Metabolism-related Genes In Liver Research Articles

Differences in expression of fat metabolism-related genes in liver and adipose tissue after ingestion of high-fat diet in obese and obesity-resistant mouse strains

Differences in expression of fat metabolism-related genes in liver and adipose tissue after ingestion of high-fat diet in obese and obesity-resistant mouse strains

Effects of age and diet forms on growth-development patterns, serum metabolism indicators, and parameters of body fat deposition in Cherry Valley ducks.

ObjectiveThis study was conducted to investigate the effects of age and diet forms on growth-development patterns, serum metabolism indicators, and parameters of body fat deposition in Cherry Valley ducks.MethodsAccording to the hatching age and initial weight, a total of 150 1-day-old male SM3 Cherry Valley ducks were randomly assigned to two diet forms (pellet vs powder form). Each treatment had with 5 replicates per treatment and 15 meat ducks per replicate. The study lasted 42 d, which was divided into two periods (1 to 21 vs 22 to 42 d).ResultsOur results showed that compared with powder group, ducks in pellet group had greater growth performance during different period (p<0.05). The inflection point was 24 d and was not numerically affected by diet forms. Increasing age (42 vs 21 d) significantly increased the weight of body fat and hepatic fat metabolism related enzyme activities in ducks (p<0.05), meanwhile, increasing age (42 vs 21 d) improved serum metabolism indicators and decreased mRNA expression levels of fat metabolism-related genes in liver (p<0.05). Ducks fed different diets (pellet vs powder form) increased growth performance as well as the weight of body fat and improved serum metabolism indicators (p<0.05). In addition, interactions were found between age and diet forms on the levels of serum metabolism indicators in ducks (p<0.05).ConclusionIn conclusion, powder feed reduced growth performance of ducks, and the day of inflection point was 24 days old. Ducks with higher age or fed with pellet diet showed higher fat deposition. The effect of age and feed forms on body fat deposition might result from changes in the contents of serum metabolism indicators, key enzyme activity of lipid production, and hepatic gene expressions.

PO-111 Effects of aerobic exercise on fatty acid metabolism in liver of NAFLD Rats

Objective Aerobic exercise can improve liver metabolic diseases such as non-alcoholic fatty liverdisease (NAFLD), but the molecular mechanism is not completely clear, which limits the applicationof aerobic exercise in the treatment and improvement of NAFLD. In this paper, the effects of aerobicexercise on the expression levels of important genes regulating fatty acid metabolism in the liver ofNAFLD rats were studied in order to explore the possible molecular mechanism of aerobic exerciseregulating hepatic fatty acid metabolism.Methods 1. Animal grouping. 36 male Sprague Dawley (SD) rats aged 21 days old were randomlydivided into three groups after 1 week of adaptive feeding: 10 in the normal diet quiet group (NCgroup), 10 in the high-fat diet quiet group (HC group) and 16 in the high-fat diet exercise group (HTgroup). 2. Training arrangements. After 12 weeks, the rats in the HT group underwent 8 weeks ofaerobic exercise with a training intensity of 25m/min, and continued exercise for 1h/d, 6d/w for atotal of 8 weeks. 3. Sample collection. After an overnight fast, rats in the three groups were weighedand anesthetized with an intraperitoneal injection of 10% chloral hydrate (0.3 ml/100 g bodyweight). Blood samples were collected from the aortaventralis, centrifuged, and kept frozen at -80 °Cfor chemical assays. The rat liver was removed, frozen in liquid nitrogen, and stored in a -80 °Cfreezer. 4. Serum lipid concentration and liver function detection. Serum levels of total cholesterol(TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoproteincholesterol (LDL-C), free fatty acid (FFA), aspartate aminotransferase (AST) and alanineaminotransferase (ALT) were detected in three groups of rats. 5. Detection of expression levels offatty acid metabolism related genes in liver. The expression levels of AMP-activated protein kinase(AMPK), silence information regulator 1 (SIRT1), peroxisome proliferator-activated receptor γcoactivator 1α (PGC-1α) in rat liver were detected by SYBR Green real-time PCR. 6. Data statistics.Results were expressed in the form of mean±standard deviation. Spss17.0 statistical software wasused to conduct one-way ANOVA to compare the differences between the groups, p&lt;0.05 indicatessignificant difference between groups.Results 1. Effects of aerobic exercise on Blood lipids and liver function. The serum levels of TC, TG,LDL-C, FFA, AST and ALT in HC group were significantly higher than those in NC group (p &lt; 0.05),while HDL-C level was significantly lower (p &lt; 0.05). The serum concentrations of TC, TG, LDL-C, FFA,AST and ALT in HT group were significantly lower than those in HC group (p &lt; 0.05), while HDL-Clevel was significantly higher (p &lt; 0.05). 2.Effects of aerobic exercise on the expression of fatty acidmetabolism regulatory genes in liver of rats. The mRNA expression levels of AMPK, SIRT1 and PGC-1α in liver of HC group were significantly lower than those of NC group (p &lt; 0. 05). While the mRNAexpression levels of AMPK, SIRT1 and PGC-1 α in liver of HT group were significantly higher thanthose of HC group (p &lt; 0. 05).Conclusions Aerobic exercise can improve serum lipid concentration and liver function in NAFLDrats. It increased the consumption of ATP, led to an increase in AMP/ATP ratio, enhanced the mRNAexpression of AMPK, SIRT1 and PGC-1α, activated AMPK - SIRT1 - PGC-1α signaling pathway,reduced hepatic fat synthesis and accelerated fatty acid oxidation in NAFLD rats liver.&#x0D;

Association of mRNA expression of iron metabolism-associated genes and progression of non-alcoholic steatohepatitis in rats.

