Induction of the Acyl-Coenzyme A Synthetase Gene by Fibrates and Fatty Acids Is Mediated by a Peroxisome Proliferator Response Element in the C Promoter

Schoonjans, Kristina; Watanabe, Mitsuhiro; Suzuki, Hiroyuki; Mahfoudi, Abderrahim; Krey, Grigorios; Wahli, Walter; Grimaldi, Paul A.; Staels, Bart; Yamamoto, Tokuo; Auwerx, Johan

doi:10.1074/jbc.270.33.19269

Cited by 357 publications

(197 citation statements)

References 58 publications

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“…40,41 Interestingly, daidzein supplementation normalized the depression of glutathione S-transferase-a3 and superoxide dismutase 2 by the HF diet, and further downregulated the expression of c-Jun N-terminal kinase and IkB kinase that is augmented by the HF diet (Table 1), which might be associated with the higher antioxidative capacity of daidzein metabolite, equol, rather than other isoflavones. 15 Besides these results, our hepatic transcript profiles showed that daidzein supplementation reduced hepatic lipid levels through the activation of ACAS and ACAD, which are involved in fatty acid b-oxidation, [42][43][44][45][46][47] and this activation was due to the upregulation of PPARa, their upstream gene. 48 Daidzein supplementation also functions as hepatic antisteatotic materials by the regulation of adipocyte metabolism.…”

Section: Discussionmentioning

confidence: 78%

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

et al. 2010

Int J Obes

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Introduction: Globally, non-alcoholic fatty liver disease (NAFLD) continues to rise and isoflavones exert antisteatotic effects by the regulation of hepatic lipogenesis/insulin resistance or adiposity/a variety of adipocytokines are related to hepatic steatosis. However, there is very little information regarding the potential effects of daidzein, the secondary abundant isoflavone, on NAFLD. Here, we have assessed the hepatic global transcription profiles, adipocytokines and adiposity in mice with high fat-induced NAFLD and their alteration by daidzein supplementation. Methods: C57BL/6J mice were fed with normal fat (16% fat of total energy), high fat (HF; 36% fat of total energy) and HF supplemented with daidzein (0.1, 0.5, 1 and 2 g per kg diet) for 12 weeks. Results: Daidzein supplementation (X0.5 g per kg diet) reduced hepatic lipid concentrations and alleviated hepatic steatosis. The hepatic microarray showed that daidzein supplementation (1 g per kg diet) downregulated carbohydrate responsive element binding protein, a determinant of de novo lipogenesis, its upstream gene liver X receptor b and its target genes encoding for lipogenic enzymes, thereby preventing hepatic steatosis and insulin resistance. These results were confirmed by lower insulin and blood glucose levels as well as homeostasis model assessment insulin resistance scores. In addition, daidzein supplementation inhibited adiposity by the upregulation of genes involved in fatty acid b-oxidation and the antiadipogeneis, and moreover augmented antisteatohepatitic leptin and adiponectin mRNA levels, whereas it reduced the mRNA or concentration of steatotic tumor necrosis factor a and ghrelin. Conclusions: These findings show that daidzein might alleviate NAFLD through the direct regulation of hepatic de novo lipogenesis and insulin signaling, and the indirect control of adiposity and adipocytokines by the alteration of adipocyte metabolism.

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Section: Discussionmentioning

confidence: 78%

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

et al. 2010

Int J Obes

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“…Treatment with these compounds results in the upregulation of genes such as acyl-CoA oxidase, bifunctional enzyme, thiolase and long-chain fatty acid acyl-CoA synthetase all of which have been shown to be regulated via PPARα (Dreyer et al, 1992;Zhang et al, 1992;Lee et al, 1995;Schoonjans et al, 1995).…”

