Browsing by Author "Fang Qiao"
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Item Atorvastatin remodels lipid distribution between liver and adipose tissues through blocking lipoprotein efflux in fish(American Physiological Society, 2023-03-01) Rui-Xin Li; Ling-Yun Chen; Samwel Mchele Limbu; Bing Yao; Yi-Fan Qian; Wen-Hao Zhou; Li-Qiao Chen; Fang Qiao; Mei-Ling Zhang; Zhen-Yu Du; Yuan LuoThe regulation of cholesterol metabolism in fish is still unclear. Statins play important roles in promoting cholesterol metabolism development in mammals. However, studies on the role of statins in cholesterol metabolism in fish are currently limited. The present study evaluated the effects of statins on cholesterol metabolism in fish. Nile tilapia (Oreochromis niloticus) were fed on control diets supplemented with three atorvastatin levels (0, 12, and 24 mg/kg diet, ATV0, ATV12, and ATV24, respectively) for 4 wk. Intriguingly, the results showed that both atorvastatin treatments increased hepatic cholesterol and triglyceride contents mainly through inhibiting bile acid synthesis and efflux, and compensatorily enhancing cholesterol synthesis in fish liver (P < 0.05). Moreover, atorvastatin treatment significantly inhibited hepatic very-low-density lipoprotein (VLDL) assembly and thus decreased serum VLDL content (P < 0.05). However, fish treated with atorvastatin significantly reduced cholesterol and triglycerides contents in adipose tissue (P < 0.05). Further molecular analysis showed that atorvastatin treatment promoted cholesterol synthesis and lipogenesis pathways, but inhibited lipid catabolism and low-density lipoprotein (LDL) uptake in the adipose tissue of fish (P < 0.05). In general, atorvastatin induced the remodeling of lipid distribution between liver and adipose tissues through blocking VLDL efflux from the liver to adipose tissue of fish. Our results provide a novel regulatory pattern of cholesterol metabolism response caused by atorvastatin in fish, which is distinct from mammals: cholesterol inhibition by atorvastatin activates hepatic cholesterol synthesis and inhibits its efflux to maintain cholesterol homeostasis, consequently reduces cholesterol storage in fish adipose tissue.Item Dietary docosahexaenoic acid reduces fat deposition and alleviates liver damage induced by D-galactosamine and lipopolysaccharides in Nile tilapia (Oreochromis niloticus)(Elsevier, 2023-06) Yi-Chan Liu; Samwel Mchele Limbu; Jin-Gang Wang; Mai Wang; Li-Qiao Chen; Fang Qiao; Yuan Luo; Mei-Ling Zhang; Zhen-Yu DuLiver health is important to maintain survival and growth of fish. Currently, the role of dietary docosahexaenoic acid (DHA) in improving fish liver health is largely unknown. This study investigated the role of DHA supplementation in fat deposition and liver damage caused by D-galactosamine (D-GalN) and lipopolysaccharides (LPS) in Nile tilapia (Oreochromis niloticus). Four diets were formulated as control diet (Con), Con supplemented with 1 % DHA, 2 % DHA and 4 % DHA diets, respectively. The diets were fed to 25 Nile tilapia (2.0 ± 0.1 g, average initial weight) in triplicates for four weeks. After the four weeks, 20 fish in each treatment were randomly selected and injected with a mixture of 500 mg D-GalN and 10 μL LPS per mL to induce acute liver injury. The results showed that the Nile tilapia fed on DHA diets decreased visceral somatic index, liver lipid content and serum and liver triglyceride concentrations than those fed on the Con diet. Moreover, after D-GalN/LPS injection, the fish fed on DHA diets decreased alanine aminotransferase and aspartate transaminase activities in the serum. The results of liver qPCR and transcriptomics assays together showed that the DHA diets feeding improved liver health by downregulating the expression of the genes related to toll-like receptor 4 (TLR4) signaling pathway, inflammation and apoptosis. This study indicates that DHA supplementation in Nile tilapia alleviates the liver damage caused by D-GalN/LPS through