Browsing by Author "Dong-Liang Lu"

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    Concentration-dependent effects of 17 β-estradiol and bisphenol A on lipid metabolism, inflammation and antioxidant response in male zebrafish (Danio rerio). Chemosphere, 237: (2019) 124422.
    (Elsevier, 2019-12) Sheng-Xiang Sun; Yun-Ni Zhang; Dong-Liang Lu; Wei-Li Wang; Samwel Mchele Limbu; Dong-Liang Li; Li-Qiao Chen; Mei-Ling Zhang; Zhen-Yu Du
    Environmental estrogenic compounds are important pollutants, which are widely distributed in natural water bodies. They produce various adverse effects on fish, but their concentration-dependent toxicities in fish metabolism and health are not fully understood. This study investigated the effects of 17β-estradiol (E2) and bisphenol A (BPA) at low and high concentrations on lipid deposition, inflammation and antioxidant response in male zebrafish. We measured fish growth parameters, gonad development, lipid contents and the activities of inflammatory and antioxidant enzymes, as well as their mRNA expressions. All E2 and BPA concentrations used increased body weight, damaged gonad structure and induced feminization in male zebrafish. The exposure of zebrafish to E2 and BPA promoted lipid accumulation by increasing total fat, liver triglycerides and free fatty acid contents, and also upregulated lipogenic genes expression, although they decreased total cholesterol content. Notably, zebrafish exposed to low concentrations of E2 (200 ng/L) and BPA (100 μg/L) had higher lipid synthesis and deposition compared to high concentrations (2000 ng/L and 2000 μg/L, respectively). However, the high concentrations of E2 and BPA increased inflammation and antioxidant response. Furthermore, BPA caused greater damage to fish gonad development and more severe lipid peroxidation compared to E2. Overall, the results suggest that the toxic effects of E2 and BPA on zebrafish are concentration-dependent such that, the relative low concentrations used induced lipid deposition, whereas the high ones caused adverse effects on inflammation and antioxidant response.
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    Dietary L-carnitine improves glycogen and protein accumulation in Nile tilapia via increasing lipid-sourced energy supply: an isotope-based metabolic tracking. Aquaculture Reports, 17: 100302.
    (Elsevier, 2020-07) Ling-Yu Li; Dong-Liang Lu; Zhe-Yue Jiang; Samwel Mchele Limbu; Fang Qiao; Liqiao Chen; Meiling Zhang; Zhen-Yu Du
    L-carnitine is a functional aquafeed additive for enhancing lipid catabolism by elevating mitochondrial fatty acid β-oxidation and modulating energy metabolism to provide a “protein sparing effect”. However, results on the effects of dietary l-carnitine on nutrient metabolism in fish are still conflicting. We explored comprehensively the effects of dietary l-carnitine on energy metabolism in Nile tilapia. We fed Nile tilapia for eight weeks with diets supplemented with l-carnitine or not. We conducted metabolic tracking tests by intraperitoneally injecting individual fish with 14C-labeled palmitic acid (PA), glucose (Glu) and an amino acid mixture (AAs). After the feeding trial, insignificant growth-promoting effect of l-carnitine was obtained in treated fish. However, l-carnitine significantly reduced the lipid content in whole body and muscle accompanied by increasing the free carnitine concentration and fatty acid β-oxidation efficiency. Moreover, l-carnitine elevated concentrations of serum glucose, pyruvate and lactate, and increased glycogen and protein deposition in muscle. These results suggest that ingested glucose and protein prefer to be reserved in carnitine-fed fish with sufficient fatty acids oxidation for energy. Nevertheless, after a 14C-labeled single nutrient injection, carnitine-fed fish showed a higher oxidation rate of [1-14C]-PA, d-[1-14C]-Glu and l-[14C (U)]-AAs. Our study indicates that, the effects of l-carnitine on nutrient metabolism are correlated with the abundance of individual macronutrients such that an inadequate lipid supply would cause dietary l-carnitine supplementation to elevate higher breakdown of glucose and protein for energy generation. The present study provides new insights on the regulation mechanism of l-carnitine on nutrient metabolism in fish.