BackgroundExcess iron is associated with non-alcoholic steatohepatitis (NASH).ResultsmRNA expression of duodenal cytochrome b, divalent metal transporter 1, ferroportin 1, hepcidin, hephaestin and transferrin receptor 1 in liver were higher in high fat, high cholesterol-containing diet (HFCD) group than in normal diet (ND) group. mRNA levels of divalent metal transporter 1 and transferrin receptor 1, which stimulate iron absorption and excretion, were enhanced in small intestine. Epithelial mucosa of small intestine in HFCD group was characterized by plasma cell and eosinophil infiltration and increased vacuoles. Iron absorption was enhanced in this NASH model in the context of chronic inflammation of small intestinal epithelial cells, consequences of intestinal epithelial cell impairment caused by HFCD. Iron is transported to hepatocytes via portal blood, and abnormalities in iron absorption and excretion occur in small intestine from changes in iron transporter expression, which also occurs in NASH liver. Knockdown of hepcidin antimicrobial peptide led to enhanced heavy chain of ferritin expression in human hepatocytes, indicating association between hepcidin production and iron storage in hepatocytes.ConclusionsIron-related transporters in liver and lower/upper portions of small intestine play critical roles in NASH development.MethodsExpression of iron metabolism-related genes in liver and small intestine was analyzed in stroke-prone spontaneously hypertensive rats (SHR-SP), which develop NASH. Five-week-old SHR-SP fed ND or HFCD were examined. mRNA and protein levels of iron metabolism-related genes in liver and small intestine from 12- and 19-week-old rats were evaluated by real-time RT-PCR and immunohistochemistry or Western blot.

Liquid chromatography mass spectrometry-based profiling of phosphatidylcholine and phosphatidylethanolamine in the plasma and liver of acetaminophen-induced liver injured mice

BackgroundAcetaminophen (APAP) overdose is one of the most common causes of acute liver failure in many countries. The aim of the study was to describe the profiling of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the plasma and liver of Acetaminophen -induced liver injured mice.MethodsA time course study was carried out using C57BL/6 mice after intraperitoneal administration of 300 mg/kg Acetaminophen 1 h, 3 h, 6 h, 12 h and 24 h. A high-throughput liquid chromatography mass spectrometry (LC-MS) lipidomic method was utilized to detect phosphatidylcholine and phosphatidylethanolamine species in the plasma and liver. The expressions of phosphatidylcholine and phosphatidylethanolamine metabolism related genes in liver were detected by quantitative Reverse transcription polymerase chain reaction (qRT-PCR) and Western-blot.ResultsFollowing Acetaminophen treatment, the content of many PC and PE species in plasma increased from 1 h time point, peaked at 3 h or 6 h, and tended to return to baseline at 24 h time point. The relative contents of almost all PC species in liver decreased from 1 h, appeared to be lowest at 6 h, and then return to normality at 24 h, which might be partly explained by the suppression of phospholipases mRNA expressions and the induction of choline kinase (Chka) expression. Inconsistent with PC profile, the relative contents of many PE species in liver increased upon Acetaminophen treatment, which might be caused by the down-regulation of phosphatidylethanolamine N-methyltransferase (Pemt).ConclusionsAcetaminophen overdose induced dramatic change of many PC and PE species in plasma and liver, which might be caused by damaging hepatocytes and interfering the phospholipid metabolism in Acetaminophen -injured liver.

Effect of rumen-protected choline supplementation on liver and adipose gene expression during the transition period in dairy cattle

