As a precursor to creatine, guanidinoacetic acid (GAA) is widely recognized to enhance growth performance and flesh quality of animals, but the underlying molecular mechanism remains unclear. This study evaluated the effects of dietary GAA supplementation on growth performance, textural properties, and flavor constituents in gibel carp CAS V (Carassius gibelio, CAS V). A total of 300 healthy gibel carp (5.01 ± 0.13 g) at 42 d of age were assigned randomly to 12 tanks (3 replicates per group, 25 fish per replicate). Fish were fed with a basal diet supplemented with graded levels of GAA (0.00, 0.03%, 0.06%, and 0.12%) for 10 weeks. Results demonstrated that GAA supplementation significantly enhanced the specific growth rate (SGR) and crude protein content in gibel carp (P < 0.05). It also enhanced muscle physicochemical attributes by increasing water holding capacity and hardness, along with boosting glycogen content and free glutamate level (P < 0.05). Mechanistically, GAA promoted myofiber development by upregulating protein and gene expression of myogenic regulatory factors (MRFs), leading to increase myofiber density and a higher frequency of myofibers with diameters between 20 and 40 μm (P < 0.05). Furthermore, GAA facilitated collagen synthesis to improve muscle hardness by activating the transforming growth factor-beta 1 (TGF-β1)/mothers against decapentaplegic homolog (SMADs) signaling pathway, upregulating transcript levels of tgf-β1, col1α1, col1α2, and smad3 (P < 0.05). Additionally, GAA increased inosine monophosphate (IMP) content in muscle (P = 0.015), which was associated with enhanced expression of AMPD1 protein and upregulation of the adsl, pkm, and ckm genes (P < 0.05). In conclusion, dietary GAA supplementation enhanced flesh quality of gibel carp via improving growth performance, nutrient deposition, texture characteristics, and flavor components.

Atractylodes macrocephala polysaccharide (AMP) exhibits antioxidant, anti-inflammatory, and intestinal protective properties. However, its effective dietary supplementation level in aquaculture remains unclear. This study aimed to define the effective range and optimal supplementation level of dietary AMP in largemouth bass (Micropterus salmoides). Fish (initial weight 3.41 +/- 0.01 g) were fed diets containing 0, 100, 200, 400, 600, and 1200 mg/kg AMP for 10 weeks. Dietary AMP improved growth performance, with 400 mg/kg producing the most consistent enhancement in weight gain rate and feed utilization. AMP supplementation at 200 mg/kg enhanced antioxidant capacity and modulated the Nrf2/Keap1 pathway, while 100-600 mg/kg reduced apoptosis-related responses and improved intestinal morphology and barrier function. Correlation analysis further revealed that antioxidant capacity was positively associated with intestinal barrier integrity and growth performance, but negatively associated with oxidative stress and apoptosis-related indices, indicating coordinated physiological responses to dietary AMP supplementation. Overall, dietary AMP exerted beneficial effects on growth and health status in largemouth bass, and 400 mg/kg is suggested as an effective and practical supplementation level based on integrated physiological responses.

Fish exhibit limited efficiency in carbohydrate utilization, necessitating research to enhance their metabolic capacity for carbohydrates. Mitochondrial fatty acid beta-oxidation (FAO) inhibition might alter carbohydrate utilization and reduce protein consumption, thereby remodeling energy homeostasis. To clarify the energy allocation in gibel carp (Carassius gibelio var. CAS V) under impeding mitochondrial FAO, diets supplemented with or without the carnitine palmitoyltransferase 1 (Cpt1) inhibitor etomoxir (ETO; 0.25 g/kg) were fed to gibel carp for 8 weeks, followed by glucose tolerance tests (GTT). The results showed that mitochondrial FAO inhibition induced ectopic lipid deposition and upregulated peroxisomal FAO. Additionally, enhanced phosphorylation level of protein kinase B (Akt) protein indicated ameliorated insulin sensitivity. Concurrently, the upregulation of gk and glut4 and the downregulation of fbp evidenced the increased glucose utilization and led to the reduced glycogen accumulation. Furthermore, significantly changed metabolites (SCMs) related to amino acids were upregulated, and differentially expressed genes (DEGs) participating in amino acid biosynthesis were identified. These molecular changes and increased protein content in muscle pointed to a protein deposition in gibel carp. In conclusion, mitochondrial FAO inhibition remodeled energy homeostasis by compensatory upregulation of peroxisomal FAO and glucose utilization, ulteriorly realizing muscle protein deposition in gibel carp.

