# Dietary Soy Impact on Host Transcriptome Profile--A Review
## 4 Discussion
Both _Acacb_ (Acetyl-CoA carboxylase 2), which is responsible for fatty acids oxidation [55], and _Ces1d_ (Carboxylesterase 1D), whose function is to hydrolyze triacylglycer-erols and monoacylglycerols [56], were overexpressed. On the other hand, genes involved in cholesterol biosynthesis (such as _Cyp2c23_ or _Cyp2c11_, members of cytochrome P450, subfamily 2) were repressed. _Cyp2c11_ is an essential component of steroid hormones and fatty acid metabolism and a biomarker for hypertension [57]. We also noticed the downregulation of _Lipc_ (Lipase C), involved in the conversion of very-low-density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL) to low-density lipoproteins (LDL) [58]. Its repression is associated with a delay in atherosclerosis in mice [59]. While the hypocholesterolem effect of the soy diet in mammals was expected, the impact in fish is puzzling, especially regarding cholesterol homeostasis. _Sc5d_ (Sterol-C5-desaturase-like), _Jffd1_ (Farnesyl-diphosphate farnesyltransferase 1), _acat2_ (Acetyl-CoA Acetyltransferase 2) are genes involved in cholesterol synthesis and absorption, and they were all upregulated with over 2-fold changes. Cytochrome P450 lanosterol 14\(\alpha\)-demethylase (_cyp51_), a key enzyme responsible for an essential step in the biosynthesis of sterols, was increased [60] while _cyp7a1_ (cholesterol 7-alpha-hydroxylase), an enzyme that oxidizes cholesterol, was decreased. Rainbow trout subjected to plant-based diet interventions show enhanced hepatic cholesterol synthesis mediated by _sereb-2, lxr-\(\alpha\)_ (liver X receptor alpha), and miR-223 [61]. Physiologically, when dietary cholesterol level is low, _cyp7a1_ is downregulated by Srebp (stend regulatory element-binding protein) [62], which leads to an increase in the hepatocytes' cholesterol level [63]. It is possible that the soy-induced upregulation of cholesterol biosynthesis is meant to compensate for its dietary lack and thus maintains cholesterol homeostasis [50]. We also found that the biosynthesis of unsaturated fatty acids, fatty acid metabolism, and fatty acid elongation pathways were also highly enriched. In rodents, _acot1_, _acot2_, _acot3_ (Acyl-CoA thioesterase), and _acaa1b_ (Acetyl-Coenzyme A acyltransferase 1), enzymes responsible for acyl-Coa and acetyl-CoA hydrolysis were upregulated [64]. Although the role of Acot enzymes in fatty acid metabolism is not fully understood, they are considered a key element in maintaining an optimal level of fatty acids' beta-oxidation [65]. In fish, we noticed a possible activation of these lipids' pathways. _Fads2_ (Fatty acid desaturase 2), known to catalyze the biosynthesis of fatty acids [66], is upregulated, while genes such as _hadhu_ and _hadhb_ (hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex), essential for fatty acid oxidation, are downregulated. They are all essential components of the multistep process that breaks down fat molecules and converts them into energy [67]. The well-known impact of soy intake on lipid metabolism in mammals (reduction in hepatic lipotoxicity by preventing the transport of fatty acids to extra-adipose tissues) might thus be explained by these coordinated transcriptome changes [68]. One should nevertheless take into account that the response to soy diet is tissue-specific: reduced lipogenesis in the liver [69], increased unsaturated fatty acid biosynthesis (monounsaturated fatty acids, polyunsaturated fatty acids, C18:1 _trans_-11, C18:2 _trans_-10, _cis_-12, _omega_-3) in the mammary gland [70]. As for the 240 fatty acid metabolism gene alterations in fish, we noticed changes that suggest an increase in fatty acid biosynthesis in the intestine. Since dietary fatty acids are taken up by enterocytes, resynthesized into triacylglycerglycerol, and stored as lipid droplets, it is conceivable that the lipids-poor soy-rich diet increases intestinal fatty acid metabolism in an attempt to maintain lipid homeostasis [68].