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The aim of this study was to evaluate the combination of maximum replacement of fishmeal (FM) and fish oil (FO) by alternative meals (AM) and oils (AO) to develop nutritious, but more eco-friendly diets for European sea bass ( Dicentrarchus labrax ) juveniles. European sea bass of 9.8 ± 1.5 g and 9.1 ± 0.5 cm were fed nine isonitrogenous (45% crude protein) and isolipidic (21%) diets containing gradually reduced levels of FM and FO as follows (%FM/%FO): 58/15, 20/6, 20/3, 10/6, 10/3, 5/6, 5/3 and 0/0. Another diet, 0/0 + , was similar to the 0/0 but supplemented with LC-PUFA from microbial and marine sources. After 90 days of feeding, European sea bass fed the 0/0 diet showed reduced (P < 0.05) final weight, final length, condition factor, perivisceral fat index and viscero-somatic index as well as feed efficiency, whereas addition of LC-PUFA significantly improved daily growth index (DGI) (0/0 + diet). Reduction of FM/FO down to 5/3 did not significantly affect fish survival or condition factor, whereas reduction to 5/6 did neither affect sea bass length or feed conversion and reduction down to 10/3 did not affected body weight, DGI and perivisceral fat or visceral weight. FM reductions down to 5% significantly reduced growth rate. FO substitution by vegetable oils (VO) led to reduced growth and increased liver to body weight ratios, liver lipid deposition and hepatocellular size. In liver and muscle, FO substitution increased n-6 fatty acids (FA) and n-6/n-3 ratio and reduced saturated FA and n-3 LC-PUFA, whereas monounsaturated FA were not increased in proportion to dietary contents. Moreover, FO reduction increased the products from Δ6 desaturase and elongases, Elovl6 and Elovl5. In conclusion, the results of this study show that it is possible to reduce dietary FM and FO levels down to 10% and 3% in mostly plant-based diets without affecting growth performance of European sea bass juveniles. [ABSTRACT FROM AUTHOR]

Background and study aims The complex series of deleterious events among diabetes patients leads to multiple organ failure. Therefore, a holistic approach of treatment is urgently required to prevent worsening of complications. The present investigation was carried out to study the possible protective effects of Roselle or Hibiscus sabdariffa Linn (HSL) calyxes aqueous extract, as an antidiabetic and antioxidant agent against oxidative liver injury in streptozotocin-induced diabetic rats. Material and methods A single dose of streptozotocin (45 mg/kg body weight, iv) was used to induced diabetes in male Sprague Dawley rats which were then divided into two groups: Diabetic control (DC) and HSL-treated diabetic (DR) group. Normal rats were divided into normal control (NC), HSL-treated control (NR). Aqueous calyxes extract of HSL (100 mg/kg/day, orally) was given for 28 consecutive days in the treated group. Weight, biochemical and histopathological (light and electron microscopic) parameters were compared in all groups. Results Supplementation of HSL significantly lowered the level of fasting blood glucose and increased plasma insulin level in DR group compared to DC group (p < 0.05). Alanine aminotransaminases and aspartate aminotransferase enzymes level were found to be significantly reduced in DR compared to DC. Microscopic examination demonstrated destruction of the liver architecture, cytoplasmic vacuolation of the hepatocytes and signs of necrosis in diabetic rats. Moreover, dilatation and congestion of blood vessels with leucocytes adherence were detected. Ultrastructural study using electron microscope showed homogeneous substance accumulation in nuclear chromatin, a decrease of organelles and mitochondrial degeneration in the diabetic rats. Conclusion Administration of HSL in diabetic rats causes significant decrease in hepatocyte destruction and prevented the changes associated with the diabetic condition. Thus, our findings provide a scientific rationale for the use of HSL as promising agent in preventing liver injury in diabetes. [ABSTRACT FROM AUTHOR]

