Systemic adaptation of lipid metabolism in response to low- and high-fat diet in Nile tilapia (Oreochromis niloticus)

Abstract

Natural selection endows animals with the abilities to store lipid when food is abundant and to synthesize lipid when it is limited. However, the relevant adaptive strategy of lipid metabolism has not been clearly elucidated in fish. This study examined the systemic metabolic strategies of Nile tilapia to maintain lipid homeostasis when fed with low- or high-fat diets. Three diets with different lipid contents (1%, 7%, and 13%) were formulated and fed to tilapias for 10 weeks. At the end of the feeding trial, the growth rate, hepatic somatic index, and the triglyceride (TG) contents of serum, liver, muscle, and adipose tissue were comparable among three groups, whereas the total body lipid contents and the mass of adipose tissue increased with the increased dietary lipid levels. Overall quantitative PCR, western blotting and transcriptomic assays indicated that the liver was the primary responding organ to low-fat (LF) diet feeding, and the elevated glycolysis and accelerated biosynthesis of fatty acids (FA) in the liver is likely to be the main strategies of tilapia toward LF intake. In contrast, excess ingested lipid was preferentially stored in adipose tissue through increasing the capability of FA uptake and TG synthesis. Increasing numbers, but not enlarging size, of adipocytes may be the main strategy of Nile tilapia responding to continuous high-fat (HF) diet feeding. This is the first study illuminating the systemic adaptation of lipid metabolism responding to LF or HF diet in fish, and our results shed new light on fish physiology.

Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio

“…The phenomena that high-fat diet impairs glucose homeostasis has been reported in rainbow trout4950. Our recent work further illustrated that glycolysis-related genes are upregulated or downregulated during low-fat diet or high-fat diet feeding, respectively51. In the present study, dietary L-carnitine supplementation improved lipid catabolism significantly, but increased the whole body glycogen deposition in the fasting state, indicating that glucose degradation was inhibited.…”

Effects of dietary lipid levels on growth, fatty acid composition, antioxidant status and lipid metabolism in juvenileOnychostoma macrolepis

“…Lipogenic genes FAS and ACC1 were highly expressed in the L3 group, suggesting that the hepatopancreas provided more fatty acids through de novo lipogenesis. Previous studies also indicated that the expression levels of FAS and ACC1 decreased with the increase in dietary lipid intake (He et al, ; Leng et al, ; Rollin, Medale, Gutieres, Blanc, & Kaushik, ). The possible reason is that the intake of exogenous lipid in higher lipid groups by juvenile O. macrolepis is sufficient, thus reducing their endogenous lipid synthesis, in order to maintain the dynamic equilibrium between the absorption and utilization of exogenous dietary lipids and endogenous lipid synthesis (Leng et al, ).…”

Comparison of effects of dietary‐specific fatty acids on growth and lipid metabolism in Nile tilapia

“…All amplifications were performed in triplicate. Specific primer nucleotide sequences of the following genes: EF1α, β‐actin, ATP citrate lyase (ACLY), acetyl‐CoA carboxylase alpha (ACCα), fatty acid synthase (FAS), diacylglycerol O‐acyltransferase 2 (DGAT2), glycerol‐3‐phosphate acyltransferase 1 (GPAT), sterol regulatory element‐binding transcription factor 1 (SREBP1), adipose triglyceride lipase (ATGL), hormone‐sensitive lipase (HSL), carnitine palmitoyltransferase I alpha (CPT1a), carnitine palmitoyltransferase I beta (CPT1b), peroxisome proliferator‐activated receptor alpha (PPARα), lipoprotein lipase (LPL), fatty acid‐binding protein 4 (FABP4), cluster determinant 36 (CD36), and acyl‐CoA oxidase (ACO) have been previously described (He et al, ; Ning et al, ).…”