Liver Total Lipids Research Articles

Biochemical composition and condition of wild blackfin snook Centropomus medius through the reproductive cycle

The blackfin snook, Centropomus medius, is a valuable fish in American and Mexican markets, mainly from catches. Nonetheless, information and studies about the biology of this species still need to be made available; thus, its aquaculture should be developed. This study aimed to describe the seasonal changes of proximate composition during a reproductive cycle of C. medius, analyzing differences between tissues and their changes related to the reproductive process. The snook specimens were collected in Magdalena Bay, Baja California Sur, Mexico, and measured every month from September 2001 to November 2002. Liver, gonads, muscle tissue, and intraperitoneal fat (IPF) were sampled and weighed. The gonadosomatic index (GSI), hepatosomatic index (HSI), IPF ratio, and condition factor index (K) were calculated. The biochemical composition was analyzed in the gonad, liver, and muscle. The reproductive period (RP) of wild C. medius in Baja California Sur, Mexico, was from June to December. The spawning period was recorded at summer temperature (25-30°C) and photoperiod (>13 h daylight) starting in September. High GSI values (gonad development), low HSI values (lipid reserve mobilization), low IPF, and low K ratio were related to elevated temperatures. Moreover, variations were observed in protein, total lipid, triglycerides, and glycogen content in muscle, liver, and gonad according to the reproductive phase. A positive correlation was demonstrated between protein contents in muscle, gonad, and K, with lower concentrations during RP, while liver protein composition showed an opposite pattern. Lipids were mainly present in the liver, and the concentration decreased during RP while muscle increased. The results obtained in this study show differences in the proximate analyses in the liver, muscle, and gonads throughout the year concerning different phases of the reproductive cycle, indicating a great dependence of this process on the mobilization of reserves during C. medius reproduction. Therefore, understanding the feeding requirements to pursue the management of this species in captivity for aquaculture development is greatly important.

Acrocomia aculeata (Jacq.) improves the antioxidant system but induces lipid accumulation in the liver of rats.

Acrocomia aculeata pulp (ACP) is a source of oleic acid, phenolic compounds, and flavonoids that protect against diseases and improve antioxidant capacity. We evaluated whether regular intake of ACP, in combination with a standard diet, improves the antioxidant system and physiological parameters. Male Wistar rats were divided into: control (C), 250 mg/kg ACP, and 500 mg/kg ACP groups. Rats received either water or the respective A. aculeata solution doses for 28 days. We observed increased food intake, lower carcass protein levels, and higher carcass lipid levels in the 500 mg/kg ACP group than in the other groups. Postprandial glucose, oral glucose tolerance test results, and the area under the curve were greater, while urea was lower in the 500 mg/kg ACP group. Total liver lipids were increased, and PPAR-α, PPARγ, and carbonylated protein levels were reduced in the 500 mg/kg ACP group. NRF2 contents and glutathione reductase, superoxide dismutase, and catalase activities were increased in the 500 mg/kg ACP group. In the 250 mg/kg ACP group, only glutathione system activity increased. Thus, ACP intake improved the enzymatic antioxidant system in the liver at the evaluated doses, although the 500 mg/kg dose induced alterations in lipid, protein, and carbohydrate metabolism.

Effects of Dietary Oxidized Phytosterol on Lipid Metabolism in Rats.

Many in vitro studies have revealed the toxic effects of oxidized phytosterols (OPSs); however, their effects on lipid metabolism are not well understood in vivo. Therefore, we examined the bioavailability of OPS and compared the effects of dietary phytosterols (PSs) or OPS on lipid metabolism in rats. OPS was detected in the plasma and liver of rats administered 50 mg of OPS for 3 days. Rats were fed the AIN76 diet (C group), basal diet plus 0.25% PS (P group), or 0.25% OPS (O group) for 4 weeks. Dietary OPS but not PS reduced hepatic fatty acid synthase activity. Liver triacylglycerol (TG) levels tended to be lower in the P group than in the C group and were significantly lower in the O group. The mRNA expression level of HMG-CoA reductase in the liver was the lowest in the O group, whereas that of CYP27A1 was the highest in the O group. The mRNA expression levels of NPC1L1 in the intestinal mucosa were significantly lower in the P and O groups than in the C group. Consistent with these modulations, plasma total cholesterol (TC) and HDL-C levels were similar between the C and P groups but tended to be higher or significantly higher in the O group. Liver TC levels were significantly lower in the P and O groups than in the C group. Moreover, fecal neutral and acidic steroid levels were the highest in the O group. The mRNA expression level of Δ6 desaturase in the liver was significantly higher in both the P and the O groups than in the C group. The Δ6 desaturation indices of fatty acids in the total liver lipids were the highest in the O group. Thus, dietary OPS may modulate lipid metabolism in the liver.