In order to investigate the effect of sodium bicarbonate(NaHCO3)on intestinal damage in largemouth bass(Micropterus salmoides)under chronic high-temperature stress,juvenile largemouth bass(20.26±0.08)g were fed diets with or without sodium bicarbonate(NaHCO3,5 g/kg)for 8 weeks.The results showed that there was no significant difference in the specific growth rate in the NaHCO3 group compared to the control group at chronic high temperatures.However,the NaHCO3 group exhibited significantly improved feed efficiency,protein deposition rate,and protein effi-ciency,along with a marked increase in intestinal amylase and trypsin activities.The addition of NaHCO3 also signifi-cantly enhanced the intestinal total antioxidant capacity(T-AOC),catalase(CAT),superoxide dismutase(SOD),and glutathione peroxidase(GPx)activities.Furthermore,NaHCO3 up-regulated the expression of cat and gpx1a genes and down-regulated the gene expression of keap1.Meanwhile,the expressions of pro-inflammatory cytokines(il-1β,tnfα,and il15)were significantly down-regulated in the group,while the expression of anti-inflammatory cytokine il10 was up-regulated.In addition,the expression of hsp90,hsp70,and hsp60 genes in the intestines of largemouth bass in the NaHCO3 group was significantly lower than that in the control group.Histologic analysis of the intestinal tract showed that high-temperature stress induced intestinal damage in largemouth bass,and the addition of NaHCO3 significantly improved the intestinal tissue morphology and up-regulated the expression of intestinal zo1,jam,occludin,and muc2.In conclusion,the addition of 5 g/kg NaHCO3 to the feed effectively alleviated chronic high-temperature stress-induced intestinal damage in largemouth bass by improving intestinal antioxidant capacity,intestinal inflammation,and intesti-nal barrier function.These findings may provide a new perspective to improve the intestinal health of fish under high-temperature stress.

Aspartic acid, a nonessential amino acid, plays crucial roles in protein synthesis, tricarboxylic acid cycle, and glycolipid metabolism in mammals. However, corresponding studies of the role of aspartic acid in fish remain limited. This study aimed to investigate the effects of aspartic acid on physiological metabolism of triploid crucian carp (Carassius auratus). The fish (48.2 +/- 2.4 g) were administered with low (0.22 g/mL, LA) or high (0.44 g/mL, HA) concentrations of L-aspartic acid solution, while normal saline was given to the control group. The results demonstrated that plasma glucose levels in both the LA and HA groups were remarkably decreased at 3 h after administration, while hepatic glycogen content increased dramatically. Furthermore, compared to the LA group, the glucose levels in the HA group were noticeably higher at 6 h. Plasma free fatty acids were remarkably decreased in both the LA and HA groups compared to control group at 3 h after administration, whereas the HA group had considerably higher plasma total cholesterol levels than the LA group. Additionally, the gene expression levels of genes involved in synthesis of fatty acids (acc, srebp1 and fasn) were significantly higher in the liver of the HA group compared with the LA group. However, aspartic acid did not affect the gene expression of key enzymes involved in hepatic fatty acid beta-oxidation. Both the LA and HA groups had significantly higher plasma levels of free aspartic acid, glutamic acid, and total essential amino acids. Additionally, the gene expression level and enzymatic activity of hepatic aspartate aminotransferase were increased (P < 0.05). In conclusion, different doses of aspartic acid induced distinct physiological and metabolic responses in triploid crucian carp. High-dose aspartic acid enhanced amino acid metabolism in the liver, thus increasing the capacity for de novo synthesis of fatty acids.