increasing lipid catabolism, decreasing lipogenesis, TLR4 signaling pathway, inflammation, and apoptosis. Our study provides novel knowledge on the role of DHA in improving liver health in cultured aquatic animals for sustainable aquaculture.Item Dietary L-carnitine alleviates the adverse effects caused by reducing protein and increasing fat contents in juvenile largemouth bass (Micropterus salmoides)(2022-05-06) Yi-Chan Liu; Samwel Mchele Limbu; Jin-Gang Wang; Jiong Ren; Fang Qiao; Mei-Ling Zhang; Zhen-Yu DuProtein ingredients for formulation of fish feeds are expensive and have limited availability. Therefore, reducing dietary protein while increasing dietary fat content is a common practice in rearing carnivorous fish species. However, the ability of dietary L-carnitine to alleviate adverse effects in such diets is currently unknown. This study investigated the role of L-carnitine supplementation in alleviating adverse effects on growth performance, energy metabolism, antioxidant capacity, and inflammation response in juvenile largemouth bass (Micropterus salmoides) fed on a low protein and high fat diet. Three diets were formulated to contain low protein and high fat (LPHF: 420 g kg-1 protein and 150 g kg-1 lipid), LPHF supplemented with L-carnitine (LPHFC: 420 g kg-1 protein and 150 g kg-1 lipid), and a control diet (CON: 480 g kg-1 protein and 130 g kg-1 lipid). The diets were fed to 30 largemouth bass (g) juveniles in triplicates for eight weeks. The results showed that the fish feed on LPHF diet increased hepatosomatic index, visceral somatic index, mesenteric fat index, whole-body crude fat content, serum and liver triglyceride concentrations, and serum non-esterified fatty acid level than those fed on CON diet. Moreover, the fish fed on LPHF diet increased serum alanine aminotransferase activity and liver malondialdehyde content and reduced superoxide dismutase (SOD) activities in the serum and liver. Furthermore, the fish fed on LPHF diet reduced the whole-body crude protein content. Interestingly, feeding the fish on the LPHFC diet decreased fat deposition and liver damage by downregulating the expression of genes related to lipogenesis, inflammation, and increased SOD activity. This study indicates that L-carnitine supplementation in largemouth bass alleviates the adverse effects caused by LPHF diet by decreasing lipogenesis and increasing lipid catabolism. Our study provides novel knowledge on strategies to improve utilization of LPHF diet in cultured aquatic animals.Item 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 DuL-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.Item Dietary L-carnitine supplementation recovers the increased pH and hardness in fillets caused by high-fat diet in Nile tilapia (Oreochromis niloticus)(Elsevier, 2022-07-15) Zhi-Yong Zhang; Samwel Mchele Limbu; Si-Han Zhao; Li-Qiao Chen; Yuan Luo; Mei-Ling Zhang; Fang Qiao; Zhen-Yu DuThe wide use of high-fat diet (HFD) causes negative effects on flesh quality in farmed fish. l-carnitine, a lipid-lowering additive, enhances mitochondrial fatty acid β-oxidation. However its roles in alleviating the effects of HFD on flesh quality in fish are unknown. We fed Nile tilapia with medium-fat diet (MFD, 6% dietary lipid), high-fat diet (HFD, 12% dietary lipid) and HFCD supplemented with l-carnitine (HFCD + 400 mg/kg l-carnitine) for 10 weeks. The HFD-fed fish had higher fat deposition, pH value, myofiber density and flesh hardness than those fed on MFD. However, feeding the fish with the HFCD improved lipid catabolism, which increased significantly lactic acid content and myofiber diameter in muscle, thus reduced pH and hardness values. HFCD also reduced endoplasmic reticulum stress and myofiber apoptosis caused by HFD in the fish. Our study suggests that dietary l-carnitine supplementation alleviates the negative effects of HFD on flesh quality of farmed fish.Item Dietary sodium acetate improves high-fat diet utilization through promoting differential nutrients metabolism