Polygoni Cuspidati Rhizoma et Radix extract attenuates high-fat diet-induced NAFLD in rats: Impact on untargeted serum metabolomics and liver lipidomics

BackgroundPolygoni Cuspidati Rhizoma et Radix (PCRR; the root and rhizome of Polygonum cuspidatum Sieb. et Zucc) has long been used to treat atherosclerosis, gastrointestinal disorders, and liver disease. However, the underlying mechanism of PCRR against liver steatosis remains unclear. PurposeThe aim of this study was to determine the potential therapeutic targets and molecular mechanisms of PCRR in improving liver steatosis. MethodsA high-fat diet (HFD)-induced simple steatosis model in rats was used to evaluate the therapeutic effect of polyphenol-rich water extract from PCRR. Its underlying mechanisms were revealed using untargeted mass spectrometry-based serum metabolomics, hepatic lipidomic profiling approaches, qPCR, and Western blotting assays. ResultsOur study showed that PCRR-treated rats displayed significant reduction of serum TC and LDL-C, hepatic TG, TC levels, and total liver lipid content under a HFD feeding condition. Untargeted metabolomics showed that PCRR significantly restored the overall levels of nine lipid classes in liver tissues and elevated the bile acid levels in the serum samples. We demonstrated that PCRR prevented HFD-induced hepatic steatosis by regulating the expressions of TG metabolism proteins, including p-AMPK, p-ACC, PPARα, and FAS, as well as the expressions of TC metabolism proteins, including p-AMPK, LDLR, and CYP7A1. Moreover, resveratrol and/or polydatin­-derived metabolites were solely detected in the serum samples of the PCRR-treated group, indicating these microbial transformed metabolites might partly contribute to the beneficial effects of PCRR. ConclusionPCRR can be employed as a therapeutic agent to improve non-alcoholic fatty liver disease via regulating lipid metabolism.

Evaluation of Short-Term Toxicity and Cholesterol-Lowering Effects in Rats Exposed to Dietary Fiber Derived from Cassava Pulp.

The dietary fiber extracted from cassava pulp, composed of crude fiber, neutral detergent fiber (NDF), and cellulose content, demonstrates promise as a functional food ingredient. The study's objectives encompassed the assessment of short-term toxicity and the evaluation of its potential cholesterol-lowering effects. The results indicated that cassava pulp dietary fiber (CDF) is well-tolerated with non-toxic thresholds determined at 10.01 g/kg body weight/day for male rats and 11.21 g/kg body weight/day for female rats during the short-term toxicity assessment. Furthermore, CDF exhibited notable cholesterol-lowering effects, significantly reducing serum triglyceride and serum total cholesterol levels, along with decreased liver total lipids and liver cholesterol levels. In contrast, it led to significant increases in fecal total lipids and cholesterol when compared to the control group. Most notably, there were no significant differences in terms of serum triglyceride, serum total cholesterol, liver total lipids, and liver cholesterol between CDF and the conventional cholesterol-lowering medication, simvastatin. These findings underscore the potential of cassava pulp dietary fiber as a natural and safe alternative for managing hyperlipidemia and related conditions. It offers a valuable avenue for the development of functional foods aimed at improving cardiovascular health and further investigation for its potential application in the field of nutraceuticals.

