mRNA Expression Of acetyl-CoA Carboxylase Research Articles

Glucagon-like peptide-1 analog liraglutide reduces fat deposition in chicken adipocytes

Previously, we reported that glucagon-like peptide-1 (GLP-1) and its analog liraglutide could inhibit fat de novo synthesis in the liver and reduce abdominal fat accumulation in broiler chickens. Nevertheless, the impact of GLP-1 on adipocyte fat deposition remains enigmatic. This study aimed to investigate the effects of GLP-1, via its analog liraglutide, on chicken chicken adipocytes in vitro. Chemical assays, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot were employed to assess the proliferation, differentiation, and fat deposition of chicken adipocytes. Our findings indicated that liraglutide significantly suppressed cell proliferation and promoted preadipocyte differentiation in comparison to the control group. This was evidenced by elevated triglyceride (TG) content and upregulated mRNA expression of lipogenesis-related enzymes, such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), as well as regulators including peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element binding protein-1 (SREBP1) and CCAAT/enhancer binding protein α (CEBPα). In mature adipocytes, liraglutide attenuated fat deposition by inhibiting fat de novo synthesis, evidenced by decreased mRNA expression of ACC, FAS, PPARγ, C/EBPα, and SREBP1, and concurrent upregulation of phosphorylated AMP-activated protein kinase (p-AMPK) and phosphorylated ACC (p-ACC). This resulted in reduced accumulation of lipid droplets and TG content in mature adipocytes. Collectively, our findings indicate that liraglutide suppresses the proliferation of preadipocytes, enhances their differentiation, and concurrently inhibits de novo lipogenesis in mature adipocytes. This observation offers profound insights into the mechanisms that underlie liraglutide's anti-adipogenic effects, which could have significant implications for the treatment of obesity in broiler chickens.

Oleuropein-Rich Jasminum Grandiflorum Flower Extract Regulates the LKB1-PGC-1α Axis Related to the Attenuation of Hepatocellular Lipid Dysmetabolism.

Diets() rich in fat are a major() cause() of metabolic disease(), and nutritional() food has been widely() used() to counteract the metabolic disorders such() as obesity() and fatty() liver(). The present study investigated the effects of oleuropein-enriched extract() from Jasminum grandiflorum L. flowers (OLE-JGF) in high-fat diet() (HFD)-fed mice and oleic acid() (OA)-treated AML-12 cells. Treatment() of HFD-fed mice with 0.6% OLE-JGF for 8 weeks significantly reduced body and liver() weights, as well as attenuating lipid dysmetabolism and hepatic steatosis. OLE-JGF administration() prominently suppressed the mRNA expressions() of monocyte chemoattractant protein()-1 (MCP-1) and cluster of differentiation 68 (CD68), and it also downregulated acetyl-CoA carboxylase (ACC) and fatty() acid() synthase (FAS) as well as sterol-regulatory-element()-binding protein() (SREBP-1c) in the liver(). Meanwhile, mitochondrial DNA and uncoupling protein() 2 (UCP2) were upregulated along with the increased expression() of mitochondrial biogenic promoters including liver() kinase B1 (LKB1), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear() factor()-erythroid-derived 2-like 2 (Nrf2), and mitochondrial transcription factor() A (Tfam), but did not change AMP-activated protein() kinase (AMPK) in liver(). The lipid droplets were decreased significantly after treatment() with 80 μM oleuropein for 24 h in OA-induced AML-12 cells. Furthermore, oleuropein significantly inhibited ACC mRNA expression() and upregulated LKB1, PGC-1α, and Tfam mRNA levels, as well as increasing the binding level of LKB1 to PGC-1α promoter in OA-induced cells. These findings indicate() that OLE-JGF reduces hepatic lipid deposition in HFD-fed mice, as well as the fact that OA-induced liver() cells may be partly() attributed to upregulation of the LKB1-PGC-1α axis, which mediates hepatic lipogenesis and mitochondrial biogenesis. Our study provides a scientific() basis() for the benefits and potential() use() of the J. grandiflorum flower as a food supplement() for the prevention() and treatment() of metabolic disease().

