Increased Liver Lipid Content Research Articles

ANGPTL3 Downregulation Increases Intracellular Lipids by Reducing Energy Utilization.

ANGPTL3 (angiopoietin-like protein 3) is a circulating protein with a key role in maintaining lipoprotein homeostasis. A monoclonal antibody against ANGPTL3 is an approved and well-tolerated treatment to reduce lipoproteins in familial hypercholesterolemia homozygotes. However, the reduction of hepatic ANGPTL3 synthesis using an antisense oligonucleotide unexpectedly resulted in a dose-dependent increase in liver lipid content and circulating transaminases, resulting in the termination of the clinical trial. Meanwhile, the use of silencing RNAs remains an area of active investigation. Our study sought to investigate whether intracellular downregulation of ANGPTL3 may lead to a primary increase in neutral lipids within the hepatocyte. We downregulated ANGPTL3 by silencing RNA in primary human hepatocytes 3-dimensional spheroids, HepG2/LX-2 3-dimensional spheroids, and in HepG2, Hep3B2, and Huh7 cultured in 2 dimensions. ANGPTL3 downregulation increased neutral lipids in all models investigated. Interestingly, ANGPTL3 induced lower intracellular deiodinase type 1 protein levels resulting in a reduction in beta-oxidation and causing an increase in triglycerides stored in lipid droplets. In conclusion, intracellular ANGPTL3 downregulation by silencing RNA led to an increase in triglycerides content due to a reduction in energy substrate utilization resembling a primary intracellular hepatocyte hypothyroidism.

GenX analogs exposure induced greater hepatotoxicity than GenX mainly via activation of PPARα pathway while caused hepatomegaly in the absence of PPARα in female mice

Despite their use as substitutes for perfluorooctanoic acid, the potential toxicities of hexafluoropropylene oxide dimer acid (HFPO-DA, commercial name: GenX) and its analogs (PFDMOHxA, PFDMO2HpA, and PFDMO2OA) remain poorly understood. To assess the hepatotoxicity of these chemicals on females, each chemical was orally administered to female C57BL/6 mice at the dosage of 0.5 mg/kg/d for 28 d. The contribution of peroxisome proliferator-activated receptors (PPARα and γ) and other nuclear receptors involving in these toxic effects of GenX and its analogs were identified by employing two PPAR knockout mice (PPARα−/− and PPARγΔHep) in this study. Results showed that the hepatotoxicity of these chemicals increased in the order of GenX < PFDMOHxA < PFDMO2HpA < PFDMO2OA. The increases of relative liver weight and liver injury markers were significantly much lower in PPARα−/− mice than in PPARα+/+ mice after GenX analog exposure, while no significant differences were observed between PPARγΔHep and its corresponding wildtype groups (PPARγF/F mice), indicating that GenX analog induce hepatotoxicity mainly via PPARα instead of PPARγ. The PPARα-dependent complement pathways were inhibited in PFDMO2HpA and PFDMO2OA exposed PPARα+/+ mice, which might be responsible for the observed liver inflammation. In PPARα−/− mice, hepatomegaly and increased liver lipid content were observed in PFDMO2HpA and PFDMO2OA treated groups. The activated pregnane X receptor (PXR) and constitutive activated receptor (CAR) pathways in the liver of PPARα−/− mice, which were highlighted by bioinformatics analysis, provided a reasonable explanation for hepatomegaly in the absence of PPARα. Our results indicate that GenX analogs could induce more serious hepatotoxicity than GenX whether there is a PPARα receptor or not. These chemicals, especially PFDMO2HpA and PFDMO2OA, may not be appropriate PFOA alternatives.

Reduced Insulin Clearance Differently Relates to Increased Liver Lipid Content and Worse Glycemic Control in Recent-Onset Type 2 and Type 1 Diabetes.