This study investigated the responses of glucolipid metabolism in gibel carp, the CAS III strain (A strain, 7.14 f 0.23 g) and the Dongting strain (DT strain, 7.72 f 0.54 g), following acute hypoxia/reoxygenation. The effects of hypoxia (0.39 f 0.02 mg/L) and reoxygenation (8.30 f 0.30 mg/L) were examined in both strains after exposure for 2 h. The results revealed significantly enhanced PI3K/AKT pathway and AMPK/HIF-1 alpha pathways, along with upregulated expression of glucose-6-phosphatase (g6pase) and lipid synthesis-related genes (acc and fas) in both gibel carp strains following acute hypoxia (P < 0.05). The observed increase in plasma glucose levels during acute hypoxia may be related to elevated expression of g6pase (P < 0.05). Regarding the genotype, the A strain exhibited significantly higher expression of glucose metabolism-related genes (pk and pepck) in the liver compared to the DT strain (P < 0.05). Conversely, the expression of lipid metabolism-related genes (hsl, lpl, ppar alpha, cpt1a, and aco3) were significantly lower in the A strain compared to the DT strain (P < 0.05). In both strains of gibel carp, reoxygenation resulted in significant activation of the PI3K/AKT and AMPK/mTOR pathways, accompanied by upregulated expression of glucose metabolism-related genes (gk, 6pfk, foxo1a, fbpase, and pepck) and lipid synthesis-related genes (srebp-1, acly, and acc) (P < 0.05). Notably, the A strain exhibited increased transcripts of glucose metabolism-related genes (gk, pk, foxo1a, g6pase, and pepck) and lipid metabolism-related genes (acly, fas, and cpt1a) compared to the DT strain (P < 0.05). Overall, this study revealed distinct regulation patterns of glucolipid metabolism in the gibel carp with different genotype under acute hypoxia/reoxygenation.

Previous nutritional studies have shown that intermediate metabolism in early fish development is highly plastic, and thus we hypothesized that there may be an early programming effect of a hyperglucidic diet on carbohydrate utilization in gibel carp. To test our hypothesis, gibel carp CAS Ⅴ (mean body weight: 0.10 g) were fed a high-carbohydrate/low protein (HC/LP) or low carbohydrate/high protein (LC/HP) diet for three weeks, and then were fed with normal feed for 12 weeks and a hyperglucidic diet for one week. We found that early HC/LP stimulus inhibited growth performance but altered the expression of glucose metabolism genes. After long-term feeding on the normal diet, the effects of early HC/LP stimulus were eliminated; these involved plasma metabolites, hepatic cholesterol, glycogen and triglyceride content, and glucose and lipid metabolism. However, the early HC stimulus group showed a better ability to maintain plasma glucose hemostasis when again given the HC diet. The capacity of carbohydrate and lipid metabolism in juvenile gibel carp was improved in the early HC diet group, as indicated by upregulated expression of genes related to glycolysis, lipid transport (gk, akt, srebp1, acc, fas, hsl, and acly) and downregulated expression of genes involved in gluconeogenesis (fbpase). Moreover, the early HC diet significantly upregulated AKT protein expression levels. The DNA methylation levels of akt in the HC/LP group were significantly lower than those in the LC/HP group. Overall, the study suggests that early HC stimulus in juvenile gibel carp can result in better carbohydrate utilization through DNA methylation of critical elements in the insulin signaling pathway.

Ammonia is recognized as an environmental stressor for fish. As resveratrol (RES) has anti-inflammatory and antioxidant properties, we hypothesized that RES could attenuate the response to ammonia exposure in gibel carp. Therefore, gibel carp were fed a diet containing RES for eight weeks, followed by acute ammonia stimulation. Stress induced by acute ammonia exposure could be ameliorated by RES, manifested by down-regulated plasma glucose, and up-regulated C3 and IgM levels. Furthermore, decreased AST and LDH; enhanced T-AOC, SOD, and GPx in the liver; and reduced damage to gill and liver tissues indicated that RES attenuated oxidative and tissue damage induced by ammonia exposure. Moreover, RES activated the Nrf2/HO-1 pathway and up-regulated the expression of several antioxidant genes. RES enhanced anti-inflammatory activity as reflected by activation of the NF-κB pathway, down-regulated the expression of pro-inflammatory cytokines (nfκb, tnf-α, and il-1β), and up-regulated the expression of anti-inflammatory cytokines (il-4 and il-10). In terms of mitochondrial function, RES up-regulated protein levels of p-AMPK, SIRT1, and PGC-1α; inhibited mitochondrial fission; promoted mitochondrial fusion and biogenesis-related gene expression. Overall, the results suggest that RES mediated the Nrf2/HO-1, NF-κB, and AMPK/SIRT1/PGC-1α pathways to attenuate oxidative stress, inflammation, and mitochondrial dysfunction induced by ammonia in gibel carp.