Effects of dietary carbohydrate on growth, feed utilization, hepatic glucose and lipid metabolism in endangered Yangtze sturgeon (Acipenser dabryanus)

The aim of this study was to determine the effects of dietary carbohydrate levels on growth performance, feed utilization and metabolism of juvenile Yangtze sturgeon (Acipenser dabryanus). Six isonitrogenous (crude protein 45 %) and isolipidic (crude lipid 10 %) experimental diets were formulated containing 7.35 %, 10.2 %, 13.4 %, 16.5 %, 19.4 % and 22.4 % carbohydrate. Triplicate groups of 15 fish (initial weight, 51.4 ± 0.16 g) were fed twice daily for 8 weeks. The significantly higher (P < 0.05) growth performance was recorded in dietary 19.4 % group compared with the dietary 7.35 % and 10.2 % groups. Meanwhile, higher dietary carbohydrate (16.5 %, 19.4 % and 22.4 %) also significantly improved feed conversion ratio compared with the lowest one (7.35 %). Protein efficiency ratio exhibited similar tendency with growth performance. And the highest muscle crude protein was found in 19.4 % group and was significantly higher than the lower dietary carbohydrate groups (7.35 %, 10.2 %, 13.4 %) (P < 0.05). Liver glycogen content was positively correlated with dietary carbohydrate levels. The highest dietary carbohydrate level (22.4 %) led to much more lipid deposition in the body. Furthermore, the highest mRNA expression of Acetyl-CoA carboxylase and fatty acid synthesis were also recorded in dietary carbohydrate 22.4 % group. mRNA expression of glycolysis related genes hexokinase was significantly (P < 0.05) up-regulated by higher levels of carbohydrate (19.4 % and 22.4 %) compared with other treatments. Quadratic broken-line analysis of weight gain against carbohydrate levels showed that the optimal value was 20.6 % of diet for Yangtze sturgeon.

Electroacupuncture improves follicular development and metabolism and regulates the expression of adiponectin, AMPK and ACC in an obese rat model of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism and follicular arrest. Electroacupuncture (EA) has been shown to be effective at improving hyperandrogenism and follicular arrest in PCOS; however, its mechanism of action remains to be deciphered. In this study, we investigated whether EA improved follicular development in an obese rat model of PCOS and regulated the expression of adiponectin, AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). EA was administered at CV3, CV4 and ST40. Changes in body weight, paraovarian fat, estrus cycle, ovarian morphology, levels of related hormones, and glucose and lipid metabolism were evaluated. In addition, protein and mRNA expression of adiponectin, AMPK and ACC was measured. The body weight and paraovarian fat of rats in the EA group were reduced, while estrus cyclicity and ovarian morphology improved. Levels of free fatty acids, triglycerides, total cholesterol and low-density lipoprotein cholesterol were significantly reduced in the EA group, as well as blood glucose levels. Furthermore, levels of testosterone and luteinizing hormone were reduced in the EA group, while estradiol levels were increased. Protein and mRNA expression of adiponectin, AMPKα1 and liver kinase B1 (LKB1) was found to be increased in the EA group, while protein and mRNA expression of ACC were significantly reduced.Conclusion: Our findings suggest that EA improved follicular development and metabolism and regulated expression levels of adiponectin, AMPKα1, LKB1 and ACC in our obese rat model of PCOS.

Use of 25-hydroxyvitamin D3 in diets for sows: A review.

Dietary supplementation with 25-hydroxyvitamin D3 (25OHD3), as an alternative source of vitamin D, is becoming increasingly popular due to its commercialization and more efficient absorbability. The addition of 25OHD3 rather than its precursor vitamin D3 can circumvent the 25-hydroxylation reaction in the liver, indicating that supplementation of 25OHD3 can rapidly improve the circulating vitamin D status of animals. Emerging experiments have reported that maternal 25OHD3 supplementation could increase sow performances and birth outcomes and promote circulating vitamin D status of sows and their offspring. Increased milk fat content was observed in many experiments; however, others demonstrated that adding 25OHD3 to lactating sow diets increased the contents of milk protein and lactose. Although an inconsistency between the results of different experiments exists, these studies suggested that maternal 25OHD3 supplementation could alter milk composition via its effects on the mammary gland. Previous studies have demonstrated that adding 25OHD3 to sow diets could improve the mRNA expressions of insulin-induced gene 1 (INSIG1) and sterol regulatory element-binding protein 1 (SREBP1) in the mammary gland cells from milk and increase the mRNA expressions of acetyl-CoA carboxylase α (ACCα) and fatty acid synthase (FAS) in the mammary gland tissue. Maternal 25OHD3 supplementation promotes skeletal muscle development of piglets before and after parturition, and improves bone properties including bone density and bone breaking force in lactating sows and their piglets. Interestingly, 25OHD3 supplementation in sow diets could improve neonatal bone development via regulation of milk fatty acid composition related to bone metabolism and mineralization. In this review, we also discuss the effects of adding 25OHD3 to sow diets on the gut bacterial metabolites of suckling piglets, and propose that butyrate production may be associated with bone health. Therefore, to better understand the nutritional functions of maternal 25OHD3 supplementation, this paper reviews advances in the studies of 25OHD3 for sow nutrition and provides references for practical application.