Diabetes may feature impaired insulin kinetics, which could be aggravated by altered hepatic metabolism and glycemic control. Thus, we examined insulin clearance and its possible determinants in individuals with recent-onset diabetes. Participants of the German Diabetes Study (GDS) with type 1 diabetes (T1D) (n = 306), type 2 diabetes (T2D) (n = 489), or normal glucose tolerance (control [CON]) (n = 167) underwent hyperinsulinemic-euglycemic clamps for assessment of whole-body insulin sensitivity (M value) and insulin clearance (ICCLAMP). Insulin clearance rates were further calculated during intravenous glucose tolerance tests (ICIVGTT) and mixed-meal tests (ICMMT). Hepatocellular lipid content (HCL) was quantified with 1H-MRS. Both T1D and T2D groups had lower ICCLAMP (0.12 ± 0.07 and 0.21 ± 0.06 vs. 0.28 ± 0.14 arbitrary units [a.u.], respectively, all P < 0.05) and ICMMT (0.71 ± 0.35 and 0.99 ± 0.33 vs. 1.20 ± 0.36 a.u., all P < 0.05) than CON. In T1D, ICCLAMP, ICIVGTT, and ICMMT correlated negatively with HbA1c (all P < 0.05). M value correlated positively with ICIVGTT in CON and T2D (r = 0.199 and r = 0.178, P < 0.05) and with ICMMT in CON (r = 0.176, P < 0.05). HCL negatively associated with ICIVGTT and ICMMT in T2D (r = -0.005 and r = -0.037) and CON (r = -0.127 and r = -0.058, all P < 0.05). In line, T2D or CON subjects with steatosis featured lower ICMMT than those without steatosis (both P < 0.05). Insulin clearance is reduced in both T1D and T2D within the first year after diagnosis but correlates negatively with liver lipid content rather in T2D. Moreover, insulin clearance differently associates with glycemic control and insulin sensitivity in each diabetes type, which may suggest specific mechanisms affecting insulin kinetics.

Effect of overconditioning on the hepatic global gene expression pattern of dairy cows at the end of pregnancy

Overconditioning is a risk factor for upregulated pre- and postpartum fat mobilization. Therefore, we hypothesized that overconditioning at the end of pregnancy leads to the accumulation of lipids in the liver and modifications of the hepatic gene expression pattern. The aim of this study was to evaluate the effect of normal- versus overconditioning on the hepatic transcriptomic profile of dairy cows at the end of pregnancy. Ten dry multiparous Holstein cows were killed 2 wk before expected calving. Body condition score (BCS) and backfat thickness (BFT) were evaluated, and blood samples for nonesterified fatty acids (NEFA) were taken before cows were killed. After cows were killed, liver biopsy samples were collected for further assessment of total lipids and RNA sequencing. Five cows were classified as normal-conditioned (median BCS = 3, range 2.75-3.5) and 5 as overconditioned (median BCS = 4, range 4-5). Regression models confirmed that normal-conditioned cows had lower BFT (1.29 ± 0.29 cm; least squares means ± standard error) and serum NEFA (0.16 ± 0.04 mmol/L) in comparison to overconditioned cows (3.14 ± 0.43 cm and 0.38 ± 0.07 mmol/L for BFT and NEFA, respectively). Total liver lipid percentage tended to be lower in normal- versus overconditioned cows (4.63 ± 0.40% and 6.06 ± 0.44%, respectively). In comparison to the mean liver lipid percentage of the normal- and overconditioned cows, 1 overconditioned cow had a relatively low (5.21%) and 1 normal-conditioned cow had a relatively high (6.07%) liver lipid percentage. Differentially expressed genes analysis (edgeR quasi-likelihood method) showed that normal-conditioned cows presented 11 upregulated and 12 downregulated genes in comparison to overconditioned cows. Linear discriminant analysis effects size revealed 133 differentially expressed genes between normal- versus overconditioned cows. Notably, the liver of normal-conditioned cows had upregulated genes associated with liver functionality (ALB, SELENOP, IGF1, and IGF2). On the other hand, overconditioned cows had upregulated genes associated with the acute-phase response (C3, HPX, and, LBP). High basal lipolysis in overconditioned cows at the end of pregnancy increased liver lipid content, and this may alter the hepatic gene expression pattern to a pro-inflammatory state.

Effects of different dietary oil sources on growth performance, antioxidant capacity and lipid deposition of juvenile golden pompano Trachinotus ovatus