Section: Transcriptional Control Of Lipid Homeostasismentioning

confidence: 99%

Metabolism and Functions of Lipids and Fatty Acids in Teleost Fish

Tocher

2003

Reviews in Fisheries Science

2,042

1,718

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Lipids and their constituent fatty acids are, along with proteins, the major organic constituents of fish, and they play major roles as sources of metabolic energy for growth including reproduction, and movement including migration. Furthermore, the fatty acids of fish lipids are rich in ω3 long chain, highly unsaturated fatty acids (n-3 HUFA) that have particularly important roles in animal nutrition, including fish and human nutrition, reflecting their roles in critical physiological processes. Indeed, fish are the most important food source of these vital nutrients for man Thus, the long standing interest in fish lipids stems from their abundance and their uniqueness. This review attempts to summarise our present state of knowledge of various aspects of the basic biochemistry, metabolism and functions of fatty acids, and the lipids they constitute part of, in fish, seeking where possible to relate that understanding as much to fish in their natural environment as to farmed fish. In doing so, it highlights the areas that require to be investigated in greater depth and also the increasing application of molecular technologies in fish lipid metabolism which will fascilitate further advances through molecular biological and genetic techniques including genomics and proteomics.

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“…13 The ACS gene contains three different first exons preceded by specific regulatory regions A, B, and C. Recently, it has been reported that C-ACS promoter activity was induced by the addition of fatty acids or fenofibric acids. 33 C-ACS promoter possesses a peroxisome proliferator activator receptor-responsive element. The peroxisome proliferator activator receptor is known to form a heterodimer with retinoid X receptor and to activate genes related to fatty acid metabolism in response to the addition of fatty acids or fibrates.…”

Section: Figmentioning

confidence: 99%

Enhanced expression of hepatic acyl-coenzyme A synthetase and microsomal triglyceride transfer protein messenger RNAs in the obese and hypertriglyceridemic rat with visceral fat accumulation

et al. 1998

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The liver plays a central role in lipoprotein metabolism. In particular, very-low density lipoprotein (VLDL) is assembled in the hepatocytes and secreted into the blood circulation. The VLDL is then catabolized to low-density lipoprotein by lipoprotein lipase and hepatic triglyceride lipase. Obese subjects, especially those with visceral fat accumulation, are frequently associated with hyperlipidemia, non-insulin-dependent diabetes mellitus (NIDDM), and hypertension. The mechanism of hyperlipidemia in visceral fat obesity has not yet been elucidated. Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model of NIDDM, characterized by obesity with visceral fat accumulation, hyperlipidemia, and late-onset insulin resistance. To elucidate the mechanism of hyperlipidemia observed in OLETF rats, we focused on the production of VLDL by the liver and investigated hepatic messenger RNA (mRNA) levels of microsomal triglyceride transfer protein (MTP), acyl-coenzyme A synthetase (ACS), and apolipoprotein B (apo B), which play important roles in VLDL synthesis and secretion. In 6-week-old OLETF rats, in which insulin resistance had not been manifested, visceral fat weight was already higher and portal free fatty acid (FFA) and VLDL-triglyceride levels were elevated compared with the control rats. Hepatic ACS activity and mRNA levels, and MTP mRNA levels were also increased in OLETF rats, whereas apo B mRNA levels were similar; these results suggest that the enhanced expression of both ACS and MTP genes associated with visceral fat accumulation before developing insulin resistance may be involved in the pathogenesis of hyperlipidemia in obese animal models with NIDDM. (HEPATOLOGY 1998;27:557-562.)

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Induction of the Acyl-Coenzyme A Synthetase Gene by Fibrates and Fatty Acids Is Mediated by a Peroxisome Proliferator Response Element in the C Promoter

Cited by 357 publications

References 58 publications

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism

Metabolism and Functions of Lipids and Fatty Acids in Teleost Fish

Enhanced expression of hepatic acyl-coenzyme A synthetase and microsomal triglyceride transfer protein messenger RNAs in the obese and hypertriglyceridemic rat with visceral fat accumulation

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