Growth performance, meat quality and lipid metabolism in finishing lambs fed diets containing rumen-unprotected and rumen-protected betaine

This study investigated the influence of dietary supplementation of rumen-unprotected betaine (RUPB) and rumen-protected betaine (RPB) on growth performance, meat quality and fatty acid profile in intramuscular and subcutaneous fat of growing lambs. A total of 24 Hu male lambs were equally divided into three groups and fed a basal diet or basal diet supplemented with 1.6 g/kg of RUPB or 2.9 g/kg of RPB for 68 days. The water loss, redness of longissimus dorsi (LD) muscle and abdominal fat percentage were reduced in RUPB and RPB groups (p < .05). RPB supplementation decreased the shear force of LD muscle (p < .05). Polyunsaturated fatty acid (PUFA) content in LD muscle was decreased in RPB group, whereas n-3PUFA content was increased in RUPB group (p < .05). RUPB and RPB supplementation reduced the content of saturated fatty acid (SFA), and increased the contents of PUFA, monounsaturated fatty acid (MUFA), and n-6PUFA in subcutaneous fat (p < .05). Furthermore, dietary RUPB and RPB supplementation increased the mRNA expression of acetyl-CoA carboxylase (ACC) and glycerol-3-phosphate acyltransferase 1 (GPAT1) in LD muscle (p<.05); it increased the mRNA expression of fatty acid synthetase (FANS) and lipoprotein lipase (LPL) but reduced the mRNA expression of GPAT1 in subcutaneous fat (p < .05). In conclusion, either RUPB or RPB supplementation may improve the meat quality and slightly change the fat deposition and fatty acid composition of intramuscular and subcutaneous fat, and RUPB is recommended as a supplement for growing male lambs based on its lower cost. Highlights Dietary supplementation of both rumen-unprotected betaine and (RUPB) and rumen-protected betaine (RPB) improved meat quality and altered the fat deposition of growing male lambs. Both RUPB and RPB supplementation changed fatty acid composition in the longissimus dorsi muscle and subcutaneous adipose tissue. RUPB is recommended as a supplement for growing lambs based on its lower cost.

The Dietary Replacement of Soybean Oil by Canola Oil Does Not Prevent Liver Fatty Acid Accumulation and Liver Inflammation in Mice.

A high-carbohydrate diet (HCD) is a well-established experimental model of accelerated liver fatty acid (FA) deposition and inflammation. In this study, we evaluated whether canola oil can prevent these physiopathological changes. We evaluated hepatic FA accumulation and inflammation in mice fed with a HCD (72.1% carbohydrates) and either canola oil (C group) or soybean oil (S group) as a lipid source for 0, 7, 14, 28, or 56 days. Liver FA compositions were analyzed by gas chromatography. The mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was measured as an indicator of lipogenesis. The mRNA expression of F4/80, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-10, as mediators of liver inflammation, were also measured. The C group stored less n-6 polyunsaturated FAs (n-6 PUFAs) and had more intense lipid deposition of monounsaturated FAs (MUFAs), n-3 PUFAs, and total FAs. The C group also showed higher ACC1 expression. Moreover, on day 56, the C group showed higher expressions of the inflammatory genes F4/80, TNF-α, IL-1β, and IL-6, as well as the anti-inflammatory IL-10. In conclusion, a diet containing canola oil as a lipid source does not prevent the fatty acid accumulation and inflammation induced by a HCD.