Vegetable oils (VO) that are used to substitute fish oil in aquafeeds may affect, not only the fatty acid composition, but also lipid metabolism and distribution. The present study was designed to investigate this issue in juvenile golden pompano Trachinotus ovatus fed eight diets formulated with typical VO with widely varying fatty acid compositions including coconut oil (CO), palm oil (PO), oil-tea camellia seed oil (OTO), olive oil (OO), canola oil (CNO), peanut oil (PNO), linseed oil (LO) and perilla oil (PFO), in comparison with fish fed fish oil (FO). After the 8-week feeding trial, fish fed the CO diet had the highest growth performance, and higher general antioxidant capacities in serum and liver than in fish fed the other VO. The crude lipid content in whole body and expression levels of fas were lower in fish fed the FO, PFO and LO diets, while lipid contents and expression levels of scd were higher in fish fed the OTO and PNO diets. Other than fish fed the PFO diet, the total lipid contents of liver in other fish fed the other VO diets were higher than that in fish fed the FO diet, with the highest contents in fish fed the OTO and OO diets. The expression levels of genes involved in fatty acid catabolism and transport, namely pparα, cpt1 and apoB100, were higher in fish fed diet PFO than in fish fed the other diets. Comparing the fatty acid compositions of tissues and diets showed that 18:1n-9, 18:3n-3 (ALA) and 22:6n-3 (DHA) were preferentially deposited in tissues of pompano, with DHA preferentially deposited in polar lipids rather than neutral lipids. However, excessive dietary ALA in PFO did not lead to increased deposition of ALA, but increased liver lipid content. The present study showed that dietary lipid sources had significant influences on growth performance and antioxidant capacity, as well as on lipid deposition. Low dietary 18:1n-9, high n-3 long-chain polyunsaturated fatty acids and an appropriate ratio of ALA/LNA (18,2n-6) could reduce lipid deposition in pompano tissues, especially liver.

Hepatic Lipidomics and Molecular Imaging in a Murine Non-Alcoholic Fatty Liver Disease Model: Insights into Molecular Mechanisms.

An imbalance between hepatic fatty acid uptake and removal results in ectopic fat accumulation, which leads to non-alcoholic fatty liver disease (NAFLD). The amount and type of accumulated triglycerides seem to play roles in NAFLD progression; however, a complete understanding of how triglycerides contribute to NAFLD evolution is lacking. Our aim was to evaluate triglyceride accumulation in NAFLD in a murine model and its associations with molecular mechanisms involved in liver damage and adipose tissue-liver cross talk by employing lipidomic and molecular imaging techniques. C57BL/6J mice fed a high-fat diet (HFD) for 12 weeks were used as a NAFLD model. Standard-diet (STD)-fed animals were used as controls. Standard liver pathology was assessed using conventional techniques. The liver lipidome was analyzed by liquid chromatography–mass spectrometry (LC–MS) and laser desorption/ionization–mass spectrometry (LDI–MS) tissue imaging. Liver triglycerides were identified by MS/MS. The transcriptome of genes involved in intracellular lipid metabolism and inflammation was assessed by RT-PCR. Plasma leptin, resistin, adiponectin, and FABP4 levels were determined using commercial kits. HFD-fed mice displayed increased liver lipid content. LC–MS analyses identified 14 triglyceride types that were upregulated in livers from HFD-fed animals. Among these 14 types, 10 were identified in liver cross sections by LDI–MS tissue imaging. The accumulation of these triglycerides was associated with the upregulation of lipogenesis and inflammatory genes and the downregulation of β-oxidation genes. Interestingly, the levels of plasma FABP4, but not of other adipokines, were positively associated with 8 of these triglycerides in HFD-fed mice but not in STD-fed mice. Our findings suggest a putative role of FABP4 in the liver-adipose tissue cross talk in NAFLD.

Hydrogen inhalation alleviates nonalcoholic fatty liver disease in metabolic syndrome rats.

Hydrogen exhibits therapeutic and preventive effects against various diseases. The present study investigated the potential protective effect and dose-dependent manner of hydrogen inhalation on high fat and fructose diet (HFFD)-induced nonalcoholic fatty liver disease (NAFLD) in Sprague-Dawley rats. Rats were randomly divided into four groups: i) Control group, regular diet/air inhalation; ii) model group, HFFD/air inhalation; iii) low hydrogen group, HFFD/4% hydrogen inhalation; and iv) high hydrogen group, HFFD/67% hydrogen inhalation. After a 10-week experiment, hydrogen inhalation ameliorated weight gain, abdominal fat index, liver index and body mass index of rats fed with HFFD and lowered the total area under the curve in an oral glucose tolerance test. Hydrogen inhalation also ameliorated the increase in liver lipid content and alanine transaminase and aspartate transaminase activities. Liver histopathologic changes evaluated with hematoxylin and eosin as well as Oil Red O staining revealed lower lipid deposition in hydrogen inhalation groups, consistent with the decrease in the expression of the lipid synthesis gene SREBP-1c. The majority of the indicators were affected following treatment with hydrogen in a dose-dependent manner. In conclusion, hydrogen inhalation may play a protective role by influencing the general state, lipid metabolism parameters, liver histology and liver function indicators in the rat model of metabolic syndrome with NAFLD.

Effect of high chronic intake of sucrose on liver metabolism in aging rats. Modulation by rutin and micronutrients.