Gestational exposure to ambient fine particulate matter disrupts maternal hepatic lipid metabolism

Pregnancy is a unique physiological stage for females as well as a vulnerable period for pollutant exposure. The effect of gestational ambient fine particulate matter (PM2.5) exposure on maternal lipid metabolism during pregnancy is rarely observed, and the mechanism is unknown. In the current study, pregnant C57BL/6 mice were randomly assigned to either ambient PM2.5 or filtered air exposure chambers since gestational day (GD) 0. Meanwhile, non-pregnant female mice were housed as controls in each exposure chamber. PM2.5 exposure exerted no significant effect on body weight gain or the body composition during pregnancy. Pregnant mice exposed to PM2.5 demonstrated improved glucose tolerance, whereas non-pregnant mice showed an increased fasting blood glucose level after PM2.5 exposure with no alterations in glucose tolerance. PM2.5 exposure exerted no significant effect on total lipid content in serum during pregnancy, while an increased serum total lipid level was found in non-pregnant mice exposed to PM2.5. PM2.5 exposure had no effect on total liver lipid levels, it increased several triacylglycerol (TAG) species and total cholesterol esters (CEs) in pregnant mice but lowered a considerable amount in non-pregnant mice’ livers. Furthermore, gestational exposure to PM2.5 enhanced the expression of key enzymes in fatty acid uptake, de novo lipid synthesis, and β oxidation, and inhibited molecules for lipid export in mice liver. Conversely, PM2.5 exposure upregulated proteins involved in hepatic lipolysis and lipid export in non-pregnant mice. These results suggest that the interference of PM2.5 exposure during pregnancy on the lipid metabolism, particularly the hepatic lipid metabolism, differs from that during non-pregnancy. This study provides toxicological evidence that PM2.5 exposure during pregnancy disrupts the lipid metabolism of the liver and provides a basis for protecting vulnerable populations.

Dietary β-glucan ameliorates metabolic stress caused by a high dietary carbohydrate level in Nile tilapia

Carbohydrates are an excellent cost-friendly energy source for fish, and they have been used to improve growth performance and reduce dietary protein levels. However, the aquaculture industry has frequently overused high dietary carbohydrate levels, which has caused metabolic disturbances in fish. This deleterious effect is often diagnosed at the end of the production cycle, affects fish health and causes significant losses to farmers. In this context, β-glucan, which is broadly known as an immunomodulator, may ameliorate the deleterious effects caused by high levels of dietary carbohydrates. Therefore, we investigated the effect of dietary β-glucan on the reduction of metabolic disturbances in Nile tilapia fed a high carbohydrate diet. A total of 352 juvenile Nile tilapias (25.39 ± 0.83 g) were fed isoproteic (280 g kg−1 PD) and isoenergetic diets (3130 kcal kg−1) containing low amounts of carbohydrates (CHO-L 270 g kg−1) or high amounts of carbohydrates (CHO-H 620 g kg−1) with four levels of β-glucan (βG; 0, 1, 3 and 6 g kg−1) for 10 weeks. We evaluated the productive performance, plasma glucose, serum triglycerides, hepatosomatic index, total liver and muscle lipid, hepatic glycogen, hepatic activity of hexokinase, glucokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase, malic enzyme, liver histopathology and innate immune responses. Fish fed a high carbohydrate diet had significantly increased productive performance and lipogenesis, presenting higher hepatosomatic indexes, triglycerides, hepatic glycogen, muscular lipid, hepatic activity of glucose-6-dehydrogenase phosphate, and malic enzyme. Additionally, histological analyses indicated expressive cytoplasm vacuolization. The innate immune responses such as leukocyte respiratory activity, complement and lysozyme were also significantly decreased for the high carbohydrate diet, indicating the occurrence of immunosuppression in fish. These results also indicate impaired metabolic functioning. However, β-glucan ameliorated metabolic stress. Specifically, we found a significant decrease in the serum levels of triglycerides, hepatosomatic index, muscular lipid, and hepatic activities of malic and glucose-6-dehydrogenase phosphate enzymes in fish fed high amounts of carbohydrates containing glucan. There was also a significant decrease in hepatic activity of the glycolytic pathway, hexokinase and pyruvate kinase. Moreover, β-glucan modulated the respiratory activity of leukocytes and complement, confirming its immunomodulating effect on fish. In conclusion, β-glucan mitigated the metabolic disturbances caused by the high levels of carbohydrates in the diet of Nile tilapia. This finding indicates that besides having an immunomodulating effect, β-glucan also has metabolic functions/benefits such as reducing glycolysis and lipogenesis.