between liver and muscle in Nile tilapia (Oreochromis niloticus)(Elsevier, 2023-02-25) Wen-Hao Zhou; Samwel Mchele Limbu; Rui-Xin Li; Yuan Luo; Jiong Ren; Fang Qiao; Mei-Ling Zhang; Zhen-Yu Duigh-fat diet (HFD) often causes many negative effects and impairs fish growth. Short-chain fatty acids (SCFAs) such as acetates modify metabolic disorders and regulate body homeostasis. However, the effects of sodium acetate on alleviating HFD in fish is currently unknown. This study investigated the role of using dietary sodium acetate to alleviate adverse effects caused by HFD in fish. Three replicates (thirty fish each) of 4.8 ± 0.30 g Nile tilapia (Oreochromis niloticus) were fed with control diet (Con), high-fat diet (HFD) or HFD containing sodium acetate diet (HFD + NaAc) for eight weeks. After the feeding trial, Nile tilapia fed with HFD increased significantly tissue lipid deposition, reduced insulin sensitivity and suppressed glucose and lipid metabolism in both liver and muscle, accompanied with signs of metabolic disorders and liver damage. Moreover, HFD feeding inhibited muscle protein synthesis and impaired fish growth performance. However, the fish fed on HFD + NaAc improved significantly oxidative stress, inflammation, apoptosis and injury in liver compared to those fed on HFD. More importantly, dietary sodium acetate supplementation enhanced insulin sensitivity, promoted glucose catabolic utilization and protein synthesis in muscle through activation of insulin and mTOR signaling pathways, respectively, and markedly improved the growth performance. In contrast, dietary sodium acetate promoted hepatic pentose phosphate pathway, hepatic glycogen accumulation, and activated lipid catabolism to alleviate hepatic lipid deposition. Our study illustrates that sodium acetate alleviates differentially the adverse effects induced by feeding Nile tilapia with HFD in muscle and liver. SCFAs such as acetate may be used for improving HFD utilization in fish nutrition.Item Different effects of two dietary levels of tea polyphenols on the lipid deposition, immunity and antioxidant capacity of juvenile GIFT tilapia (Oreochromis niloticus) fed a high-fat diet. Aquaculture, 542: 736896. https://doi.org/10.1016/j.aquaculture.2021.736896(Elsevier, 2021-05-11) Yu-Cheng Qian; Xue Wang; Jiong Ren; Jie Wang; Samwel Mchele Limbu; Rui-Xin Li; Wen-Hao Zhou; Fang Qiao; Mei-Ling Zhang; Zhen-Yu DuLong-term feeding of fish with a high-fat diet (HFD) causes excess fat deposition and an impairment of immune function. In the present study, we aimed to determine whether dietary tea polyphenols (TPs) would ameliorate the adverse effects of HFD-feeding in GIFT tilapia. Juvenile GIFT tilapias (5.4 ± 0.9 g) were raised in twelve 200-L tanks (three tanks per diet, 20 fish per tank) and fed a control diet (6% fat, 36% protein), an HFD (12% fat, 36% protein), or an HFD supplemented with 50 mg/kg or 200 mg/kg TP for 8 weeks. The fish were hand-fed 5% of their body weight per day in three feeds, and maintained at 28 ± 1 °C under a 14-h light/10-h dark cycle. The fish in each tank were bulk weighed and counted fortnightly, and the daily feed amount was adjusted accordingly. At the end of the trial, the cumulative survival rate was calculated, and the weight gain and feed conversion ratio were calculated according to the bulk weight of fish in each tank. Tissues were collected from nine fish per diet, their organs were weighed, and biochemical and molecular indices were subsequently measured. HFD-feeding significantly increased lipid deposition, reduced cumulative survival from 96% to 75%, reduced hepatic alkaline phosphate activity (AKP) and serum total antioxidant capacity (T-AOC); and reduced the hepatic expression of immunoglobulin M (IgM), transforming growth factor-beta (TGF-β) and glutathione-S-transferase (GST) genes versus the control diet. The addition of TPs at 50 or 200 mg/kg both ameliorated the HFD-induced increase in lipid droplets in the liver (50 mg/kg TP from 40.83% to 17.27%; 