High-sugar intake and senescence share common deleterious effects, in particular in liver, but combination of these two factors was little studied. Our aims were to examine the effect of a high-sucrose diet in liver of old rats and also the potential benefices of a polyphenol/micronutrient supplementation. Four groups of 22-month-old male rats fed during 5months with a diet containing either 13 or 62% sucrose, supplemented or not with rutin, vitamin E, A, D, selenium, and zinc were compared. We measured liver macronutrient composition, glycation/oxidative stress, enzyme activities (lipogenesis, β-oxidation, fructokinase), gene expression (enzymes and transcription factors), in vivo protein synthesis rates and plasma parameters. Sucrose induced an increase in plasma and liver lipid content, and a stimulation of liver protein synthesis rates. Gene expression was little changed by sucrose, with lower levels for LXR-α and LXR-β. Polyphenol/micronutrient supplementation tended to limit liver triglyceride infiltration through variations in fatty acid synthase, acyl coA oxidase, and possibly ATP-citrate lyase activities. In conclusion, despite differences in enzymatic regulations, and blunted responses of gene expression, high-sucrose diet was still able to induce a marked increase in liver lipid content in old animals. However, it probably attenuated the positive impact of polyphenol/micronutrients.

Effect of thermal stress on metabolic and oxidative stress biomarkers of Hoplosternum littorale (Teleostei, Callichthyidae)

The present study aimed to investigate in Hoplosternum littorale (Hancock, 1828) the effects of different water temperatures (10°C, 25°C-control group- and 33°C) on physiologic and metabolic traits following acute (1day) and chronic (21days) exposures. We analyzed several biomarker responses in order to achieve a comprehensive survey of fish physiology and metabolism under the effect of this natural stressor. We measured morphological indices, biochemical and hematological parameters as well as oxidative stress markers. To evaluate energy consumption, muscle and hepatic total lipid, protein and glycogen concentrations were also quantified. Extreme temperatures exposures clearly resulted in metabolic adjustments, being liver energy reserves and plasma metabolites the most sensitive parameters detecting those changes. We observed reduced hepatosomatic index after acute and chronic exposure to 33°C while glycogen levels decreased at both temperatures and time of exposure tested. Additionally, acute and chronic exposures to 10°C increased liver lipid content and plasma triglycerides. Total protein concentration was higher in liver and lower in plasma after chronic exposures to 10°C and 33°C. Acute exposition at both temperatures caused significant changes in antioxidant enzymes tested in the different tissues without oxidative damage to lipids. Antioxidant defenses in fish failed to protect them when they were exposed for 21days to 10°C, promoting higher lipid peroxidation in liver, kidney and gills. According to multivariate analysis, oxidative stress and metabolic biomarkers clearly differentiated fish exposed chronically to 10°C. Taken together, these results demonstrated that cold exposure was more stressful for H. littorale than heat stress. However, this species could cope with variations in temperature, allowing physiological processes and biochemical reactions to proceed efficiently at different temperatures and times of exposure. Our study showed the ability of H. littorale to resist a wide range of environmental temperatures and contributes for the understanding of how this species is adapted to environments with highly variable physicochemical conditions.

Resolution of glucose intolerance in long-term high-fat, high-sucrose-fed mice.

The high-fat, high-sucrose diet (HFSD)-fed C57Bl/6 mouse is a widely used model of prediabetes. However, studies typically implement a relatively short dietary intervention lasting between 4 and 16 weeks; as a result, little is known about how a long-term HFSD influences the metabolic profile of these mice. Therefore, the aim of this investigation was to examine the effects of consuming a HFSD for 42 weeks on the development of hyperinsulinaemia and glucose intolerance in male C57Bl/6 mice. Two cohorts of HFSD mice were studied at independent institutes and they underwent an oral glucose tolerance test (OGTT) with measures of plasma insulin and free fatty acids (FFA). Age-matched chow-fed control mice were also studied. The HFSD-fed mice were hyperinsulinaemic and grossly obese, being over 25 g heavier than chow-fed mice, which was due to a marked expansion of subcutaneous adipose tissue. This was associated with a 3-fold increase in liver lipid content. Glucose tolerance, however, was either the same or better than control mice due to the preservation of glucose disposal as revealed by a dynamic stable isotope-labelled OGTT. In addition, plasma FFAs were suppressed to lower levels in HFSD mice during the OGTT. In conclusion, we have made the paradoxical observation that long-term HFSD feeding results in the resolution of glucose intolerance in the C57Bl/6 mouse. Mechanistically, we propose that the gross expansion of subcutaneous adipose tissue increases the glucose disposal capacity of the HFSD-fed mouse, which overcomes the prevailing insulin resistance to improve glucose tolerance.