Effect of Sub-Lethal, Carbaryl and Cartap Exposures on Lipid and Cholesterol Contents in Liver, Kidney and Gills of Channa Punctatus (BLOCH)

Channa punctatus were exposed for 24, 48, 72 and 96 h to sub-lethal concentration (30% of LC50 for 96h) of carbaryl and cartap (carbamate pesticides) in order to record their effect on total lipid and cholesterol contents in liver, kidney and gills. The normal lipid content in liver, kidney and gills ranged from 17.95±0.41 to18.21±0.38 mg/g, 15.55i-0.51 to16.21±0.35 mg/g and 8.53±0.39 to 9.58±0.33 mg/g, whereas cholesterol contents varied between 3.60±0.06 to 3.81±0.04 mg/g, 1.61±0.05 to 1.72±0.02 mg/g and 0.71±0.02 to 0.77±0.10 mg/g, respectively. The treatment elicited significant decline in lipid and cholesterol contents throughout the exposure period suggesting response of the fish to the pesticide intoxication.

Investigating Performance of the SLIM-Based High Resolution Ion Mobility Platform for Separation of Isomeric Phosphatidylcholine Species.

Lipids are structurally diverse molecules that play a pivotal role in a plethora of biological processes. However, deciphering the biological roles of the specific lipids is challenging due to the existence of numerous isomers. This high chemical complexity of the lipidome is one of the major challenges in lipidomics research, as the traditional liquid chromatography-mass spectrometry (LC-MS) based approaches are often not powerful enough to resolve these isomeric and isobaric nuances within complex samples. Thus, lipids are uniquely suited to the benefits provided by multidimensional liquid chromatography-ion mobility-mass spectrometry (LC-IM-MS) analysis. However, many forms of lipid isomerism, including double-bond positional isomers and regioisomers, are structurally similar such that their collision cross section (CCS) differences are unresolvable via conventional IM approaches. Here we evaluate the performance of a high resolution ion mobility (HRIM) system based on structures for lossless ion manipulation (SLIM) technology interfaced to a high resolution quadrupole time-of-flight (QTOF) analyzer to address the noted lipidomic isomerism challenge. SLIM implements the traveling wave ion mobility technique along an ∼13 m ion path, providing longer path lengths to enable improved separation of isomeric features. We demonstrate the power of HRIM-MS to dissect isomeric PC standards differing only in double bond (DB) and stereospecific number (SN) positions. The partial separation of protonated DB isomers is significantly enhanced when they are analyzed as metal adducts. For sodium adducts, we achieve close to baseline separation of three different PC 18:1/18:1 isomers with different cis-double bond locations. Similarly, PC 18:1/18:1 (cis-9) can be resolved from the corresponding PC 18:1/18:1 (trans-9) form. The separation capacity is further enhanced when using silver ion doping, enabling the baseline separation of regioisomers that cannot be resolved when measured as sodium adducts. The sensitivity and reproducibility of the approach were assessed, and the performance for more complex mixtures was benchmarked by identifying PC isomers in total brain and liver lipid extracts.

PDK inhibition promotes glucose utilization, reduces hepatic lipid deposition, and improves oxidative stress in largemouth bass (Micropterus salmoides) by increasing pyruvate oxidative phosphorylation.

