Effects of high-fat diets on growth performance, endoplasmic reticulum stress and mitochondrial damage in blunt snout breamMegalobrama amblycephala

Abstract

This study aimed to investigate the relationship between fat deposition and endoplasmic reticulum stress of blunt snout bream through changing dietary lipid levels and adding lipolytic agents. The results showed that high fat diet (HFD) remarkably increased VSI, IPF, whole‐body lipid, tissue lipid contents, plasma levels of LDL‐C, TC and TG contents, cytosolic cytochrome c activity and Ca2+ content and the transcriptions of GRP78, IRE1, XBP1s and SREBP1, whereas the opposite was true for plasma HDL‐C content, SDH and Na+, K+‐ATPase activities in the mitochondria, Ca2+‐ATPase activity in the ER and the transcriptions of XBP1u, PPARα and CPT I. In addition, simvastatin supplementation remarkably decreased VSI, tissue lipid contents, plasma LDL‐C and TC levels, cytosolic cytochrome c activity and Ca2+ content and the transcriptions of GRP78, IRE1, XBP1s and SREBP1, while the opposite was true for plasma HDL‐C level, Ca2+‐ATPase activity and the transcriptions of XBP1u, PPARα and CPT I. Furthermore, the histological results showed that large lipid droplets and ultrastructural impairments of the mitochondria, nucleus and ER were present in hepatocytes of fish fed the HFD, while simvastatin supplementation had the potential to alleviate these damages. Taken together, these results indicated that there was an interaction between lipid deposition and endoplasmic reticulum stress induced by HFD.

Effects of Dietary Protein and Lipid Levels on Growth, Body Composition, Blood Biochemistry, Antioxidant Capacity and Ammonia Excretion of European Grayling (Thymallus thymallus)

“…Additionally, we detected elevated serum CHO concentration at higher dietary protein levels which agrees with the study on red-spotted grouper (Wang et al, 2017). Several authors noted that TG level in blood has an inverse relationship with protein content of feed (Zhang et al, 2010;Jin et al, 2015) but has a positive relationship with fat content (Li et al, 2017;Cao et al, 2019). Likewise, in this study serum TG concentration doubled at higher dietary lipid level indicating more active transport of lipids.…”

Dietary berberine regulates lipid metabolism in muscle and liver of black sea bream (Acanthopagrus schlegelii) fed normal or high-lipid diets

“…HL diets causing excessive lipid deposition in liver have been widely reported in different fish species (15,32,43) . HL diets have been reported to result in cellular swelling, nuclear translocation, lipid droplet accumulation (6,44) and hypertrophied liver cells with larger cell diameter (32,45) , which were also observed in the present study. These pathologies might also inhibit lipoprotein secretion and fatty acid oxidation, which then result in a vicious cycle (46) .…”

“…Since the liver is the central organ involved in carbohydrate, lipid and protein metabolism, its impairment eventually causes poor health condition and induces other diseases (e.g. inflammatory reaction and oxidative stress) (6) . Excessive lipid accumulation also poses severe health problems and reduces harvest yields, which is directly responsible for economic losses (7) .…”

Dietary fenofibrate attenuated high-fat-diet-induced lipid accumulation and inflammation response partly through regulation of pparα and sirt1 in juvenile black seabream (Acanthopagrus schlegelii)

“…Although, serum and hepatic TAG and CHOL were not significantly reduced after fenofibrate treatment in the present study, there was a trend of decreasing TAG contend in both serum and liver in fish fed the diet supplemented with fenofibrate compared to fish fed HFD. These results were consistent with previous studies in blunt snout bream (Cao et al, 2019b;Dai et al, 2018;Zhou et al, 2019) and common carp (Cyprinus carpio) (Abasubong et al, 2018) fed high fat diets. The aminotransferase enzymes, AST and ALT, play important roles in fish as in mammals and are used generally as key indicators of liver function and cellular damage (Ma et al, 2018).…”