Apolipoprotein CIII Overexpression-Induced Hypertriglyceridemia Increases Nonalcoholic Fatty Liver Disease in Association with Inflammation and Cell Death.

Nonalcoholic fatty liver disease (NAFLD) is the principal manifestation of liver disease in obesity and metabolic syndrome. By comparing hypertriglyceridemic transgenic mice expressing apolipoprotein (apo) CIII with control nontransgenic (NTg) littermates, we demonstrated that overexpression of apoCIII, independent of a high-fat diet (HFD), produces NAFLD-like features, including increased liver lipid content; decreased antioxidant power; increased expression of TNFα, TNFα receptor, cleaved caspase-1, and interleukin-1β; decreased expression of adiponectin receptor-2; and increased cell death. This phenotype is aggravated and additional NAFLD features are differentially induced in apoCIII mice fed a HFD. HFD induced glucose intolerance together with increased gluconeogenesis, indicating hepatic insulin resistance. Additionally, the HFD led to marked increases in plasma TNFα (8-fold) and IL-6 (60%) in apoCIII mice. Cell death signaling (Bax/Bcl2), effector (caspase-3), and apoptosis were augmented in apoCIII mice regardless of whether a HFD or a low-fat diet was provided. Fenofibrate treatment reversed several of the effects associated with diet and apoCIII expression but did not normalize inflammatory traits even when liver lipid content was fully corrected. These results indicate that apoCIII and/or hypertriglyceridemia plays a major role in liver inflammation and cell death, which in turn increases susceptibility to and the severity of diet-induced NAFLD.

Impact of Dietary L‐Malic Acid Supplementation on Growth, Feed Utilization, Ash Deposition, and Hepatic Lipid Metabolism of Juvenile Genetically Improved Farmed Tilapia, Oreochromis niloticus

AbstractA 9‐wk feeding trial was conducted to investigate the effects of L‐malic acid (LMA) supplementation on growth, feed utilization, body composition, whole‐body mineral concentrations, and hepatic lipid metabolism of juvenile genetically improved farmed tilapia. LMA was included in the diets at 0, 0.8, or 3.2%. LMA‐supplemented treatments began to demonstrate weight gain improvement at 7 wk. After 9 wk, feed intake, weight gain, feed conversion ratio, and protein efficiency ratio were improved with either 0.8% or 3.2% LMA. Although whole‐body Fe, Mn, and Cu concentrations decreased, increased Ca and P concentrations contributed to improve whole‐body ash deposition with LMA inclusion. The concentrations of Na, K, Mg, and Zn and the Ca/P ratio of the whole body were not impacted by dietary treatments. Dietary LMA inclusion promoted whole‐body lipid deposition, which largely resulted from enhanced lipid accumulation in the liver and muscle tissues. In line with the increased liver lipid content, hepatic transcript levels of cytosolic malic enzyme 1 and acetyl‐CoA carboxylase a were upregulated, while mRNA levels of carnitine palmitoyltransferase 1A (CPT1A) and CPT1B were downregulated with LMA supplementation. However, increasing dietary LMA supply from 0.8 to 3.2% did not produce additional effects on most of the tested parameters, at least for a 9‐wk period. Taken together, it could be concluded that 0.8% LMA was superior to 3.2% LMA in tilapia feed and its inclusion could improve growth and feed utilization and enhance ash deposition and hepatic lipid accumulation.

VNN1 promotes atherosclerosis progression in apoE−/− mice fed a high-fat/high-cholesterol diet

Accumulated evidence shows that vanin-1 (VNN1) plays a key part in glucose metabolism. We explored the effect of VNN1 on cholesterol metabolism, inflammation, apoptosis in vitro, and progression of atherosclerotic plaques in apoE−/− mice. Oxidized LDL (Ox-LDL) significantly induced VNN1 expression through an ERK1/2/cyclooxygenase-2/PPARα signaling pathway. VNN1 significantly increased cellular cholesterol content and decreased apoAI and HDL-cholesterol (HDL-C)-mediated efflux by 25.16% and 23.13%, respectively, in THP-1 macrophage-derived foam cells (P < 0.05). In addition, VNN1 attenuated Ox-LDL-induced apoptosis through upregulation of expression of p53 by 59.15% and downregulation of expression of B-cell lymphoma-2 127.13% in THP-1 macrophage (P < 0.05). In vivo, apoE−/− mice were divided randomly into two groups and transduced with lentivirus (LV)-Mock or LV-VNN1 for 12 weeks. VNN1-treated mice showed increased liver lipid content and plasma levels of TG (124.48%), LDL-cholesterol (119.64%), TNF-α (148.74%), interleukin (IL)-1β (131.81%), and IL-6 (156.51%), whereas plasma levels of HDL-C (25.75%) were decreased significantly (P < 0.05). Consistent with these data, development of atherosclerotic lesions was increased significantly upon infection of apoE−/− mice with LV-VNN1. These observations suggest that VNN1 may be a promising therapeutic candidate against atherosclerosis.