Molecular mechanism of non-alcoholic fatty liver disease induced and aggravated by chronic stress through HSL/ATGL-FFA which promotes fat mobilization

Abstract Objective To study the effects of social stress (CS) and social stress combined with high-fat diet on fat mobilization as a candidate mechanism for the induction or aggravation of non-alcoholic fatty liver disease (NAFLD). Methods Thirty-two male Wistar rats (250 ± 10 g) were randomly allocated to a blank control group (BC), a high-fat diet group (HFD), a CS group, and a combined CS and high-fat diet group (CS + HFD). Rats were sacrificed and tissues were collected after 8 weeks. Liver and body mass were measured and used to calculate the liver index. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and free fatty acids (FFAs) were measured. Liver sections were examined microscopically after oil red O and hematoxylin and eosin staining. The relative mRNA expression of acetyl-CoA carboxylase (ACCase), hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase in liver, and hormone-sensitive lipase (HSL), and adipose triglyceride lipase (ATGL) in subcutaneous adipose tissue, were measured by real-time PCR. The liver concentrations of triglyceride, reactive oxygen species, and ACCase were measured by ELISA and HSL activity was determined using turbidimetry. Results NAFLD developed in the CS, HFD, and CS + HFD groups, with the most severe NAFLD being in the CS + HFD group. Serum AST, ALT, and FFA, liver index, and hepatic triglyceride, FFA, and tumor necrosis factor-α were significantly higher in both the CS and CS + HFD groups. However, food intake and ACCase mRNA expression were lower. The mRNA expression of HSL and ATGL in adipose tissue was much higher, and HSL activity was higher in the CS group than in the BC group, and in the CS + HFD group than in the HFD group. Conclusion We have successfully established two models of stress-induced NAFLD, suggesting stress can induce and aggravate NAFLD by promoting fat mobilization through upregulation of HSL and ATGL.

Effects of maternal 25-hydroxycholecalciferol on nutrient digestibility, milk composition and fatty-acid profile of lactating sows and gut bacterial metabolites in the hindgut of suckling piglets

ABSTRACTTo investigate the effects of maternal 25-hydroxycholecalciferol (25OHD3) supplementation during lactation on nutrient digestibility and milk composition of sows and gut bacterial metabolites and their metabolites in the hindgut of suckling piglets, 24 Large White × Landrace sows were assigned randomly to one of two dietary treatments (Diet ND: 2000 IU vitamin D3/kg feed; Diet 25-D: 50 μg 25OHD3/kg feed). The experiment began on d 107 of gestation and continued until weaning on d 21 of lactation. Maternal 25OHD3 supplementation increased (p < 0.05) total litter weight gain during lactation. Milk fat content, immunoglobulin G level on d 21 of lactation and 25OHD3 concentration on d 7, 14, and 21 of lactation were higher (p < 0.05) in sows fed with 25OHD3. Apparent total tract digestibility of dietary calcium was higher (p < 0.05) in 25-D sows than ND sows. With respect to fatty-acid profile, C16:0 and saturated fatty acids in milk were higher (p < 0.05), but C20:4n-6, the ratios of monounsaturated fatty acids to saturated fatty acids and polyunsaturated fatty acids to saturated fatty acids were lower (p < 0.05) in 25-D sows than ND sows. 25OHD3 supplementation increased the mRNA expressions of acetyl-CoA carboxylase α and fatty-acid synthase in the mammary gland of lactating sows. For gut bacterial metabolites, concentration of butyrate in the caecal digesta was higher (p < 0.05) in piglets suckling 25-D sows than piglets suckling ND sows. In conclusion, 25OHD3 supplementation in maternal diets changed dietary calcium digestibility, milk composition and milk fatty-acid profile of lactating sows and altered gut bacterial metabolites in the hindgut of suckling piglets.

Molecular identification of sterol regulatory element‐binding protein‐1c from Helicoverpa armigera pheromone gland

AbstractSterol regulatory element‐binding protein‐1c (SREBP‐1c) is a basic helix‐loop‐helix type transcription factor that regulates the fatty acid and cholesterol biosynthesis. Lepidoptera sex pheromone is a product of fatty acid biosynthesis followed by carbon chain modifications. However, the role of SREBP‐1c on sex pheromone biosynthesis remains elusive. In the present study, Helicoverpa armigera was used as a model to investigate the role of SREBP‐1c on sex pheromone biosynthesis (HaSREBP‐1c). Sequence analysis demonstrated that the open reading frame of HaSREBP‐1c consists of 3201 bp nucleotides that encode 1066 amino acid residues. Blast searches based on amino acid sequences demonstrated that HaSREBP‐1c shares higher amino acid identity with lepidopteran homologues. Development expression profiles demonstrated that HaSREBP‐1c transcript could be detected at 72 hr before adult emergence, then gradually increased, and finally reached its peak at 24 hr after adult emergence. The spatial expression pattern demonstrated that HaSREBP‐1c was ubiquitously expressed in all examined tissues. The decrease of HaSREBP‐1c messenger RNA (mRNA) levels as shown by RNA interference caused significant decreases in acetyl‐coA carboxylase (ACC) mRNA levels and subsequent sex pheromone production. Behavior analysis demonstrated that the decrease of HaSREBP‐1c mRNA level caused a significant decrease in the female’s ability to attract males. Altogether our results demonstrated that HaSREBP‐1c acts as a transcription factor to regulate ACC mRNA expression and, therefore, to influence female sex pheromone biosynthesis.