Abstract: It was estimated, in a rat model of moderate and relatively high chronic human exposure to cadmium (Cd), whether enhanced zinc (Zn) consumption may prevent Cd-induced liver injury and if the possible protective effect of this bioelement depends on its intake. For this purpose, the structure and function of the liver of the rats that received Zn (30 and 60mg/l) or/and Cd (5 and 50mg/l) for 6months were evaluated. The treatment with Cd led to, dependent on the exposure level, pathological changes in the liver, including enhanced apoptosis and induction of inflammatory and necrotic processes. Moreover, the serum activities of hepatic marker enzymes (alanine transaminase and aspartate transaminase) and the concentration of proinflammatory cytokine – tumor necrosis factor α were increased. The supplementation with 30 and 60mg Zn/l (enhancing daily Zn intake by 79% and 151%, respectively) partially or totally prevented from some of the Cd-induced changes in the liver structure and function; however, it provided no protection from necrosis, and the administration of 60mg Zn/l during the higher Cd exposure even intensified this process. At both levels of Cd treatment, the use of 30mg Zn/l was more effective in preventing liver injury than that of 60mg Zn/l. The hepatoprotective impact of Zn may be explained, at least partly, by its antioxidative, antiapoptotic and anti-inflammatory action, ability to stimulate regenerative processes in the liver tissue, and indirect action resulting in a decrease in the liver pool of the non-metallothionein-bound Cd2+ ions able to exert toxic action. The results provide strong evidence that enhanced Zn consumption may be beneficial in protection from Cd hepatotoxicity; however, its excessive intake at relatively high exposure to Cd may intensify liver injury. [Copyright &y& Elsevier]

Abstract: Aim: To compare the effects of preoperative chemotherapy on liver parenchyma morphology, as well as morbidity and mortality after liver resection for colorectal liver metastases. Methods: Prospectively collected data on 173 patients undergoing liver resection for CLM between 1/2003 and 9/2005 was analysed in three groups: A: preoperative oxaliplatin (Ox, n =70); B: other chemotherapeutic agents (OC, n =60); and C: surgery alone without chemotherapy (SA, n =43). Blood transfusion, hospital stay, operative procedure, peak postoperative bilirubin levels, complications and histopathology of the resected liver were compared. Results: Intra-operative blood transfusion requirement (34%) and biliary complications (16%) was higher in patients receiving oxaliplatin-based chemotherapy (p =0.01 and p =0.06, respectively). Oxaliplatin-based chemotherapy was also associated with sinusoidal dilatation of mild grade in 52.8% vs. 26.6% and 23.3% patients (p =0.007 and p =0.004) in other groups, respectively. Steatosis was similarly distributed across the study group. Postoperative mortality was 2, 1 and 4 patients, respectively (p =ns). Conclusion: Oxaliplatin-based preoperative chemotherapy is associated with vascular alterations in the liver parenchyma without significantly increasing the risk of steatosis, or postoperative morbidity and mortality. [Copyright &y& Elsevier]

Summary: This study investigated the possible protective effects of melatonin as an antioxidant against streptozotocin (STZ)-induced diabetic liver injury in rats. Wistar rats were divided into four groups: untreated control (UC), melatonin-treated control (MC), untreated diabetic (UD), and melatonin-treated diabetic (MD). Experimental diabetes was induced by a single-dose (60mg/kg, intraperitoneally (ip)) STZ injection, and melatonin was injected (200μg/kg/day, ip) for 4 weeks. Upon light and electron microscopic examination, we observed that melatonin improved the morphological and histopathological changes of the liver caused by diabetes. Malondialdehyde levels in the liver homogenates of UD rats were higher than those of controls and were markedly reduced after melatonin treatment. Although no significant difference was observed with respect to antioxidant status, the superoxide dismutase activity tended to be higher in the UD rats than in the treated rats. Our findings showed that melatonin administration partially reduced liver injury in STZ-induced diabetic rats. [Copyright &y& Elsevier]