Peripartal rumen-protected methionine supplementation to higher energy diets elicits positive effects on blood neutrophil gene networks, performance and liver lipid content in dairy cows.

BackgroundMain objectives were to determine to what extent Smartamine M (SM) supplementation to a prepartal higher-energy diet could alter neutrophil (PMN) and liver tissue immunometabolic biomarkers, and whether those responses were comparable to those in cows fed a prepartal lower-energy diet (CON).ResultsTwenty-eight multiparous Holstein cows were fed CON (NEL = 1.24 Mcal/kg DM) during d −50 to d −22 relative to calving. From d −21 to calving, cows were randomly assigned to a higher-energy diet (OVE, n = 9; NEL = 1.54 Mcal/kg DM), OVE plus SM (OVE + SM, n = 10; SM = 0.07 % of DM) or remained on CON (n = 9). All cows received the same basal lactation diet (NEL = 1.75 Mcal/kg DM). Supplementation of SM (OVE + SM) continued until 30 d postpartum. Liver biopsies were harvested at d −10, 7, and 21 relative to parturition. Blood PMN isolated at −10, 3, and 21 d relative to calving was used to evaluate gene expression. As expected, OVE increased liver lipid content postpartum; however, cows fed OVE + SM or CON had lower concentrations than OVE. Compared with OVE, cows in CON and OVE + SM had greater DMI postpartum and milk production. Furthermore, cows fed OVE + SM had the greatest milk protein and fat percentage and lowest milk SCC despite having intermediate PMN phagocytic capacity. Adaptations in PMN gene expression in OVE + SM cows associated with the lower SCC were gradual increases from −10 to 21 d in genes that facilitate migration into inflammatory sites (SELL, ITGAM), enzymes essential for reducing reactive oxygen metabolites (SOD1, SOD2), and a transcription factor(s) required for controlling PMN development (RXRA). The greater expression of TLR4 on d 3, key for activation of innate immunity due to inflammation, in OVE compared with CON cows suggests a more pronounced inflammatory state. Feeding OVE + SM dampened the upregulation of TLR4, despite the fact that these cows had similar expression of the pro-inflammatory genes NFKB1 and TNF as OVE. Cows in CON had lower overall expression of these inflammation-related genes and GSR, which generates reduced glutathione, an important cellular antioxidant.ConclusionsAlthough CON cows appeared to have a less stressful transition into lactation, SM supplementation was effective in alleviating negative effects of energy-overfeeding. As such, SM was beneficial in terms of production and appeared to boost the response of PMN in a way that improved overall cow health.Electronic supplementary materialThe online version of this article (doi:10.1186/s40104-016-0077-9) contains supplementary material, which is available to authorized users.

Effect of replacing dietary menhaden oil with pollock or soybean oil on muscle fatty acid composition and growth performance of juvenile Pacific threadfin (Polydactylus sexfilis)