Prebiotic attenuation of olanzapine-induced weight gain in rats: analysis of central and peripheral biomarkers and gut microbiota

Olanzapine is an effective antipsychotic drug but since it causes significant weight gain, it is not well tolerated by psychosis patients. The prebiotic, B-GOS®, attenuates metabolic dysfunction in obese subjects, and in rodents, alters central NMDA receptors and may affect serotonin receptors that are relevant in psychosis. We have determined whether B-GOS® influenced olanzapine-associated weight gain and central NMDA and serotonin receptors. Circulating acetate, IL-1β, IL-8 and TNFα, liver acetyl-CoA carboxylase (ACC), white adipose tissue (WAT) acetate receptor GPR43, and specific faecal bacteria genera were also measured to provide mechanistic information. Adult female Sprague-Dawley rats were administered a B-GOS® (0.5 g/kg/day) solution or water for 21 days, and received a single, daily, intraperitoneal injection of olanzapine or saline on days 8–21. The intake of B-GOS® significantly attenuated olanzapine-induced weight gain without altering frontal cortex 5-HT2AR blockade. Cortical GluN1 levels were elevated by olanzapine in the presence of B-GOS®. Plasma acetate concentrations increased following B-GOS® or olanzapine administration alone, but reduced when prebiotic and drug were administered in combination. This pattern was paralleled by hepatic ACC mRNA expression. The abundance of WAT GPR43 mRNA was reduced by olanzapine, only in the absence of B-GOS®. Co-administration of B-GOS® and olanzapine also elevated plasma TNFα, which is reported to influence lipid metabolism. Finally, B-GOS® elevated faecal Bifidobacterium spp. and reduced some bacteria in the Firmicutes phylum, whilst olanzapine treatment either alone or with B-GOS®, was without effect. These data suggest that inclusion of B-GOS® as an adjunct to olanzapine treatment in schizophrenia may prevent weight gain and have benefits on cognitive function in psychosis. The role of acetate in these effects requires further investigation.

P.1.015 - Influence of prebiotic intake on olanzapine-mediated weight gain, central receptors, peripheral biomarkers, and gut microbiota

Olanzapine is the first-line antipsychotic treatment for schizophrenia, but often leads to secondary health concerns such as metabolic syndrome and weight gain. Studies in rats have shown that chronic olanzapine administration induces weight gain [1] and reduces hippocampal glutamate N-methyl-D-Aspartate receptor (NMDAR) levels, the latter which may hinder the recovery of cognitive function in schizophrenia patients. We have shown that dietary augmentation of beneficial gut bacteria using the commercially available prebiotic Bimuno ™ galacto-oligosaccharides (B-GOS ® ) increases central levels of NMDAR subunits in rodents [2,3]. The aim of this study was to determine whether the effects of olanzapine on weight gain and peripheral effects are influenced by B-GOS® intake in rats. Adult female Sprague-Dawley rats were provided with a B-GOS ® (0.5g/kg/day) solution or water for 21 days, and received a single, daily, intraperitoneal injection of olanzapine or saline on days 8-21. Weight gain and water intake were monitored daily. We determined whether B-GOS ® influenced olanzapine-associated weight gain, and central NMDAR and serotonin receptor expression. Circulating levels of acetate, IL-1β, IL-8 and TNFα as well as liver acetyl-CoA Carboxylase (ACC), white adipose tissue acetate receptor GPR43, and specific faecal bacteria genera were also measured to provide mechanistic information. Two-way ANOVAs were used to analyse all data, with repeated measures included to explore weight gain. Olanzapine induced significant weight gain (p ® -fed rats. Significant effect of treatment was observed on hippocampal GluN1 mRNA abundance (p = 0.034), where olanzapine significantly increased (+17%) levels in the absence of B-GOS ® (p = 0.040). Plasma acetate concentrations increased following B-GOS ® or olanzapine administration alone, but reduced when prebiotic and drug were administered in combination. This pattern was paralleled by hepatic ACC mRNA expression. The abundance of WAT GPR43 mRNA was reduced by olanzapine, only in the absence of B-GOS ® . Co-administration of B-GOS ® and olanzapine also elevated plasma TNFα, which is reported to influence lipid metabolism. Finally, B-GOS ® elevated faecal Bifidobacterium Spp. and reduced some bacteria in the Firmicutes phylum, whilst olanzapine treatment either alone or with B-GOS ® , was without effect. The current study demonstrates a potential strategy to reduce olanzapine-mediated weight gain in schizophrenia without compromising a key central pharmacological action of this antipsychotic. We also demonstrate a NMDAR augmenting effect, supporting a potential pro-cognitive effect of the prebiotic. Our data also implies that elevated TNFα in B-GOS ® /olanzapine rats may contribute to the reduction in olanzapine-induced weight gain as pro-inflammatory TNFα is a recognised appetite suppressant. These data suggest that inclusion of B-GOS ® as an adjunct to olanzapine treatment in schizophrenia may prevent weight gain and have benefits on cognitive function in psychosis.

