Browsing by Author "Rui-Xin Li"

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    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 Luo
    The 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.
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    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 Du
    igh-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.
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    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 Du
    Long-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.
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    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.
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    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 Du
    Pyruvate 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.
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    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 Du
    Dietary 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.