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    Inhibition of lipophagy suppresses lipid metabolism in zebrafish liver cells, Frontiers in Physiology, 10; Article 1077; 1-9.
    (Frontiers Media SA, 2019-08-21) Jing Wang; Si-Lan Han; Dong-Liang Lu; Ling-Yu Li; Samwel Mchele Limbu; Dongliang Li; Meiling Zhang; Zhen-Yu Du
    Lipophagy degrades lipid droplets (LDs) through the lysosomal degradative pathway, thus plays important roles in regulating lipid metabolism in mammals. However, information on the existence and functions of lipophagy in fish lipid metabolism is still limited. In the present study, we confirmed the existence of lipophagy by observing the structures of LDs sequestered in autophagic vacuoles in the zebrafish liver cell line (ZFL) via electronic microscopy. Moreover, starved cells increased the mRNA expression of the microtubule-associated protein 1A/1B light chain 3 beta (LC3), which is a marker protein for autophagy and protein conversion from LC3-I to LC3-II. Inhibiting autophagy with chloroquine increased significantly the LDs content and decreased fatty acid β-oxidation and esterification activities in the ZFL cells cultured in the fed state. Furthermore, inhibiting autophagy function downregulated the mRNA expression of the genes and their proteins related to lipid metabolism. Altogether, the present study verified the existence of lipophagy and its essential regulatory roles in lipid metabolism in fish cells.
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    Mitochondrial fatty acid β-oxidation inhibition promotes carbohydrate catabolism and protein deposition through energy homeostasis remodelling. The Journal of Nutrition, nxaa187, https://doi.org/10.1093/jn/nxaa187.
    (Oxford University Press, 2019-09) Ling-Yu Li; Jia-Min Li; Li-Jun Ning; Dong-Liang Lu; Yuan Luo; Qiang Ma; Samwel Mchele Limbu; Dong-Liang Li; Li-Qiao Chen; Irfan J. Lodhi; Pascal Degrace; Mei-Ling Zhang; Zhen-Yu Du
    Background Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. Objectives This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. Methods Carnitine-depleted male Nile tilapia (initial weight: 4.29 ± 0.12 g; 3 mo old) were established by feeding them with mildronate diets (1000 mg/kg/d) for 6 wk. Zebrafish deficient in the carnitine palmitoyltransferase 1b gene (cpt1b) were produced by using CRISPR/Cas9 gene-editing technology, and their males (154 ± 3.52 mg; 3 mo old) were used for experiments. Normal Nile tilapia and wildtype zebrafish were used as controls. We assessed nutrient metabolism and energy homeostasis–related biochemical and molecular parameters, and performed 14C-labeled nutrient tracking and transcriptomic analyses. Results The mitochondrial FAO decreased by 33.1–88.9% (liver) and 55.6–68.8% (muscle) in carnitine-depleted Nile tilapia and cpt1b-deficient zebrafish compared with their controls (P < 0.05). Notably, glucose oxidation and muscle protein deposition increased by 20.5–24.4% and 6.40–8.54%, respectively, in the 2 fish models compared with their corresponding controls (P < 0.05). Accordingly, the adenosine 5′-monophosphate–activated protein kinase/protein kinase B–mechanistic target of rapamycin (AMPK/AKT-mTOR) signaling was significantly activated in the 2 fish models with inhibited mitochondrial FAO (P < 0.05). Conclusions These data show that inhibited mitochondrial FAO in fish induces energy homeostasis remodeling and enhances glucose utilization and protein deposition. Therefore, fish with inhibited mitochondrial FAO could have high potential to utilize carbohydrate. Our results demonstrate a potentially new approach for increasing protein deposition through energy homeostasis regulation in cultured animals.