We previously reported that supplementation of rumen-protected choline (RPC) reduces the hepatic triacylglycerol concentration in periparturient dairy cows during early lactation. Here, we investigated the effect of RPC on the transcript levels of lipid metabolism-related genes in liver and adipose tissue biopsies, taken at wk −3, 1, 3, and 6 after calving, to elucidate the mechanisms underlying this RPC-induced reduction of hepatic lipidosis. Sixteen multiparous cows were blocked into 8 pairs and randomly allocated to either 1 of 2 treatments, with or without RPC. Treatments were applied from 3wk before to 6wk after calving. Both groups received a basal diet and concentrate mixture. One group received RPC supplementation, resulting in an intake of 14.4g of choline per day, whereas controls received an isoenergetic mixture of palm oil and additional soybean meal. Liver and adipose tissue biopsies were taken at wk −3, 1, 3, and 6 to determine the mRNA abundance of 18 key genes involved in liver and adipose tissue lipid and energy metabolism. Milk samples were collected in wk 1, 2, 3, and 6 postpartum for analysis of milk fatty acid (FA) composition. The RPC-induced reduction in hepatic lipidosis could not be attributed to altered lipolysis in adipose tissue, as no treatment effect was observed on the expression of peroxisome proliferator-activated receptor γ, lipoprotein lipase, or FA synthase in adipose tissue, or on the milk FA composition. Rumen-protected choline supplementation increased the expression of FA transport protein 5 and carnitine transporter SLC22A5 in the liver, suggesting an increase in the capacity of FA uptake and intracellular transport, but no treatment effect was observed on carnitine palmitoyl transferase 1A, transporting long-chain FA into mitochondria. In the same organ, RPC appeared to promote apolipoprotein B-containing lipoprotein assembly, as shown by elevated microsomal triglyceride transfer protein expression and apolipoprotein B100 expression. Cows supplemented with RPC displayed elevated levels of glucose transporter 2 mRNA and a reduced peak in pyruvate carboxylase mRNA immediately after calving, showing that supplementation also resulted in improved carbohydrate metabolism. The results from this study suggest that RPC supplementation reduces liver triacylglycerol by improved FA processing and very-low-density lipoprotein synthesis, and RPC also benefits hepatic carbohydrate metabolism.

Differential Expression of Metabolism-related Genes in Liver of Diabetic Obese Rats

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat, a model of spontaneous type 2 diabetes (T2D), develops hyperglycemic obesity with hyperinsulinemia and insulin resistance after the age of 25 weeks, similar to patients with noninsulin-dependent diabetes mellitus (DM). In the present study, we determined whether there are differences in the pattern of gene expression related to glucose and lipid metabolism between OLETF rats and their control counterparts, Long-Evans Tokushima (LETO) rats. The experiment was done using 35-week-old OLETF and LETO rats. At week 35 male OLETF rats showed overt T2D and increases in blood glucose, plasma insulin, plasma triglycerides (TG) and plasma total cholesterol (TC). Livers of diabetic OLETF and LETO rats also showed differences in expression of mRNA for glucose and lipid metabolism related genes. Among glucose metabolism related genes, GAPDH mRNA was significantly higher and FBPase and G6Pase mRNA were significantly lower in OLETF rats. For lipid metabolism related genes, HMGCR, SCD1 and HL mRNA were substantially higher in OLETF rats. These results indicate that gluconeogenesis in OLETF rats is lower and glycolysis is higher, which means that glucose metabolism might be compensated for by a lowering of the blood glucose level. However, lipid synthesis is increased in OLETF rats so diabetes may be aggravated. These differences between OLETF and LETO rats suggest mechanisms that could be targeted during the development of therapeutic agents for diabetes.

Expression profiles of lipid metabolism-related genes in liver of apoE(-/-)/LDLR(-/-) mice

To explore the relationship between the expression characteristics of lipid metabolism-related genes in the liver and early atherosclerotic lesions in apolipoprotein E and low density lipoprotein receptor gene double knockout (apoE(-/-)/LDLR(-/-)) mice. RT-PCR was used to detect the differential expression of lipid metabolism-related genes in the liver of apoE(-/-)/LDLR(-/-) and wild type (WT) mice. Serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) level as well as aortic morphology were also analyzed. Among the 11 lipid metabolism-related genes, apolipoprotein B100 (apoB100) mRNA levels were significantly higher in apoE(-/-)/LDLR(-/-)mice compared with WT mice. At 14 days, 1, 2 and 3 months of age, the level of mRNA expression were 1.55, 1.47, 1.50 and 2.42 folds of those of the age matched WT mice respectively. The fatty acid transporter (FAT/CD36) mRNA expression levels were higher in 14-day and 3-month old mice at 1.30 and 1.35 folds of those of the age matched WT mice, respectively. Apolipoprotein A IV (apoA IV) and Apolipoprotein AV (apoAV) mRNA levels were significantly down-regulated (0.89 fold decrease in 14-day, and 0.90 folds decrease in 3-month, respectively). The mRNA expression levels of apolipoprotein AI (apo AI), apolipoprotein F (apo F), peroxidase proliferator-activated receptor alpha (PPAR-alpha), liver X receptor alpha (LXRalpha), angiopoietin-like protein 3 (ANGPTL3), acyl-coenzymeA oxidase 1 (ACOX1) and carnitine palmitoyl transferase 1 (CPT1) had no significant changes. Serum TC, TG and LDL-C were higher than those of age matched WT mice at 7, 2 and 30 folds, respectively. Furthermore, apoE(-/-)/LDLR(-/-) mice demonstrated typical early atherosclerotic lesions at sinus and root regions of aorta in an age dependent manner. Alterations of the expression of lipid metabolism-related genes in liver play important roles in the development of AS in the apoE(-/-)/LDLR(-/-) mice at early ages.