Atmospheric ammonia alters lipid metabolism-related genes in the livers of broilers (Gallus gallus).

Atmospheric ammonia in animal housing is reported to have adverse effects on livestock performance and animal health. Previous experiments have found that 75ppm ammonia reduced the production performance and altered body fat distribution quality of broilers. In this study, we examined the body fat distribution, serum metabolites and lipid metabolism gene expression of broiler exposed to ammonia. A total of 400 chickens were randomly allocated to four groups with four replicates and received ammonia treatments at 0, 25, 50 and 75ppm, respectively, for 3weeks. The average daily feed intake and weight gain were decreased when broiler was exposed to ammonia concentration exceeding 50ppm (p<.05). The increased abdominal fat and reduced thickness of subcutaneous adipose were found in broilers of 75ppm group (p<.05). When ammonia exceeded 50ppm, the content of fat in breast muscle of broiler was increased, and when ammonia was higher than 25ppm, the fat in liver was increased (p<.05). It showed that the fat content in liver was a sensitive index for broilers exposed to ammonia. Furthermore, ammonia exposure had no significant effect on total cholesterol and triglyceride in serum, but significantly increased the relative mRNA expression of acetyl-CoA carboxylase (p=.046) and malic enzyme in liver (p=.038), which indicated that ammonia exposure may increase the de novo fat synthesis in liver. In addition, ammonia increased the high-density lipoprotein cholesterol (p=.02) and activity of hepatic lipase in serum (p<.001), which indicated that ammonia exposure may improve the transportation of cholesterol to liver. To conclude, our results indicated that ammonia exposure might increase the de novo fat synthesis in liver and increased the transportation of cholesterol to liver. In addition, the concentration of ammonia in poultry house should be limited lower than 25ppm based on the variation of hepatic fat content.

Anti-diabetic activities of catalpol in db/db mice.

The objective was to investigate the hypoglycemic action of catalpol in spontaneous diabetes db/db mice. 40 db/db mice were randomly divided into fi ve groups: model control gourp; db/db plus catalpol 40, 80, 120 mg/kg body wt. groups and db/db plus metformin 250 mg/kg group. Age-matched db/m mice were selected as normal control group. The mice were administered with corresponding drugs or solvent by gavage for 4 weeks. The oral glucose tolerance test was carried out at the end of 3rd week. After 4 weeks of treatment, the concentrations of fasting blood glucose (FBG), glycated serum protein (GSP), insulin (INS), triglyceride (TG), total cholesterol (TC) and adiponection (APN) in serum were detected. The protein expressions of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and glucose transporter-4 (GLUT-4) in skeletal muscle and adipose tissues were detected by western blot. Real time RT-PCR was used to detect the mRNA expressions of acetyl-CoA carboxylase (ACC) and Hydroxymethyl glutaric acid acyl CoA reductase (HMGCR) in liver. Our results showed that catalpol could significantly improve the insulin resistance, decrease the serum concentrations of INS, GSP, TG, and TC. The concentrations of APN in serum, the protein expression of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and GLUT-4 in peripheral tissue were increased. Catalpol could also down regulate the mRNA expressions of ACC and HMGCR in liver. In conclusion, catalpol ameliorates diabetes in db/db mice. It has benefi t eff ects against lipid/glucose metabolism disorder and insulin resistance. The mechanism may be related to up-regulating the expression of phosphorylation-AMPKα1/2.