Abstract This study investigated effect of different dietary lipid sources on juvenile Pacific threadfin (Polydactylus sexfilis), a tropical marine fish, based on growth performance, proximate composition of whole fish and muscle fatty acid composition. The objectives were 1) to compare the nutritional value of menhaden oil to pollock oil, a product generated by the Alaskan fish processing industry; and 2) to evaluate the potential of replacing pollock oil with soybean oil in diets for juvenile Pacific threadfin. Six experimental diets were formulated to contain 42% crude protein and 12% crude lipid including 4% lipid from fishmeal and 8% added oil. The 8% added oil was provided by menhaden oil pollock oil (P) or soybean (S) oil mixed with pollock oil. Diets containing the mixed oil were named as P8S0, P6S2, P4S4, P2S6, and P0S8 to denote the level of pollock oil (decreasing from 8 to 0%) and soybean oil (increasing from 0 to 8%). Pacific threadfin (average body weight of 18.6 g) were fed each of the experimental diets for 8 weeks. Growth performance, proximate composition of whole body and muscle were similar among fish fed with different diets. Pollock oil and menhaden oil were shown to have a similar effect on the nutritional composition of fish or tissue. In contrast, the diet containing 8% soybean oil significantly increased liver lipid content compared to the other test diets. The fatty acid composition of muscle reflected the dietary fatty acids. Fish fed the soybean oil diets exhibited significantly lower levels of n-3 long chain polyunsaturated fatty acid (n-3 LC-PUFA) and higher levels of 18:2n-6 and 18:3n-3 than those fed the fish oil diets. Results of this study suggest that pollock oil can replace menhaden oil without any adverse effect on growth performance or nutritional quality of fish. Total replacement of pollock oil with soybean oil had no detrimental effect on growth performance of juvenile Pacific threadfin but altered the fatty acid composition of fish muscle tissue. These results are useful in formulating practical feeds at reduced cost for Pacific threadfin culture. However, a longer term study will be needed to investigate whether the changes in muscle fatty acid composition will influence the welfare as well as the market value of Pacific threadfin.

Natural induction of spontaneous liver steatosis in Greylag Landaise geese (Anser anser)

The present experiment aimed at demonstrating that the Greylag geese (Anser anser), commonly used for the production of foie gras, are able to develop spontaneous hyperphagia and subsequent liver steatosis under specific handling conditions and without overfeeding. One hundred and eighty male geese were used in this experiment. After a period of feed restriction, at the age of 19 wk, corn was provided ad libitum. From wk 21 to 23, the daylight duration was progressively reduced from 10 to 7 h and kept as such until the end of the experiment (wk 31). Thirty birds were slaughtered at wk 19, 23, 25, 27, 29, and 31. During the first 2 wk after corn delivery, the average consumption rose up to 600 g/bird/d and decreased slowly thereafter to reach 270 g at wk 31. The liver weight increased from 95 (wk 19) to 514 g (wk 31), and most of these changes were due to the increase in liver lipid content from 6 to 50% of liver weight. There was no mortality during the experimental period. Histological observations indicate that the accumulation of fat in the livers occurred through a large increase in the size of the hepatocytes without modification of the cell boundaries and without any sign of inflammation or degeneration. Our data clearly show that under specific management conditions of feeding and photoperiod, the geese are able to initiate spontaneous liver steatosis. These results demonstrate their natural ability to store fat in the liver without any visible sign of tissue alteration. However, the variability in the response remains very high (at wk 31, the CV in liver weight was 45%). Further research is needed to better understand the origin of this variability.

Effect of dietary protein, lipid and carbohydrate contents on the liver composition and enzyme activity of Cyprinus carpio communis fingerlings

This study aimed to determine a feed formulation with best protein to energy ratio which would result in better liver composition and enzyme activity of Cyprinus carpio communis. Fingerlings having average weight 1.64 g ± 0.13 and length 5.26 ± 0.10 cm were fed on four different formulated feeds and a control feed (each in a triplicate set), 6% of their body weight, three times a day, during 90 days. Feeds were formulated using ground nut oil cake, mustard oil cake, rice bran, wheat bran, fish meal and soybean meal in order to suffice the balanced need of protein and energy of the common carp. Liver composition and acid and alkaline phosphatase activity of fingerlings were measured. There was a significant increase in liver lipid content with the increase in dietary carbohydrate level. The ACP and ALP activity was the maximum in the fingerlings fed on the diet having optimum protein to energy ratio of 20.54 mg protein/Kj. This work concluded that a diet containing 40% protein, 9.31% lipid and 10.08% carbohydrate is the best one for a more profitable and successful culture of the common carp. Key words: Protein to energy ratio, carp production, acid phosphatase, alkaline phosphatase.

Effects of ovariectomy and resistance training on lipid content in skeletal muscle, liver, and heart; fat depots; and lipid profile

The aim of the present study was to investigate the effects of resistance training on skeletal muscle lipid content, liver lipid content, heart lipid content, fat depots, and lipid profile in ovariectomized rats. Wistar adult female rats were divided into 4 groups (n = 10 per group): sedentary (Sed-Intact), sedentary ovariectomized (Sed-Ovx), strength trained (ChronicEx-intact), and strength trained ovariectomized (ChronicEx-Ovx). A 12-week strength-training period was used, during which the animals climbed a 1.1-m vertical ladder with weights attached to their tails. The sessions were performed once every 3 days, with 4-9 climbs and 8-12 dynamic movements per climb. Ovariectomy increased liver lipid content and fat depots, and heart and muscle lipid content. There was an increase in the atherogenic index and a negative change in lipid profile because of the ovariectomy. Resistance training decreased lipid content in the liver, soleus, and tibialis anterior, decreased fat depots (mesenteric and retroperitoneal), and changed the lipid profile, independently of ovarian hormone status. These results indicate the potential benefits of resistance training as an alternative strategy to control the effects of ovariectomy on fat depot, lipid profile, and tissue lipid content.