Abstract: There are few reports of dietary copper (Cu) toxicity to warm water species of freshwater fish, and little is known about recovery from dietary Cu exposure. In this study Nile tilapia (Oreochromis niloticus) were fed to satiation on a Cu-loaded diet (2000mgCukg−1 dry weight (dw) feed), or a control diet (3mgCukg−1 dw feed), for 42 days. All fish were then fed the control diet for a further 21 days to assess recovery. Nutritional performance, haematology, histology, and tissue ion content (Cu, Na+, and K+) were measured. No mortalities occurred during the experiment. Dietary copper exposure was confirmed by elevated Cu concentrations in the intestine (30-fold), liver (three-fold) and gills (2.7-fold) of Cu-exposed fish compared to controls after 42 days (ANOVA, P <0.05). Copper-exposed fish showed a reduction in food intake, and weight gain by day 21 of exposure, compared to controls (ANOVA, P <0.05) and this persisted throughout the experiment. There were no treatment-dependent effects on food conversion ratio or hepatosomatic index, and all fish showed normal tissue Na+ and K+, and haematology throughout the experiment. Gill and intestine did not show overt pathology, but fatty change was observed in the liver of Cu-fed fish during exposure. The recovery phase on normal food was characterised by a reduction in intestinal and branchial Cu levels back to control values. However, the liver of the Cu-fed fish showed a further 1.7-fold rise in Cu content and marked hepatic lipidosis (increased intracellular fat stores) post-exposure, suggesting redistribution of Cu to the liver and delayed hepatotoxicity. [Copyright &y& Elsevier]

In the present study, we tested the hypothesis that dietary oligofructose (FOS) can modulate both the response to an endotoxic shock induced by lipopolysaccharide (LPS) administration and the activity of resident hepatic macrophages, i.e., Kupffer cells. Male Wistar rats (n = 5-9 per group) were fed a standard diet or a diet supplemented with 10 g/100 g FOS for 3 wk. LPS (10 mg/kg) or saline were injected i.p. after dietary treatment. After LPS injection, serum levels of tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine, and prostaglandin E(2) (PGE(2)), an immunosuppressive mediator, were higher in FOS-treated rats than in control rats. Alanine aminotransferase (ALT) activity was approximately 50% lower than in controls 24 h after LPS administration in FOS-treated rats, suggesting less hepatic injury; this was confirmed through histological analysis. FOS treatment increased the number of large phagocytic Kupffer cells, as assessed by histological examination of the liver after colloidal carbon injection into the portal vein. Precision-cut liver slices (PCLS) from FOS-treated rats released more TNF-alpha and PGE(2) into the incubation medium than PCLS from control rats, independently of LPS challenge in vitro. This would suggest that the higher Kupffer cell phagocytic activity and secretion capacity due to FOS supplementation improve LPS clearance in liver tissue and reduce hepatocyte alterations. This study supports the hypothesis that oligofructose might decrease liver tissue injury after endotoxic shock and sepsis. [ABSTRACT FROM AUTHOR]

Hepatobiliary characteristics of untreated obese patients and those of patients reducing weight through very-low-calorie diets (VLCDs) are reviewed. In untreated obesity, hepatobiliary abnormalities are prevalent. Fatty change is common and may be related to insulin resistance. Moreover, portal inflammation and fibrosis are prevalent findings, also in the absence of alcohol abuse. The liver plays a key role in the hyperinsulinism and hyperlipidemia, and hepatic drug metabolism is influenced by enhanced glucuronidation and sulphatation. Predisposition to gallstone formation can be ascribed to increased biliary cholesterol secretion in concert with changed nucleating factors and altered gallbladder motility. Weight loss by VLCD reduces fatty change but may induce slight portal inflammation and fibrosis. Insulin resistance and pharmacokinetic abnormalities regress. During VLCD the risk of gallstone formation is markedly increased. The deleterious effects described of a rapid weight loss should draw some attention to the liver and biliary tract during VLCD treatment. [ABSTRACT FROM AUTHOR]

To investigate the growth and metabolic responses of largemouth bass (Micropterus salmoides) to dietary vitamin c supplementation levels, quadruplicate groups of 30 largemouth bass juveniles were fed eight experimental diets with graded level of VC in cages floated in concrete tanks for 60 days. The result showed that growth, survival rate and digestive enzyme activity were strongly positively influenced by AMP100, AMP125 and AMP150. Treatment AMP125 significantly (P < 0.05) enhanced growth compared with AMP0, AMP25, AMP50 and AMP75. Tissue VC increased as VC level in diet increased, whole body crude protein and moisture were influenced by dietary VC supplementation. Dietary VC significantly influenced muscle amino acid and hepatic amino acyl transferase activity. Furthermore, AMP100, AMP125, AMP150 and AMP175 significantly triggered the up-regulation of Insulin-like growth factors (IGFs) and growth hormone (GH) gene mRNA expression level in liver and muscle compared with AMP0. Also, AMP125 and AMP150 maintained liver morphology. Nevertheless, dietary VC enhances digestive enzyme activity, hepatic amino acyl transferase activity and growth-related gene mRNA expression. Therefore, 120.46–145.35 mg/kg is adequate to improve the utilization of amino acid for growth, expression of growth-related genes and liver integrity in juvenile largemouth bass. • Dietary VC significantly increases digestive enzyme and hepatic amino acyl transferase activity. • Dietary VC significantly enhances muscle amino acid usage for growth. • Dietary VC significantly up-regulates IGFs and GH genes. • Dietary VC 120.46–145.35 mg/kg improves liver integrity in largemouth bass. [ABSTRACT FROM AUTHOR]