Effect of the cryopreservation method used, the embryonic stage and the use of conjugated linoleic acid isomers on the cryotolerance of in vitro-produced bovine embryos

Conjugated linoleic acid (CLA) might be able to improve the cryotolerance of in vitro-produced (IVP) embryos. The effect of two CLA isomers on the cryotolerance of bovine IVP embryos, as well as that of the stage of embryonic development and the method used for cryopreservation was evaluated by three experiments. In Experiment 1, oocytes (n = 3,917) were fertilized in vitro and cultured with 0, 50, 100, or 200 ?M trans-10, cis-12 (t10, c12 CLA). In Experiment 2, fertilized oocytes (n = 2,131) were cultured with 100 ?M t10, c12 or cis-9, trans-11 (c9, t11 CLA), or a combination of both isomers. The embryos were vitrified at the blastocyst (BL) or the expanded blastocyst (EB) stage. In Experiment 3, oocytes (n = 1,720) were fertilized and cultured with or without 100 ?M t10, c12 CLA, and the blastocysts were vitrified or frozen. Blastocyst development rate as well as the rates of re-expansion and hatching after thawing was recorded. Moreover, the mean cell number and mRNA expression of acetyl-CoA carboxylase (ACC1) and stearoyl-CoA desaturase (SCD1) as well as fatty acid synthase (FASN) multienzyme complex were determined. In Experiment 1, the highest concentration of t10, c12 CLA that did not reduce blastocyst development rate was 100 ?M. In Experiment 2, the rates of re-expansion and hatching among the EBs obtained through IVP after supplementation with t10, c12 CLA (73.1% and 57.7%), with c9, t11 CLA (80.0% and 68.6%), with the combination (78.3% and 52.2%), and with the control group (85.4% and 58.3%) were similar. At the BL stage, the rates of re-expansion and hatching were lower than those at the EB stage, and CLA combination allowed a hatching rate (8.0%) lower than that observed in the control group (40.0%). In Experiment 3, the hatching rates for vitrified EBs (vitrified control; 67.4%) and vitrified CLA EBs (65.8%) were higher than those obtained for frozen EBs, exposed (13.3%) or not exposed (28.6%) to CLA. In addition, in Experiment 3, the hatching rate was higher at the EB stage in vitrified groups, while the rates of BL and EB were similar in frozen groups, thus proving that vitrification was more efficient than freezing for IVP bovine embryos. In Experiment 3, CLA isomer t10, C12 did not influence the embryonic cell number or mRNA expression of ACC1 and SCD1 enzymes, but decreased the mRNA expression of FASN. In conclusion, 100 ?M CLA did not affect subsequent embryonic development. However, neither CLA isomer improved the cryotolerance of IVP bovine embryos.

Effect of the cryopreservation method used, the embryonic stage and the use of conjugated linoleic acid isomers on the cryotolerance of in vitro-produced bovine embryos

&lt;p&gt;Conjugated linoleic acid (CLA) might be able to improve the cryotolerance of &lt;em&gt;in vitro-&lt;/em&gt;produced (IVP) embryos. The effect of two CLA isomers on the cryotolerance of bovine IVP embryos, as well as that of the stage of embryonic development and the method used for cryopreservation was evaluated by three experiments. In Experiment 1, oocytes (n = 3,917) were fertilized &lt;em&gt;in vitro &lt;/em&gt;and cultured with 0, 50, 100, or 200 ?M &lt;em&gt;trans-&lt;/em&gt;10&lt;em&gt;, cis-&lt;/em&gt;12 (t10, c12 CLA). In Experiment 2, fertilized oocytes (n = 2,131) were cultured with 100 ?M t10, c12 or &lt;em&gt;cis-&lt;/em&gt;9&lt;em&gt;, trans-&lt;/em&gt;11 (c9&lt;em&gt;, &lt;/em&gt;t11 CLA), or a combination of both isomers. The embryos were vitrified at the blastocyst (BL) or the expanded blastocyst (EB) stage. In Experiment 3, oocytes (n = 1,720) were fertilized and cultured with or without 100 ?M t10, c12 CLA, and the blastocysts were vitrified or frozen. Blastocyst development rate as well as the rates of re-expansion and hatching after thawing was recorded. Moreover, the mean cell number and mRNA expression of acetyl-CoA carboxylase (ACC1) and stearoyl-CoA desaturase (SCD1) as well as fatty acid synthase (FASN) multienzyme complex were determined. In Experiment 1, the highest concentration of t10, c12 CLA that did not reduce blastocyst development rate was 100 ?M. In Experiment 2, the rates of re-expansion and hatching among the EBs obtained through IVP after supplementation with t10, c12 CLA (73.1% and 57.7%), with c9, t11 CLA (80.0% and 68.6%), with the combination (78.3% and 52.2%), and with the control group (85.4% and 58.3%) were similar. At the BL stage, the rates of re-expansion and hatching were lower than those at the EB stage, and CLA combination allowed a hatching rate (8.0%) lower than that observed in the control group (40.0%). In Experiment 3, the hatching rates for vitrified EBs (vitrified control; 67.4%) and vitrified CLA EBs (65.8%) were higher than those obtained for frozen EBs, exposed (13.3%) or not exposed (28.6%) to CLA. In addition, in Experiment 3, the hatching rate was higher at the EB stage in vitrified groups, while the rates of BL and EB were similar in frozen groups, thus proving that vitrification was more efficient than freezing for IVP bovine embryos. In Experiment 3, CLA isomer t10, C12 did not influence the embryonic cell number or mRNA expression of ACC1 and SCD1 enzymes, but decreased the mRNA expression of FASN. In conclusion, 100 ?M CLA did not affect subsequent embryonic development. However, neither CLA isomer improved the cryotolerance of IVP bovine embryos.&lt;/p&gt;