200 mg/kg TP to 25.33%), and increased the cumulative survival rate of the tilapia. The addition of 50 mg/kg TP had a marked effect increasing cumulative survival to 90%, and increasing the activities of serum acid phosphatase (ACP), T-AOC; and IgM, TGF-β, nuclear factor-κB (NF-κB), superoxide dismutase (SOD), and GST gene expression to the highest level of the HFD-fed groups. The 50 mg/kg TP-containing diet also significantly increased the hepatic expression of carnitine palmitoyltransferase 1 alpha (CPT1α) versus the control diet. In contrast, the tilapia fed an HFD supplemented with 200 mg/kg TPs had the lowest expression of adipose triglyceride lipase, hormone-sensitive lipase, CPT1α, fatty acid synthase and acetyl-CoA carboxylase alpha genes of any of the groups, which implies that the lower and higher levels of TP supplementation have differing effects on lipid metabolism. The 200 mg/kg supplement had lower cumulative survival rate (82%), and smaller effects on serum ACP and hepatic AKP activities than the 50 mg/kg dose, and had no significant effect on serum T-AOC or the expression of IgM, TGF-β, GST, or NF-κB genes in the tilapia. These results indicate that the beneficial effects of TPs on the lipid metabolism and health of fish fed an HFD are dose-related. Moreover, they are likely to be largely mediated through lipid catabolism.Item Environmental estrogen exposure converts lipid metabolism in male fish to a female pattern mediated by AMPK and mTOR signaling pathways. Journal of Hazardous Materials, 394: 122537.(Elsevier, 2020-07-15) Sheng-Xiang Sun; Jun-Lin Wu; Hong-Bo Lv; Hai-Yang Zhang; Jing Zhang; Samwel Mchele Limbu; Fang Qiao; Li-Qiao Chen; Yi Yang; Mei-Ling Zhang; Zhenyu DuEnvironmental estrogens, including bisphenol A (BPA) and 17β-estradiol (E2), which are widely used in industries and medicine, pose a severe ecological threat to fish due to feminization induction. However, the related metabolic basis for reproductive feminization in male fish has not been well addressed. We first found that female zebrafish exhibited higher lipid accumulation and lipogenesis activity than males. Next, we exposed male and female zebrafish to E2 (200 ng/L) or BPA (100 μg/L) for six weeks, and observed an early-phase reproductive feminization in males, accompanied with reduced spermatids, significant fat deposition and lipogenic gene expressions that mimicked female patterns. Cellular signaling assays revealed that, E2 or BPA modulated lipid metabolism in males mainly through lowering 5′ AMP-activated protein kinase (AMPK) and upregulating the lipogenic mechanistic target of rapamycin (mTOR) pathways. For the first time, we show that environmental estrogens could alter lipid metabolism in male fish to a female pattern (metabolic feminization) prior to gonad feminization in male fish, to allows males to accumulate efficiently lipids to harmonize with the feminized gonads. This study suggests that negative effects of environmental estrogens, as hazardous materials, on vertebrate health are more complicated than originally thought.Item High cholesterol intake remodels cholesterol turnover and energy homeostasis in Nile tilapia (Oreochromis niloticus)(2023-02-16) Rui-Xin Li; Ling-Yun Chen; Samwel Mchele Limbu; Yu-Cheng Qian; Wen-Hao Zhou; Li-Qiao Chen; Yuan Luo; Fang Qiao; Mei-Ling Zhang· · ·The roles of dietary cholesterol in fish physiology are currently contradictory. The issue reflects the limited studies on the metabolic consequences of cholesterol intake in fish. The present study investigated the metabolic responses to high cholesterol intake in Nile tilapia (Oreochromis niloticus), which were fed with four cholesterol-contained diets (0.8, 1.6, 2.4 and 3.2%) and a control diet for eight weeks. All fish-fed cholesterol diets showed increased body weight, but accumulated cholesterol (the peak level was in the 1.6% cholesterol group). Then, we selected 1.6% cholesterol and control diets for further analysis. The high cholesterol diet impaired liver