In omnivorous fish, the pyruvate dehydrogenase kinases (PDKs)-pyruvate dehydrogenase E1α subunit (PDHE1α) axis is essential in the regulation of carbohydrate oxidative catabolism. Among the existing research, the role of the PDKs-PDHE1α axis in carnivorous fish with poor glucose utilization is unclear. In the present study, we determined the effects of PDK inhibition on the liver glycolipid metabolism of largemouth bass (Micropterus salmoides). DCA is a PDK-specific inhibitor that inhibits PDK by binding the allosteric sites. A total of 160 juvenile largemouth bass were randomly divided into two groups, with four replicates of 20 fish each, fed a control diet and a control diet supplemented with dichloroacetate (DCA) for 8 weeks. The present results showed that DCA supplementation significantly decreased the hepatosomatic index, triglycerides in liver and serum, and total liver lipids of largemouth bass compared with the control group. In addition, compared with the control group, DCA treatment significantly down-regulated gene expression associated with lipogenesis. Furthermore, DCA supplementation significantly decreased the mRNA expression of pdk3a and increased PDHE1α activity. In addition, DCA supplementation improved glucose oxidative catabolism and pyruvate oxidative phosphorylation (OXPHOS) in the liver, as evidenced by low pyruvate content in the liver and up-regulated expressions of glycolysis-related and TCA cycle/OXPHOS-related genes. Moreover, DCA consumption decreased hepatic malondialdehyde (MDA) content, enhanced the activities of superoxide dismutase (SOD), and increased transforming growth factor beta (tgf-β), glutathione S-transferase (gst), and superoxide dismutase 1 (sod1) gene expression compared with the control diet. This study demonstrated that inhibition of PDKs by DCA promoted glucose utilization, reduced hepatic lipid deposition, and improved oxidative stress in largemouth bass by increasing pyruvate OXPHOS. Our findings contribute to the understanding of the underlying mechanism of the PDKs-PDHE1α axis in glucose metabolism and improve the utilization of dietary carbohydrates in farmed carnivorous fish.

Assessment of Areca Nut Bioactivities in Western Diet-Induced Mice NAFLD Model.

The areca nut is often consumed as a chewing food in the Asian region. Our previous study revealed that the areca nut is rich in polyphenols with high antioxidant activity. In this study, we further assessed the effects and molecular mechanisms of the areca nut and its major ingredients on a Western diet-induced mice dyslipidemia model. Male C57BL/6N mice were divided into five groups and fed with a normal diet (ND), Western diet (WD), WD with areca nut extracts (ANE), areca nut polyphenols (ANP), and arecoline (ARE) for 12 weeks. The results revealed that ANP significantly reduced WD-induced body weight, liver weight, epididymal fat, and liver total lipid. Serum biomarkers showed that ANP ameliorated WD-enhanced total cholesterol and non-high-density lipoprotein (non-HDL). Moreover, analysis of cellular signaling pathways revealed that sterol regulatory element-binding protein 2 (SREBP2) and enzyme 3-hydroxy-3-methylglutaryld coenzyme A reductase (HMGCR) were significantly downregulated by ANP. The results of gut microbiota analysis revealed that ANP increased the abundance of beneficial bacterium Akkermansias and decreased the abundance of the pathogenic bacterium Ruminococcus while ARE shown the opposite result to ANP. In summary, our data indicated that areca nut polyphenol ameliorated WD-induced dyslipidemia by increasing the abundance of beneficial bacteria in the gut microbiota and reducing the expressions of SREBP2 and HMGCR while areca nut ARE inhibited this improvement potential.

Histological and in vivo Study on Novel Polyelectrolyte Complex Vildagliptin Loaded Microbeads in Streptozotocin-induced Rat Model.

This study aimed to investigate the effect of vildagliptin-containing polyelectrolyte complex microbeads formulation in a streptozotocin-induced diabetic rat model. Vildagliptin-containing polyelectrolyte complex microbeads were given to diabetic rats at a dose of 2.5 mg/kg body weight in order to study their antidiabetic, hypolipidemic histopathological conditions. A portable glucometer was used to measure the blood glucose level using a reagent strip. After vildagliptin formulation was administered orally to healthy streptozotocin-induced rats, other parameters, such as liver profile and total lipid levels, were assessed. Vildagliptin-containing polyelectrolyte complex microbeads were found to significantly decrease high glucose levels and improve kidney, liver, and hyperlipidaemia caused due to diabetes. Vildagliptin-containing polyelectrolyte complex microbeads also had a favourable impact on alterations in the liver and pancreatic histopathology in diabetes caused by streptozotocin. Vildagliptin-containing polyelectrolyte complex microbeads have the ability to enhance a variety of lipid profiles, including those related to body weight, liver, kidney, and total lipid profiles. Vildagliptin-containing polyelectrolyte complex microbeads have also been found to be effective in preventing the histological alterations in the liver and pancreas occurred in streptozotocin-induced diabetes.

