Abstract
An 8-week feeding trial was conducted to investigate how dietary taurine supplementation attenuates the lipid deposition induced by dietary high lipid in juvenile orange-spotted grouper (Epinephelus coioides). Three isonitrogenous (47% crude protein) semipurified diets were formulated to contain two levels of lipid and termed as 10% lipid diet, 15% lipid diet, and 15% lipid with 1% taurine (namely, diet 10L, diet 15L, and diet 15L + T, respectively). Groupers fed diet 15L + T showed higher weight gain and feed efficiency compared with diet 15L. Groupers fed diet 15L showed higher liver lipid contents, plasma total cholesterol (TC), and leptin contents vs. those fed diet 10L. Diet 15L + T decreased hepatosomatic index, liver lipid content, and plasma TC and adiponectin contents, and increased liver 3-hydroxy-3-methy1 glutary1 coenzyme A reductase content compared with diet 15L. Fish fed diet 15L had higher contents of chenodeoxycholic acid, deoxycholic acid, and lithocholic acid, and lower contents of glycodeoxycholic acid (GDCA), glycolithocholic acid, glycoursodeoxycholic acid, taurodeoxycholic acid (TDCA), and β-, γ-, and ω-muricholic acid (MCA) when compared with fish fed diet 10L. Diet 15L + T downregulated the contents of glycocholic acid, glycochenodeoxycholic acid, taurohyodeoxycholic acid, tauromuricholic acid, TDCA, ursodeoxycholic acid, GDCA, and β-MCA vs. diet 15L. Diet 15L upregulated expression of peroxisome proliferator-activated receptor α (pparα) gene but downregulated expression of acyl-CoA carboxylase (acc), fatty acid synthase (fas), and glucose-6-phosphate dehydrogenase (g6pd) genes in comparison with diet 10L. The gene expression level of fas and 6pgd was downregulated and the pparα gene expression level was upregulated in fish fed diet 15L + T compared with those in fish fed diet 15L. Overall, this study indicated that dietary taurine supplementation can attenuate the liver lipid deposition of groupers caused by feeding 15% lipid through accelerating lipid absorption of taurine-conjugated bile acids and fatty acid β-oxidation and inhibiting lipogenesis.
Highlights
Taurine (2-aminoethanesulfonic acid), as a free amino acid, does not participate in protein synthesis but is known to play a wide range of key roles in animal physiology, such as immune regulation, osmoregulation, antioxidation, nervous system development and regeneration, and bile acid (BA) conjugation (Huxtable, 1992; Salze and Davis, 2015; Wu, 2020; Xu et al, 2020)
The diet taurine downregulated the contents of all differential BAs, namely, glycodeoxycholic acid (GDCA), glycocholic acid (GCA), glycochenodeoxycholic acid (GCDCA), taurohyodeoxycholic acid (THDCA), tauromuricholic acid (TMCA), tauroursodeoxycholic acid (TUDCA), ursodeoxycholic acid (TUDCA), and β-MCA in comparison with taurine free diet at 15% lipid (Figure 3F)
feed intake (FI) was not affected by dietary taurine levels at 15% lipid in this study, the trend of feed efficiency (FE) in response to dietary taurine addition was similar to weight gain (WG)
Summary
Taurine (2-aminoethanesulfonic acid), as a free amino acid, does not participate in protein synthesis but is known to play a wide range of key roles in animal physiology, such as immune regulation, osmoregulation, antioxidation, nervous system development and regeneration, and bile acid (BA) conjugation (Huxtable, 1992; Salze and Davis, 2015; Wu, 2020; Xu et al, 2020). BAs are regarded as biosurfactants, which emulsify lipid into micelles to facilitate its digestion and absorption by allowing for more cleavage sites for lipase (Suga et al, 2019; Romano et al, 2020). The emulsification of long-chain triglycerides (TGs) is achieved by conjugated BAs, which are better emulsifiers than BAs due to their hydrophilic and lipophilic properties (Gupta and Kim, 2003). Previous studies demonstrated that dietary taurine addition increased taurine-conjugated BAs contents in rockfish (Sebastes schlegeli) and tiger puffer (Takifugu rubripes) (Kim et al, 2015; Xu et al, 2020). Taurine may regulate lipid metabolism through accelerating BAs to form taurine-conjugated BAs
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