• Vaccine using rLPG3 in mice improves the liver enzymatic antioxidant defenses. • rLPG3 + SAP vaccine preserves hepatic architecture and reduces granuloma formation in L. infantum chagasi infection. • rLPG3 + SAP vaccine reduces the hepatic parasitism in 99 % in mice infected with L. infantum chagasi. In this work, we aimed to evaluate the effects of the Leishmania infantum chagasi infection on the liver of vaccinated mice, considering parameters of tissue damage and the inflammatory response elicited by vaccination. We used recombinant LPG3 protein (rLPG3) as immunogen in BALB/c mice before challenge with promastigote forms of L. infantum chagasi. The animals were separated into five groups: NI: non-infected animals; NV: non-vaccinated; SAP: treated with saponin; rLPG3: immunized with rLPG3; rLPG3 + SAP: immunized with rLPG3 plus SAP. The experiment was conducted in replicate, and the vaccination protocol consisted of three subcutaneous doses of rLPG3 (40 μg + two boosters of 20 μg). The mice were challenged two weeks after the last immunization. Our results showed that rLPG3 + SAP immunization decreased the parasite burden in 99 %, conferring immunological protection in the liver of the infected animals. Moreover, the immunization improved the antioxidant defenses, increasing CAT and GST activity, while reducing the levels of oxidative stress markers, such as H 2 O 2 and NO 3 /NO 2, and carbonyl protein in the organ. As a consequence, rLPG3 + SAP immunization preserved tissue integrity and reduced the granuloma formation, inflammatory infiltrate and serum levels of AST, ALT, and ALP. Taken together, these results showed that rLPG3 vaccine confers liver protection against L. infantum chagasi in mice, while maintaining the liver tissue protected against the harmful inflammatory effects caused by the vaccine followed by the infection. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the effects of dietary fish oil replacement by soybean oil and l -carnitine supplementation on growth performance, fatty acid composition, plasma biochemical parameters, lipid metabolism, hepatic antioxidant ability and morphology of juvenile largemouth bass, Micropterus salmoides. Five isonitrogenous and isoenergetic experimental diets were formulated by replacing 0 (Diet 1), 50% (Diet 2) and 100% (Diet 3) of fish oil by soybean oil, and 50% (Diet 4) and 100% (Diet 5) of fish oil by soybean oil supplemented with 0.02% l -carnitine. After 8 weeks of growth trial, dietary fish oil replacement by soybean oil and l -carnitine supplementation significantly increased final body weight and weight gain rate except for fish fed Diet 3 (P < 0.05). No significant effects were observed in the composition of back muscle and liver among all groups (P > 0.05). Dietary fish oil replacement by soybean oil not only caused oxidative stress and liver damage, but also decreased the content of long-chain polyunsaturated fatty acid such as ARA, EPA and DHA in muscle and liver of fish. However, dietary l -carnitine supplementation could improve growth performance, lipid metabolism and liver health of fish. In conclusion, 50% of fish oil can be replaced by soybean oil with no adverse effects on growth performance, plasma biochemical parameters and liver health, and dietary 0.02% l -carnitine supplementation was beneficial to the health of fish fed dietary fish oil replacement by soybean oil. • It was possible to replace dietary fish oil (FO) with soybean oil (SO) in diets of largemouth bass. • Dietary FO replacement by SO caused oxidative stress and liver damage. • Dietary l -carnitine supplementation was beneficial to the health of fish fed dietary FO replacement by SO. [ABSTRACT FROM AUTHOR]