Effects of Chronic Alcohol Consumption and Iron Deficiency on Maternal Folate Status and Reproductive Outcome in Mice

The influence of chronic alcohol consumption with or without iron deficiency on reproductive performance and folate status was studied. Female CBA/J mice were fed isocaloric liquid diets prior to and during pregnancy. A 2 × 2 factorial design was employed with ethanol-derived calories (EDC) and iron (Fe) as dietary variables. Groups received 0% EDC and 30 ppm Fe (CA); 0% EDC and 2 ppm Fe (CD); 20% EDC and 30 ppm Fe (EA); and 20% EDC and 2 ppm Fe (ED). Animals were killed on day 18 of gestation. Mean body weights were reduced in CD, EA and ED groups, while daily caloric intakes reduced only in CD and ED groups. Maternal values for hemoglobin, transferrin saturation and red cell folates decreased with iron deficiency and/or 20% EDC; hematocrit, serum iron and serum folates decreased only with iron deficiency. Blood ethanol levels were similar in EA and ED groups. Maternal liver total lipids and alcohol dehydrogenase activity increased only with 20% EDC, while dihydrofolate reductase activity decreased with iron deficiency and/or 20% EDC. Iron deficiency and/or 20% EDC adversely affected gestational performances in mice as indicated by increased resorptions and decreased percentages of live fetuses/litters and live fetal weights. Data indicate that iron deficiency and/or chronic ethanol consumption induce adverse effects on maternal reproductive performance of CBA/J mice possibly via alteration of folate metabolism.

Rutin and Hesperidin Revoke the Hepatotoxicity Induced by Paclitaxel in Male Wistar Rats via Their Antioxidant, Anti-Inflammatory, and Antiapoptotic Activities.

Paclitaxel, one of the most effective chemotherapeutic drugs, is used to treat various cancers but it is exceedingly toxic when used long-term and can harm the liver. This study aimed to see if rutin, hesperidin, and their combination could protect male Wistar rats against paclitaxel (Taxol)-induced hepatotoxicity. Adult male Wistar rats were subdivided into 5 groups (each of six rats). The normal group was orally given the equivalent volume of vehicles for 6 weeks. The paclitaxel-administered control group received intraperitoneal injection of paclitaxel at a dose of 2 mg/Kg body weight twice a week for 6 weeks. Treated paclitaxel-administered groups were given paclitaxel similar to the paclitaxel-administered control group together with oral supplementation of rutin, hesperidin, and their combination at a dose of 10 mg/Kg body weight every other day for 6 weeks. The treatment of paclitaxel-administered rats with rutin and hesperidin significantly reduced paclitaxel-induced increases in serum alanine transaminase, aspartate transaminase, lactate dehydrogenase, alkaline phosphatase, and gamma-glutamyl transferase activities as well as total bilirubin level and liver lipid peroxidation. However, the levels of serum albumin, liver glutathione content, and the activities of liver superoxide dismutase and glutathione peroxidase increased. Furthermore, paclitaxel-induced harmful hepatic histological changes (central vein and portal area blood vessel congestion, fatty changes, and moderate necrotic changes with focal nuclear pyknosis, focal mononuclear infiltration, and Kupffer cell proliferation) were remarkably enhanced by rutin and hesperidin treatments. Moreover, the elevated hepatic proapoptotic mediator (caspase-3) and pro-inflammatory cytokine (tumor necrosis factor-α) expressions were decreased by the three treatments in paclitaxel-administered rats. The cotreatment with rutin and hesperidin was the most effective in restoring the majority of liver function and histological integrity. Therefore, rutin, hesperidin, and their combination may exert hepatic protective effects in paclitaxel-administered rats by improving antioxidant defenses and inhibiting inflammation and apoptosis.

Effects of Tributyrin Supplementation on Liver Fat Deposition, Lipid Levels and Lipid Metabolism-Related Gene Expression in Broiler Chickens.