Glutamate (Glu) plays important physiological roles in protein synthesis and muscle flesh quality. Despite existing studies on the effects of Glu on fish muscle quality, the underlying mechanism thereof remains unclear. To illustrate the effects of Glu on the flesh quality of triploid crucian carp, fish were fed a diet with added 3.2% Glu (no additional Glu was used as a control). Results showed that dietary Glu promoted the expression levels of genes related to the growth of muscle fibers, thereby promoting the development of the sarcolemma and regulating the hardness and springiness of muscle. Moreover, dietary Glu improved muscle protein deposition via AMPK/mTOR signaling pathway activation. Besides, aspartate, Glu, and inosine monophosphate (IMP) levels in muscle were markedly enhanced by dietary Glu supplementation. In summary, Glu improves flesh quality and growth of triploid crucian carp by regulating protein synthesis, protein retention and flavor compound deposition.

This study investigated the potential role of curcumin (CUR) in preventing oxidative stress and ferroptosis induced by ammonia exposure in gibel carp. Experimental fish (initial weight: 11.22 ± 0.10 g, n = 150) were fed diets supplemented with or without 0.5% CUR for 56 days, followed by a 24 h ammonia (32.5 mg/L) exposure. Liver damages (aspartate aminotransferase (AST), alanine aminotransferase (ALT), adenosine deaminase (ADA), and alkaline phosphatase (ALP)) and oxidative stress enzyme activities (reactive oxygen species (ROS), malondialdehyde (MDA); and the content of antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GPx)) were induced by ammonia stress. The antioxidant capacity was decreased, as indicated by inhibited gene expression of nuclear factor erythroid 2-related factor 2 (nrf2), heme oxygenase-1 (ho-1), catalase (cat), and sod. Ferroptosis was induced by ammonia stress, as suggested by upregulated mRNA levels of nuclear receptor coactivator 4 (ncoa4), transferrin receptor 1 (tfr1), and iron-responsive element-binding protein 2 (ireb2), and downregulated expression of glutathione peroxidase 4 (gpx4), ferroportin (fpn), and ferritin heavy chain 1 (fth1). In addition, both mRNA and protein levels of ferroptosis markers acyl-CoA synthetase long-chain family member 4 (ACSL4) and prostaglandin-endoperoxide synthase 2 (PTGS2) were upregulated, while cystine/glutamate antiporter (SLC7A11) was downregulated. However, liver injury and ferroptosis in fish induced by ammonia could be attenuated by CUR. Collectively, these findings demonstrate that CUR ameliorates oxidative stress and attenuates ammonia stress-induced ferroptosis. This study provides a new perspective on potential preventive strategies against ammonia stress in gibel carp by dietary CUR.

Introduction Resveratrol (RES) is a polyphenol organic compound with antioxidant and anti-inflammatory properties. This study aimed to determine whether and how RES can alleviate liver injury in lipopolysaccharide (LPS)-induced gibel carp. Methods Gibel carp were fed a diet with or without RES and were cultured for 8 weeks, followed by LPS injection. Results and discussion The results suggested that RES attenuated the resulting oxidative stress and inflammation by activating the Nrf2/Keap1 pathway and inhibiting the NF-κB pathway, as confirmed by changes in oxidative stress, inflammation-related gene expression, and antioxidant enzyme activity. Furthermore, RES cleared damaged mitochondria and enhanced mitochondrial biogenesis to mitigate reactive oxygen species (ROS) accumulation by upregulating the SIRT1/PGC-1α and PINK1/Parkin pathways and reducing p62 expression. Overall, RES alleviated LPS-induced oxidative stress and inflammation in gibel carp through mitochondria-related mechanisms.