Liver phosphorus content in Holstein-Friesian cows during the transition period

Hepatic lipidosis and hypophosphatemia are frequently observed in high-yielding periparturient dairy cows. Objectives of this study were to investigate the association of the liver P content with the degree of liver fat accumulation and serum P concentration and to characterize the change in liver P content throughout the transition period. In a cross-sectional study, liver biopsies obtained from 33 Holstein-Friesian cows 14 d postpartum (p.p.) were assayed for total lipid (TLip), triacylglycerol, DNA, P, Mg, K, Na, and Ca content. Serum samples obtained at the time of biopsy were analyzed for indices of liver function and injury and the serum P concentration was determined. From this cross-sectional study, 6 cows were selected for a longitudinal study and liver tissue obtained from the 6 cows on d −65, −30, −14, 1, 14, 28, and 49 relative to calving was assayed. The amounts of P, K, Mg, Na, and Ca were expressed as amount in dry weight (DW), wet weight (WW), nonfat wet weight (NFWW), and indexed to DNA. In the cross-sectional study, PDW and PWW decreased with increasing TLip, whereas PNFWW and PDNA were independent of TLip. Values for PDNA varied widely, whereas PNFWW varied within a narrow range. Stepwise regression analysis revealed the strongest associations between PDW and the amount of tissue water (partial R2=0.74) and the log to the base 10 of triacylglycerol (partial R2=0.05). The PWW was associated with the log to the base 10 of triacylglycerol (partial R2=0.20), but no associations were found for PNFWW. These findings indicate that decreased electrolyte content in dry and wet liver tissue with increased liver lipid content is predominantly due to the decrease in tissue water and therefore the distribution volume of electrolytes. In the longitudinal study, PDW, PWW, and PNFWW were decreased on d 14 p.p. Similar directional decreases were found for K, Mg, and Na, but P was the only electrolyte that was significantly decreased in liver tissue at d 14 p.p. This finding indicates that the P content of liver tissue decreases in early lactation due to a reduction in hepatocellular cytosol volume as well as a decrease in cytosolic P concentration, with the latter having biological relevance. The clinical significance of decreased cytosolic P concentration in the hepatocytes of dairy cows in early lactation remains to be determined.

Effect of 6-month calorie restriction and exercise on serum and liver lipids and markers of liver function.

Nonalcoholic fatty liver disease (NAFLD) and its association with insulin resistance are increasingly recognized as major health burdens. The main objectives of this study were to assess the relation between liver lipid content and serum lipids, markers of liver function and inflammation in healthy overweight subjects, and to determine whether caloric restriction (CR) (which improves insulin resistance) reduces liver lipids in association with these same measures. Forty-six white and black overweight men and women (BMI = 24.7-31.3 kg/m(2)) were randomized to "control (CO)" = 100% energy requirements; "CR" = 25%; "caloric restriction and increased structured exercise (CR+EX)"= 12.5% CR + 12.5% increase in energy expenditure through exercise; or "low-calorie diet (LCD)" = 15% weight loss by liquid diet followed by weight-maintenance, for 6 months. Liver lipid content was assessed by magnetic resonance spectroscopy (MRS) and computed tomography (CT). Lipid concentrations, markers of liver function (alanine aminotransferase (ALT), alkaline phosphatase (ALK)), and whole-body inflammation (tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP)) were measured in fasting blood. At baseline, increased liver lipid content (by MRS) correlated (P < 0.05) with elevated fasting triglyceride (r = 0.52), ALT (r = 0.42), and hsCRP (r = 0.33) concentrations after adjusting for sex, race, and alcohol consumption. With CR, liver lipid content was significantly lowered by CR, CR+EX, and LCD (detected by MRS only). The reduction in liver lipid content, however, was not significantly correlated with the reduction in triglycerides (r = 0.26; P = 0.11) or with the changes in ALT, high-density lipoprotein (HDL)-cholesterol, or markers of whole-body inflammation. CR may be beneficial for reducing liver lipid and lowering triglycerides in overweight subjects without known NAFLD.