The objective of this study was to investigate the effects of tributyrin supplementation on liver fat metabolism in broiler chickens. Two hundred and forty broilers were randomly allocated into two experimental groups (6 replicates per treatment; 20 chickens in each replicate): the control group (CN), which received a basal diet, and the tributyrin group (TB), which received a basal diet supplemented with 1 g/kg of tributyrin. The experimental period lasted 37 days. The results showed that in the liver, broilers supplemented with tributyrin had higher content of high-density lipoprotein cholesterol (HDL-C) (p < 0.05). Liver hepatic lipase (HL), lipoprotein lipase (LPL) and total lipid (TL) activity were significantly lower than in the TB group than that in the NC group. Meanwhile, the diet supplemented with tributyrin had more lipid droplets than the NC group, whereas the TB and NC groups showed no histological abnormalities in the liver. Furthermore, the mRNA expression levels of peroxisome proliferators-activated receptor α (PPARα), proliferators-activated receptor γ (PPARγ), fatty acid synthase (FAS), LPL and adipose triglyceride lipase (ATGL) in the liver were significantly upregulated in the TB group (p < 0.05), while those of the long-chain acyl-CoA-synthetase 1 (ACSL1) mRNA between the TB group and the NC group were not different (p > 0.05). These findings indicated that the diet supplemented with tributyrin could increase fat deposition appropriately by promoting fat synthesis without causing liver tissue damage, which demonstrated that tributyrin can be considered a valid feed additive for broiler chickens.

Fatty acid profile of the liver lipids under acute fungicide action and intake of a biologically active preparation in rats

The widespread use of fungicides in agriculture leads to a negative consequences for both humans and the environment. The acute effect of fungicides containing tebuconazole alone or in combination with triadimefon on fatty acid (FAs) composition of the total lipids in the liver of rats was studied. FAs content was analyzed by gas chromatography with the use of flame ionization detector. The results obtained indicate that the acute effect of triazole fungicides one-time oral administration to rats is characterized by toxic reactions and is accompanied by the total liver lipids FAs profile redistribution, similar for the studied fungicides. In particular, the reduction in the total content of monounsaturated FAs (by 26% – 37%) and in the ω3/ω6 ratio was observed. It was demonstrated that the subsequent two-week introduction of the preparation based on Milk thistle seeds oil extract had a positive effect and improved the FAs profile of lipids in dynamics after fungicide intake. Keywords: fatty acids, fungicides, Milk thistle seeds extract, rat liver lipids, triazoles

The association between elevated body mass index and wide blood chemistry panel results in apparently healthy individuals

BackgroundBlood chemistry panel and body mass index (BMI) are common ways to evaluate individual health. The study aimed to compare a wide range of blood chemistry tests between obese, overweight, and normal weight populations that are otherwise apparently healthy. MethodsWe conducted a cross-sectional study of all adults (20-65 years) with BMI ≥18.5 kg/m2 who underwent routine annual health check-ups. Participants who had any known morbidity or taking medication were excluded. BMI was categorized using the current World Health Organization criteria. After fasting, glucose, renal and liver functions, albumin and total protein levels, lipid profile, electrolytes levels and inflammatory marker were observed and compared between BMI categories. ResultsThe study included 10,211 adults (median BMI 25.1 kg/m2, 48.8% normal weight, 39.7% overweight, 11.5% obese). The mean age was 40.78 years (SD 9.69) and 35.4% were female. Triglyceride level was 23.5% in overweight and 50.6% higher in obese participants (p < 0.001). Liver enzymes were higher in overweight (5.6-18.7%, p < 0.001) and obese participants (13.4-48.3%, p < 0.001). C-reactive protein level was 134% higher in overweight and 430% higher in obese participants (p < 0.001). Differences were also documented in other blood tests. ConclusionsOverweight and obesity were found to be associated with significant abnormalities in blood tests. A periodic wide panel of blood tests, especially for overweight and obese populations, is essential to identify and intervene as secondary prevention before the onset of symptoms.

Inhibition of pyruvate dehydrogenase kinase improves carbohydrate utilization in Nile tilapia by regulating PDK2/4-PDHE1α axis and insulin sensitivity.

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 control diet without dichloroacetate (DCA) (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 dose DCA3.75 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.