Atractylodes macrocephala polysaccharide (AMP) can enhance antioxidant defense and anti-inflammation, as the tolerance levels of AMP in aquaculture is important for additive utilization. However, the tolerance dose of AMP is unknown. We assess the tolerance levels of AMP in juvenile largemouth bass (3.38 ± 0.11 g) by feeding them a 0, 400, 4000, or 8000 mg/kg AMP supplemented diet for 10 weeks. The 400 mg/kg AMP dose increased growth performance. The Nrf2/Keap1 signaling pathway was activated, as indicated by Keap1 and Nrf2 protein levels in the liver. Enhanced activity of antioxidant enzymes (SOD, GPx), together with increased mRNA levels of antioxidant genes (sod, gpx) and decreased accumulation of reactive oxygen species (ROS) and MDA, was found in the liver, implying the antioxidant effect of AMP. Nutrient absorption was enhanced by AMP, as reflected by the increased length of intestinal villi and microvilli. However, 4000 and 8000 mg/kg AMP induced oxidant stress, as indicated by increased plasma ALT and AST content and decreased mRNA levels of antioxidant genes (sod, gpx) in the liver and intestinal tissues. Inflammatory reactions were also induced by high doses of AMP, as reflected by enhanced levels of pro-inflammatory cytokines (tnfα, nfκb) in the liver, intestinal, and kidney tissues and inhibited levels of anti-inflammatory cytokines (tgfβ, iκb). Histological analysis reveals inflammatory cell infiltration and tissue damage. Thus, the safe tolerance margin of AMP supplement for largemouth bass was 400–4000 mg/kg.

Previous studies have found that vitamin C (VC) has protective effects in fish. However, the efficacy of VC on hypoxia-induced liver injury in fish remains unknown. Therefore, to investigate the protective mechanism of VC on liver injury after acute hypoxic stimulation in fish, gibel carp were fed a diet containing VC for eight weeks, then were subjected to acute hypoxia stimulation. The specific growth rate of fish was increased by the supplementation of VC. Plasma stress markers (glucose, lactic acid, and cortisol) were decreased by the VC supplementation. Moreover, the levels of the inflammatory cytokines (tnf-α, il-2, il-6, and il-12) were increased by enhancing the Nrf2/Keap1 signaling pathway. Upregulation of the antioxidant enzymes activity (CAT, SOD, and GPx); T-AOC; and anti-inflammatory factors (il-4 and tgf-β) highlighted the antioxidant and anti-inflammatory activities of VC. The results showed that VC reduced the apoptotic index of the fish hypothalamus. The expression of GRP78 protein in the liver and endoplasmic reticulum stress and apoptosis induced by hypoxia were inhibited by VC. Taken together, the results indicate that VC can attenuate oxidative damage, inflammation, and acute hypoxia induced apoptosis in gibel carp via the Nrf2/Keap1 signaling pathway. The results identify a new defense strategy of gibel carp in response to hypoxic conditions.

实验以初重为(11.33±0.03)g的异育银鲫(Carassius auratus gibelio)为研究对象,分别投喂脂肪水平为4％(L4)、8％(L8)、12％(L12)、16％(L16)和20％(L20)的5种等氮饲料进行为期340d的长养殖周期实验,以探究饲料脂肪水平对长养殖周期异育银鲫生长性能、消化酶活性和脂代谢的影响.期间共取样5次,生长阶段分为63d(D63,幼鱼期)、110d(D110,养成前期)、223d(D223,越冬期)、275d(D275,越冬后)和340d(D340,养成中后期).实验结果显示,以增重率为评价指标,幼鱼期D63的异育银鲫适宜脂肪水平为8％,养成前期D110的异育银鲫适宜脂肪水平为12％,而其他生长阶段饲料脂水平对增重率无显著影响.饲料脂肪水平对幼鱼期异育银鲫肠道消化酶活性有显著影响,脂肪酶活性随脂肪水平的升高呈现先降低后升高的趋势,幼鱼期(D63)异育银鲫肠道胰蛋白酶和淀粉酶活性高于越冬期和养成中后期的异育银鲫,表明幼鱼期的异育银鲫对脂肪的利用较低.幼鱼期(D63)异育银鲫脂肪合成相关基因pparγ和fas的表达量饲料脂肪水平升高呈先升高后下降的趋势,且在L8组表达量最高,而脂解基因lpl和cpt1a的表达量在低脂组L4显著低于其他各组.pparγ和cpt1a在越冬后期(D275)的表达量随饲料脂肪水平的升高呈现先上升后下降,而fas表达量在L4组显著高于其他组,表明不同生长阶段异育银鲫对饲料脂肪摄入的响应策略不一致,摄入过高或过低均会导致代谢紊乱.适宜的脂水平(8％—12％)可促进幼鱼期和养成前期异育银鲫的生长,增强脂肪利用率和脂代谢能力,而较大规格的异育银鲫对脂肪的变化不敏感.