function and reduced mitochondria number in fish. Furthermore, high cholesterol intake triggered protective adaptation via (1) inhibiting endogenous cholesterol synthesis, (2) elevating the expression of genes related to cholesterol esterification and efflux, and (3) promoting chenodeoxycholic acid synthesis and efflux. Accordingly, high cholesterol intake reshaped the fish gut microbiome by increasing the abundance of Lactobacillus spp. and Mycobacterium spp., both of which are involved in cholesterol and/or bile acids catabolism. Moreover, high cholesterol intake inhibited lipid catabolic activities through mitochondrial β-oxidation, and lysosome-mediated lipophagy, and depressed insulin signaling sensitivity. Protein catabolism was elevated as a compulsory response to maintain energy homeostasis. Therefore, although high cholesterol intake promoted growth, it led to metabolic disorders in fish. For the first time, this study provides evidence for the systemic metabolic response to high cholesterol intake in fish. This knowledge contributes to an understanding of the metabolic syndromes caused by high cholesterol intake or deposition in fish.Item Inhibition of pyruvate dehydrogenase kinase increases carbohydrate utilization in Nile tilapia by regulating PDK2/4-PDHE1α axis and insulin sensitivity(Elsevier, 2022-06-24) Yuan Luo; Wen-Hao Zhou; Rui-Xin Li; Samwel Mchele Limbu; Fang Qiao; Li-Qiao Chen; Mei-Ling Zhang; Zhen-Yu DuPyruvate dehydrogenase kinases (PDKs)-pyruvate dehydrogenase E1α subunit (PDHE1α) axis plays an important role in regulating glucose metabolism in mammals. However, the regulatory function of PDKs-PDHE1α axis in the glucose metabolism of fish is not well known. This study determined whether PDKs inhibition could enhance PDHE1α activity, and improve glucose catabolism in fish. Nile tilapia fingerlings (1.90 ± 0.11 g) were randomly divided into 4 treatments in triplicate (30 fish each) and fed with control diet without dichloroacetate (DCA0) (38% protein, 7% lipid and 45% corn starch) and the control diet supplemented with DCA, which inhibits PDKs through binding the allosteric sites, at 3.75 (DCA3.75), 7.50 (DCA7.50) and 11.25 g/kg (DCA11.25), for 6 wk. The results showed that DCA3.75, DCA7.50 and DCA11.25 significantly increased weight gain, carcass ratio and protein efficiency ratio (P < 0.05) and reduced feed efficiency (P < 0.05) of Nile tilapia. To investigate the effects of DCA on growth performance of Nile tilapia, we selected the lowest doseDCA3.75 for subsequent analysis. Nile tilapia fed on DCA3.75 significantly reduced the mesenteric fat index, serum and liver triglyceride concentration and total lipid content in whole fish, and down-regulated the expressions of genes related to lipogenesis (P < 0.05) compared to the control. The DCA3.75 treatment significantly improved glucose oxidative catabolism and glycogen synthesis in the liver, but significantly reduced the conversion of glucose to lipid (P < 0.05). Furthermore, the DCA3.75 treatment significantly decreased the PDK2/4 gene and protein expressions (P < 0.05), accordingly stimulated PDHE1α activity by decreasing the phosphorylated PDHE1α protein level. In addition, DCA3.75 treatment significantly increased the phosphorylated levels of key proteins involved in insulin signaling pathway and glycogen synthase kinase 3β (P < 0.05). Taken together, the present study demonstrates that PDK2/4 inhibition by using DCA promotes glucose utilization in Nile tilapia by activating PDHE1α, and improving insulin sensitivity. Our study helps to understand the regulatory mechanism of glucose metabolism for improving dietary carbohydrate utilization in farmed fish.Item More simple more worse: Simple carbohydrate diets cause alterations in glucose and lipid metabolism in Nile tilapia (Oreochromis niloticus).