivo to regulation of hepatic lipid metabolism and steatosis.Methods and resultsIn mice with depleted n-3 polyunsaturated fatty acids, we observed an accumulation of trans-11,trans-13 CLA and cis-9,cis-11 conjugated linoleic acids in the liver tissue that were associated with an increased triglyceride content and expression of lipogenic genes. We used an in vitro model to evaluate the impact of these two conjugated linoleic acids on hepatic lipid metabolism. In HepG2 cells, we observed that only trans-11,trans-13 conjugated linoleic acids recapitulated triglyceride accumulation and increased lipogenic gene expression, which is a phenomenon that may implicate the nuclear factors sterol regulatory element binding protein 1c (SREBP-1c) and carbohydrate-responsive element-binding protein (ChREBP).ConclusionThe trans-11,trans-13 conjugated linoleic acids can stimulate hepatic lipogenesis, which supports the conclusion that gut microbiota and related metabolites should be considered in the treatment of non-alcoholic liver disease.
Highlights
Non-alcoholic fatty liver disease represents a major worldwide health problem with a prevalence of 20% in the general population that increases up to 70% in obese and type 2 diabetic subjects [1]
The trans-11,trans-13 conjugated linoleic acids can stimulate hepatic lipogenesis, which supports the conclusion that gut microbiota and related metabolites should be considered in the treatment of non-alcoholic liver disease
This accumulation of hepatic TG following colonization is attributed to a stimulation of de novo fatty acid synthesis, which is mainly controlled by a transcription factor called sterol regulatory element binding protein-1c (SREBP-1c) [5]; several other transcription factors, such as the Liver X Receptor, could play a role [6, 7]
Summary
Non-alcoholic fatty liver disease represents a major worldwide health problem with a prevalence of 20% in the general population that increases up to 70% in obese and type 2 diabetic subjects [1]. Colonization of germ-free mice with gut microbiota harvested from conventionally raised mice leads to increased body fat mass and hepatic TG content [5]. This accumulation of hepatic TG following colonization is attributed to a stimulation of de novo fatty acid synthesis, which is mainly controlled by a transcription factor called sterol regulatory element binding protein-1c (SREBP-1c) [5]; several other transcription factors, such as the Liver X Receptor, could play a role [6, 7]. In addition to cis-9,trans-11 CLA, several other CLA isomers, such as trans-10,cis-12 CLA have been described as intermediates of LA biohydrogenation [18]
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