To investigate the physiological responses to different energy sources under feeding restriction in fish, gibel carp were fed a high lipid, low carbohydrate diet (HL diet, 12% lipid, 16% carbohydrate) or a high carbohydrate, low lipid diet (HC diet, 34% carbohydrate, 4% lipid) to satiation or 70% satiation (restriction) for 56 d; then, growth performance, nutrient metabolism, endoplasmic reticulum (ER) stress, autophagy, and apoptosis were determined. Fish that were fed the HL diet had higher final body weight, specific growth rate, and feed efficiency, lower phosphorylation levels of AKT and mTOR proteins and lower mRNA levels of gk than the HC group. When fed to 70% satiation, fish had lower feed intake, feeding rate, final body weight, and specific growth rate, and lower plasma glucose and nonesterified fatty acid levels. Feeding restriction induced the transcript level of gk and suppressed the mRNA level of acly, acc, fas. There were no significant differences in ER stress, autophagy and apoptosis between feeding levels or diets. Interactions between feeding level and diet were observed in plasma triglyceride level and the gene expression levels of fbpase and srebp1. Thus, gibel carp utilized HL diet better than HC diet, which was unalerted by feeding restriction.

Previous studies have shown that emodin (EMO) has a wide range of pharmacological activities, with the potential to protect against a variety of diseases. However, it is not clear whether EMO can alleviate impairment induced by acute hypoxia in gibel carp. Thus, an acute hypoxia experiment was conducted using gibel carp fed with EMO diets for eight weeks. The results showed that EMO decreased hypoxia signaling by down-regulating protein levels of hypoxia-inducible factor (HIF-1α). This also protected the liver from oxidative damage induced by acute hypoxia, as indicated by the upregulation of mRNA levels and antioxidant enzyme activity of genes related to nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. Moreover, EMO also inhibited endoplasmic reticulum (ER) stress in the liver and hypothalamus induced by acute hypoxia. EMO enhanced autophagy and inhibited apoptosis in gibel carp by mediating the AMPK/mTOR signaling pathway. Overall, EMO could alleviate impairment in gibel carp induced by acute hypoxia via the AMPK/mTOR pathway.

Our previous studies in gibel carp (Carassius gibelio) have shown that cadmium (Cd) exposure elicits deleterious effects depending on the genetic background, and thus we hypothesized that mitigation via nutritional intervention may vary between strains. Therefore, two gibel carp strains (the A and F strains) were fed diets supplemented with 0% or 1% taurine for 8 weeks prior to 96 h Cd exposure, and the responses of antioxidant pathways, endoplasmic reticulum (ER) stress, autophagy, and apoptosis were investigated. The results showed that taurine supplementation had no effect on the growth performance of gibel carp. After Cd exposure, histological damage to mitochondria and ER, induction of oxidative stress and antioxidant responses, occurrence of ER stress, and apoptotic signals were observed in the livers. Upon the diet effects, taurine supplementation alleviated the ER-stress-induced autophagy and apoptosis after Cd exposure and stimulated antioxidant pathways. Regarding the difference between strains, taurine played a protective role in alleviating Cd toxicity through the antioxidant response, ER stress, and autophagy in the F strain, whereas such effects were achieved by the attenuation of apoptosis in the A strain. Taken together, our results demonstrate the potential use of taurine in the mitigation of heavy metal toxicity in aquatic organisms.