Wild Rice and Brown Rice Reduce Liver and Serum Lipids in Wistar Rats fed Either a Total Western Diet or a High Fat Diet

ObjectivesNon-alcoholic fatty liver disease (NAFLD) prevalence is increasing, and no pharmacological intervention exists to treat it. Here, we determined the effect of feeding wild rice and brown rice on liver lipids and the gut microbiome when fed two different high fat background diets meant to induce fatty liver. MethodsIn the HFD trial, male Wistar rats (n = 8 per group) were fed either a high fat diet (HF), or a HF containing either 20% wild rice (WR) or 20% brown rice (BR) for 8 weeks. Cecal contents, liver, and epididymal fat pads were harvested. Microbiome analysis of cecal contents was conducted by 16S sequencing. In the TWD trial, male Wistar rats (n = 12 per group) were fed the AIN-93G diet (Basal), the Total Western Diet (TWD; a high fat diet that mimics the average American diet), or the TWD containing 30% WR (WR) for 10 weeks, then liver and epididymal fat pads were harvested. ResultsIn the HFD trial, both WR and BR significantly reduced total liver lipids compared to HF (p < 0.0001). However, epididymal fat pad weight was not reduced in either of the rice groups compared to HF (p > 0.05). Serum cholesterol was also reduced in WR compared to HF (p < 0.0188). In the TWD trial, the TWD elevated total liver lipids compared to Basal, but WR reduced liver lipids significantly (p < o.oo6) compared to TWD. WR did not lower epididymal fat pad weight (p > 0.1) compared to TWD. Additionally, p-AMPK/AMPK was increased in WR compared to TWD (p < 0.003). This shift in AMPK activation was not seen in the HFD trial (p > 0.05). In the HFD trial microbiome analysis, the beta-diversity measure of community dissimilarity indicated that WR had a significantly different microbial profile compared to the animals fed the HF diet (p < 0.003) while BR had an increased abundance of lactobacillus (p < 0.03) compared to animals fed the HF diet. ConclusionsWild rice feeding reduced fatty liver, using two different high fat background diets, and altered the gut microbiome. Wild rice should be further explored as a dietary approach to prevent development of non-alcoholic fatty liver disease (NAFLD), and to investigate whether hepatic lipid reductions are mediated by changes in the gut microbiome. Funding SourcesThe TWD trial was sponsored by the Whiteside Institute for Clinical Research and the HFD trial was sponsored by the Minnesota Cultivated Wild Rice Council.

Dietary l-carnitine regulates liver lipid metabolism via simultaneously activating fatty acid β-oxidation and suppressing endoplasmic reticulum stress in large yellow croaker fed with high-fat diets.

Dietary l-carnitine (LC) is a nutritional factor that reduces liver lipid content. However, whether dietary LC can improve lipid metabolism via simultaneous activation of mitochondrial fatty acid (FA) β-oxidation and suppression of endoplasmic reticulum (ER) stress is still unknown. Large yellow croaker were fed with a high-fat diet (HFD) supplemented with dietary LC at 0, 1·2 or 2·4 ‰ for 10 weeks. The results indicated that a HFD supplemented with LC reduced the liver total lipid and TAG content and improved serum lipid profiles. LC supplementation administered to this fish increased the liver antioxidant capacity by decreasing serum and liver malondialdehyde levels and enhancing the liver antioxidant capacity, which then relieved the liver damage. Dietary LC increased the ATP dynamic process and mitochondrial number, decreased mitochondrial DNA damage and enhanced the protein expression of mitochondrial β-oxidation, biogenesis and mitophagy. Furthermore, dietary LC supplementation increased the expression of genes and proteins related to peroxisomal β-oxidation and biogenesis. Interestingly, feeding fish with LC-enriched diets decreased the protein levels indicative of ER stress, such as glucose-regulated protein 78, p-eukaryotic translational initiation factor 2a and activating transcription factor 6. Dietary LC supplementation downregulated mRNA expression relative to FA synthesis, reduced liver lipid and relieved liver damage through regulating β-oxidation and biogenesis of mitochondria and peroxisomes, as well as the ER stress pathway in fish fed with HFD. The present study provides the first evidence that dietary LC can improve lipid metabolism via simultaneously promoting FA β-oxidation capability and suppressing the ER stress pathway in fish.