(Elsevier, 2022-03-15) Wen-Hao Zhou; Chen-Chen Wu; Samwel Mchele Limbu; Rui-Xin Li; Li-Qiao Chen; Fang Qiao; Yuan Luo; Mei-Ling Zhang; Tao Han; Zhen-Yu DuDietary carbohydrates are widely used in aquafeeds as cheap energy source and improve quality of feeds. However, comprehensive assessment of the effects of dietary carbohydrate complexity on fish metabolism and liver health is currently lacking. This study investigated the effect of replacing 50% of starch by using sucrose, fructose and glucose. Four isonitrogenic (400 g/kg protein) and isolipidic (60 g/kg fat) feeds containing starch (polysaccharide), sucrose (disaccharide) and fructose and glucose (monosaccharides) were fed to three replicates of 4.5 ± 0.30 g Nile tilapia (Oreochromis niloticus) for eight weeks. Afterwards, growth performance, feed utilization efficiency, glucose and lipid metabolism and liver health were evaluated. The results showed that the Nile tilapia fed on monosaccharide diets had significantly lower growth and feed utilization efficiency than those fed on disaccharide and polysaccharide diets. The Nile tilapia fed on monosaccharide diets reduced significantly lipid deposition, hepatosomatic index (HSI), serum alanine transaminase (ALT) and aspartate aminotransferase (AST) and expression of lipid metabolism genes than those fed on polysaccharide diet. The Nile tilapia fed on disaccharide diet increased significantly the serum insulin, muscle glycogen, and muscle glycogen synthase (gs) gene expression compared with those fed on polysaccharide diet. Interestingly, the Nile tilapia fed on monosaccharide diets reduced significantly the glycogen content while they increased insulin, glucose and the expression of liver gluconeogenesis genes such as glucose-6-phosphatase (g6pase) and phosphoenolpyruvate carboxykinase (pepck) than those fed on polysaccharide diet. Contrary, the Nile tilapia fed on disaccharide diet downregulated liver glucose catabolism and lowered serum triglyceride (TG) levels than those fed on polysaccharide but enhanced muscle peroxisome proliferator activated receptor alpha (pparα) and carnitine palmitoyltransferase 1a (cpt1a) gene expression, liver gluconeogenesis and pentose phosphate pathways. These results indicate that Nile tilapia utilizes better dietary polysaccharides and disaccharides than monosaccharides. Feeding Nile tilapia on monosaccharide diets caused insulin resistance and glucose metabolism disorders manifested by hyperinsulinism and hyperglycemia, respectively. The carbohydrate complexity affects the nutritional metabolism and liver health of fish.Item Reduced fatty acid β-oxidation improves glucose catabolism and liver health in Nile tilapia (Oreochromis niloticus) juveniles fed a high-starch diet. Aquaculture, 535 (2021) 736392. https://doi.org/10.1016/j.aquaculture.2021.736392(Elsevier, 2021-03-30) Ling-Yu Li; Yue Wang; Samwel Mchele Limbu; Jia-Min Li; Fang Qiao; Li-Qiao Chen; Mei-Ling Zhang; Zhen-Yu DuFish are poor users of dietary carbohydrates and often display prolonged hyperglycemia and fat deposition after feeding high digestible carbohydrate diets. Recently, fatty acid β-oxidation (FAO) inhibition has been reported to increase glucose oxidation in fish. Therefore, this study tested the assumption that the inhibition of FAO with mildronate (MD, a carnitine synthesis inhibitor) might also increase glucose utilization and alleviate adverse effects induced by high starch diet (HSD) in Nile tilapia, Oreochromis niloticus. Nile tilapia juveniles (6.13 ± 0.11 g) were cultured in nine 200-L tanks (30 fish per tank) and divided into three groups (three tanks per group). The fish were fed twice a day (9:00 and 18:30) at 4% body weight by using a normal starch diet (NSD, 30% corn starch), a HSD (45% corn starch), or a HSD supplemented with MD (25 g/kg of diet, HSD + MD) for eight weeks. These three feeds contained approximately 35.8% protein and 6.4% lipid. The fish each tank were weighed every two weeks, and the feeding amount was adjusted accordingly. After the feeding trial, the fish fed on HSD showed higher hepatosomatic index (HSI), visceral somatic index (VSI), serum triglyceride concentration and whole-body and tissue (liver and muscle) lipid contents than those fed on NSD. The fish fed on HSD also had higher relative area of vacuolation in the liver, hepatic malondialdehyde (MDA) content, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in the serum than those fed on NSD. Moreover, the fish fed on HSD increased serum glucose and insulin concentrations, and hepatic lactate, pyruvate and glycogen contents, but reduced whole-body protein content and dietary protein utilization than those fed on NSD, indicating that HSD induced fat deposition, liver damage, glucose intolerance and lowered protein-sparing effect. However, the fish fed on HSD + MD decreased hepatic carnitine content and FAO activity, attenuated the indexes related to fat deposition and liver damage, improved blood glucose clearance and whole-body protein deposition than those fed on HSD, suggesting that the adverse effects caused by HSD were reversed after FAO inhibition. Furthermore, the fish fed on HSD down-regulated the expression of genes associated with glucose uptake, glycolysis, FAO process, and lipolysis compared to those fed on HSD + MD and NSD, yet up-regulated lipogenic and proteolytic genes. These data suggested that inhibition of FAO improved glucose utilization and alleviated the HSD-induced adverse effects in Nile tilapia. This work demonstrates that, modifying mitochondrial FAO activity regulates the ability of fish to adapt to HSD intake through remodeling energy homeostasis. Our study provides new insights into improving carbohydrate utilization in aquatic animals.Item The responses of germ-free zebrafish (Danio rerio) to varying bacterial concentrations, colonization time points and exposure duration. Frontiers in Microbiology 10; Article 2156; 1 - 13.(Frontiers Media SA, 2019-09-18) Fang Tan; Samwel Mchele Limbu; Ye Qian; Fang Qiao; Zhen-Yu Du; Meiling ZhangColonizing germ-free (GF) zebrafish with specific bacterial species provides the possibility of understanding the influence on host biological processes including gene expression, development, immunity, and behavioral responses. It also enlightens our understanding on the host-microbe interactions within the physiological context of a living host. However, the responses of GF zebrafish to various colonization conditions such as bacterial concentrations, colonization time points, and exposure duration remain unclear. To address this issue, we explored the responses of GF zebrafish by using two bacterial species at varying concentrations, colonization time points and exposure duration. Therefore, we mono-associated GF zebrafish with Escherichia coli DH5α or Bacillus subtilis WB800N at concentrations ranging from 102 to 107 CFU/ml either at 3 day post fertilization (dpf) or 5 dpf for 24 or 48 h. We evaluated the responses of GF zebrafish by analyzing the survival rate, colonization efficiency, nutrients metabolism, intestinal cell proliferation, innate immunity, stress, and behavior responses by comparing it to conventionally raised zebrafish (CONR) and GF zebrafish. The results indicated that the final bacteria concentrations ranging from 102 to 104 CFU/ml did not cause any mortality when GF mono-associated larvae were exposed to either E. coli DH5α or B. subtilis WB800N at 3 or 5 dpf, while concentrations ranging from 106 to 107 CFU/ml increased the mortality, particularly for 5 dpf owing to the decrease in dissolved oxygen level. The E. coli DH5α mainly induced the expression of genes related to nutrients metabolism, cell proliferation and immunity, while B. subtilis WB800N mainly upregulated the expression of genes related to immunity and stress responses. Moreover, our data revealed that GF zebrafish showed higher levels of physical activity than CONR and the microbial colonization reduced the hyperactivity of GF zebrafish, suggesting colonization of bacteria affected behavior characteristics. This study provides useful information on bacterial colonization of GF zebrafish and the interaction between the host and microbiota.