实验以初重(6.20±0.01)g的团头鲂(Megalobrama amblycephala)幼鱼为研究对象,分别投喂高糖低脂(HCLL,45％糖和2％脂)、中糖中脂(MCML,30％糖和8％脂)和低糖高脂(LCHL,15％糖和14％脂)的3种等氮饲料56d,以探究饲料不同糖和脂水平对团头鲂生长性能、鱼体生化组成、营养沉积及血浆代谢物的影响.实验结果显示,饲料糖和脂水平对团头鲂摄食率无显著性影响.随饲料糖水平降低和脂水平升高,团头鲂幼鱼特定生长率和饲料效率提高.高糖低脂饲料未造成肝脏糖原或甘油三酯含量的显著沉积,且各饲料组间肝体比、脏体比及肥满度均无显著性差异.饲料糖和脂水平对团头鲂鱼体生化组成无显著性影响,但随饲料糖水平降低和脂水平增加,团头鲂蛋白沉积率升高,脂肪沉积率降低.另外,血浆葡萄糖、甘油三酯、游离脂肪酸和胆固醇含量各组间均无显著性差异.低糖高脂组血浆低密度脂蛋白胆固醇显著升高,表明肝脏将脂质转运至外周组织以维持肝脏脂稳态.研究结果表明,团头鲂对饲料脂利用优于糖类,且具有较好地应答饲料糖和脂水平的代谢机制,研究结果可为团头鲂的饲料配方设计提供支撑.

研究探讨了饲料淀粉对全养殖周期异育银鲫(Carassius auratus gibelio)生长性能和糖代谢的影响.实验以玉米淀粉为主要糖源,分别设计淀粉水平为3％(S3)、13％(S13)、23％(S23)、33％(S33)和43％(S43)的5种等氮等脂饲料,在长江故道江面网箱中饲养初始体重为(12.0±0.1)g的异育银鲫幼鱼340d,期间根据鱼体养成阶段共取样5次,生长阶段分为63d(D63,幼鱼期)、110d(D110,养成前期)、223d(D223,越冬期)、275d(D275,越冬后)和340d(D340,养成中后期).研究结果表明,幼鱼期D63异育银鲫后肠淀粉酶活力较低且对饲料淀粉水平变化不敏感,自养成前期D110之后鱼体后肠淀粉酶活力增强且随饲料淀粉水平的变化产生波动.幼鱼期D63异育银鲫glut2 mRNA相对表达量无显著差异,其他阶段异育银鲫glut2 mRNA相对表达量水平随饲料淀粉水平升高而升高.各个生长阶段异育银鲫糖酵解的敏感度高于糖异生代谢,幼鱼期D63与养成前期D110异育银鲫糖脂转化能力较强.幼鱼期D63异育银鲫适宜饲料淀粉水平为23％;养成前期D110异育银鲫适宜饲料淀粉水平减为13％;越冬后D275组异育银鲫整体代谢旺盛,43％淀粉组生长最好;而在养成中后期D340异育银鲫饲料淀粉需求则再次降到33％.研究结果表明,异育银鲫在养殖周期的不同阶段对饲料淀粉的需求和利用存在显著的差异,可以为异育银鲫不同养殖阶段特有饲料配方的设计提供支撑.

Normally, fish will decrease food intake or even stop feeding during the winter. In previous studies, two widely cultured gibel carp strains (strain A and strain F) showed differences in lipid and glucose metabolism. Therefore, we hypothesized that the physiological changes during the overwintering period would be different between the two strains. Thus, the two strains were starved for 77 days, after which the levels of glucose and lipid metabolism, ER stress, autophagy, and apoptosis were determined. The starvation increased hepatic glycogenolysis and fatty acid β-oxidation but suppressed lipogenesis in both strains overwintering. Considering the effects of genotype, strain F had higher levels of ER stress and autophagy but lower levels of apoptosis than strain A, suggesting that strain F might be more resistant to overwintering starvation. The interactions between strains and starvation periods were observed in plasma triglyceride contents and the mRNA levels of pyruvate kinase (pk), sterol regulatory element binding protein 1 (srebp1), activating transcription factor 4 (atf4), and autophagy protein 12 (atg12). In conclusion, long-term starvation during winter could induce hepatic glycogenolysis and fatty acid β-oxidation but suppress lipogenesis, ER stress, autophagy, and apoptosis in gibel carp, and strain F may be more resistant to starvation during winter. Taken together, these results discovered the responses to prolonged starvation stress during winter in two strains of gibel carp and could provide information for genotype selection, especially for selecting strains better adapted to winter.