The effect and mechanism of dietary monocalcium phosphate restriction on hepatic lipid deposition and immune status in obscure puffer, Takifugu obscurus

A 12-week chronic feeding trial was conducted to determine the effect and mechanism of dietary monocalcium phosphate (CaH2PO4) restriction on hepatic lipid deposition and immune status in obscure puffer, Takifugu obscurus. Fish with an initial mean weight of 7.21 ± 0.05 g were fed a phosphorus (P)-sufficient diet (P6, diet supplemented with 0.6% P) or P-deficient diet (P0, diet supplemented without P). Sampling occurred at weeks 3, 6, 9 and 12, respectively. During the feeding trial, fish fed the P0 diet showed poor growth performance, reduced feed intake, whole body P and ash as well as vertebrae P contents, which are signs of P deficiency. Dietary P restriction increased hepatic vacuoles and lipid droplets, lipid content of whole body and liver, viscerosomatic and hepatosomatic indices, whereas reduced whole body protein content and lipolytic enzyme activities, including carnitine palmitoyltransferase 1 (CPT-1) and lipoprotein lipase (LPL). But peroxisome proliferators-activated receptor α (pparα) mRNA level was up-regulated by dietary P deficiency on week 3, and then down-regulated on weeks 6, 9 and 12. Meanwhile, dietary P deficiency increased hepatic mRNA expressions of 6-phosphogluconate dehydrogenase (6pgd), malic enzyme (me), acetyl-CoA carboxylase (acc)-α and acc-β, while decreased cpt-1 and fatty acid binding protein (fabp). Additionally, dietary P deficiency decreased the mRNA level of complement 3 (c3) while increased heat shock proteins (HSPs, including hsp90 and hsp70) on weeks 9 and 12. Dietary P restriction also induced apoptosis by up-regulating the mRNA levels of caspase-3, caspase-8 and caspase-9 and down-regulating the levels of B-cell lymphoma 2 (bcl-2) and Bax inhibitor-1 (bi-1). In conclusion, our study indicated that dietary P deficiency induced lipid deposition and impaired the immune status of obscure puffer.