Docosahexaenoic acid (DHA) and hepatic gene transcription. Jump, D. B, Botolin, D., Wang, Y., Xu, J., Demeure, O., & Christian, B. 153(1):3–13, 5, 2008.
Docosahexaenoic acid (DHA) and hepatic gene transcription. [link]Paper  doi  abstract   bibtex   
The type and quantity of dietary fat ingested contributes to the onset and progression of chronic diseases, like diabetes and atherosclerosis. The liver plays a central role in whole body lipid metabolism and responds rapidly to changes in dietary fat composition. Polyunsaturated fatty acids (PUFA) play a key role in membrane composition and function, metabolism and the control of gene expression. Certain PUFA, like the n-3 PUFA, enhance hepatic fatty acid oxidation and inhibit fatty acid synthesis and VLDL secretion, in part, by regulating gene expression. Our studies have established that key transcription factors, like PPARalpha, SREBP-1, ChREBP and MLX, are regulated by n-3 PUFA, which in turn control levels of proteins involved in lipid and carbohydrate metabolism. Of the n-3 PUFA, 22:6,n-3 has recently been established as a key controller of hepatic lipid synthesis. 22:6,n-3 controls the 26S proteasomal degradation of the nuclear form of SREBP-1. SREBP-1 is a major transcription factor that controls the expression of multiple genes involved fatty acid synthesis and desaturation. 22:6,n-3 suppresses nuclear SREBP-1, which in turn suppresses lipogenesis. This mechanism is achieved, in part, through control of the phosphorylation status of protein kinases. This review will examine both the general features of PUFA-regulated hepatic gene transcription and highlight the unique mechanisms by which 22:6,n-3 impacts gene expression. The outcome of this analysis will reveal that changes in hepatic 22:6,n-3 content has a major impact on hepatic lipid and carbohydrate metabolism. Moreover, the mechanisms involve 22:6,n-3 control of several well-known signaling pathways, such as Akt, Erk1/2, Gsk3beta and PKC (novel or atypical). 22:6,n-3 control of these same signaling pathways in non-hepatic tissues may help to explain the diverse actions of n-3 PUFA on such complex physiological processes as visual acuity and learning.
@article{Jump-2008-ID17,
  title     = {Docosahexaenoic acid ({DHA}) and hepatic gene transcription.},
  abstract  = {The type and quantity of dietary fat ingested contributes to the onset and
               progression of chronic diseases, like diabetes and atherosclerosis. The
               liver plays a central role in whole body lipid metabolism and responds
               rapidly to changes in dietary fat composition. Polyunsaturated fatty acids
               ({PUFA}) play a key role in membrane composition and function, metabolism
               and the control of gene expression. Certain {PUFA}, like the n-3 {PUFA},
               enhance hepatic fatty acid oxidation and inhibit fatty acid synthesis and
               {VLDL} secretion, in part, by regulating gene expression. Our studies have
               established that key transcription factors, like {PPAR}alpha, {SREBP}-1,
               Ch{REBP} and {MLX}, are regulated by n-3 {PUFA}, which in turn control
               levels of proteins involved in lipid and carbohydrate metabolism. Of the
               n-3 {PUFA}, 22:6,n-3 has recently been established as a key controller of
               hepatic lipid synthesis. 22:6,n-3 controls the 26S proteasomal degradation
               of the nuclear form of {SREBP}-1. {SREBP}-1 is a major transcription factor
               that controls the expression of multiple genes involved fatty acid
               synthesis and desaturation. 22:6,n-3 suppresses nuclear {SREBP}-1, which in
               turn suppresses lipogenesis. This mechanism is achieved, in part, through
               control of the phosphorylation status of protein kinases. This review will
               examine both the general features of {PUFA}-regulated hepatic gene
               transcription and highlight the unique mechanisms by which 22:6,n-3 impacts
               gene expression. The outcome of this analysis will reveal that changes in
               hepatic 22:6,n-3 content has a major impact on hepatic lipid and
               carbohydrate metabolism. Moreover, the mechanisms involve 22:6,n-3 control
               of several well-known signaling pathways, such as Akt, Erk1/2, Gsk3beta and
               {PKC} (novel or atypical). 22:6,n-3 control of these same signaling
               pathways in non-hepatic tissues may help to explain the diverse actions of
               n-3 {PUFA} on such complex physiological processes as visual acuity and
               learning.},
  author    = {Jump, Donald B and Botolin, Daniela and Wang, Yun and Xu, Jinghua and
               Demeure, Olivier and Christian, Barbara},
  volume    = {153},
  number    = {1},
  pages     = {3--13},
  year      = {2008},
  month     = {5},
  url       = {http://www.pubmed.org/18343222},
  pmcid     = {2430187},
  pmid      = {18343222},
  doi       = {10.1016/j.chemphyslip.2008.02.007},
  keywords  = {Animals, Humans, Liver, Signal Transduction, Transcription Factors,
               Docosahexaenoic Acids, Gene Expression Regulation, Glycolysis, Lipid
               Metabolism, Lipogenesis, Transcription, Genetic},
  file      = {FULLTEXT:pdfs/000/000/000000017.pdf:PDF}
}
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