Effect of neonatal overfeeding on associated enzymes of lipid metabolism in rat liver

Objective To investigate the effect of neonatal overfeeding on the expression of lipid metabolic associated enzymes and molecular mechanisms in the livers of rats. Methods Male Sprague-Dawley rats were randomly assigned to litter sizes of three group (small litters, SL group) or ten (normal litters, NL group) on postnatal day 3.Body weight, milk intake, liver and fat pad (epididymal and retroperitonea) weight, and hepatic histological analysis were recorded in week 2 and week 3, respectively.The levels of lipids were detected by the automatic biochemical analyzer.The mRNA expressions of acetyl-CoA carboxylase (ACC), lipoprotein lipase (LPL), liver-type fatty acid-binding protein (L-FABP), carnitine palmitoyltransferase 1(CPT1), microsomal triglyceride transfer protein (MTP), sterol regulatory element-binding protein-1c (SREBP-1c) and peroxisome proliferator activated receptor α (PPARα)in liver were determined by real time PCR; the protein expressions of SREBP-1c and PPARα were determined by Western lot. Results As early as week 2, the body weight of rats in SL group began to elevate (t=-5.997, P<0.001) and food intake (t=-3.462, P=0.002) compared with the rats in NL group, and persistent to weaning (body weight: t=-17.019, P<0.001; food intake: t=-2.276, P=0.031). By the time of 3 weeks old, SL rats increased visceral fat pad [retroperitonea (t=-7.643, P<0.001), epididymal (t=5.997, P=0.001)], liver weight (t=-7.812, P<0.001), hepatosomatic index (t=-3.829, P=0.003) and serum triglyceride (TG) level (t=-2.703, P=0.022) compared with those of NL rats, as well as the level of hepatic ACC mRNA (t=-3.751, P=0.007), LPL (t=-2.721, P=0.017) and L-FABP mRNA (t=-2.521, P=0.026) .While CPT1 mRNA (t=-1.531, P=0.155) and MTP mRNA (t=-1.741, P=0.098) levels remained unchanged in both groups.Hepatic SREBP-1c mRNA expression increased in SL rats after 2 to 3 weeks (t=-2.836, P=0.016), paralleled with ACC and LPL mRNA expression; while the mRNA and protein expression of PPARα remained unchanged (t=-0.854, P=0.411). Conclusions Postnatal overfeeding can promote higher liver pad and dyslipidemia at the time of weaning.The process may be regulated by up-regulated expression of ACC, LPL and L-FABP.SREBP-1c may be participated in the regulation of ACC, a rate-limiting enzyme involved in lipogenesis. Key words: Nutritional programming; Liver; Lipid metabolism; Rat

발효울금 50% 에탄올 추출물의 라디칼 소거능 및 지방형성 억제 효과

In this study, free radical scavenging activities (ABTS, DPPH, NBT, TBARS, and ORAC) and anti-obesity potential were evaluated using 50% ethanol extract from fermented Curcuma longa L. (FCE50). FCE50 showed free radical scavenging activities and anti-oxidant potential. Lipid accumulation and intracellular TG content were significantly reduced by 25.8% and 28.6%, respectively, by 250 μg/mL of FCE50 compared to adipocytes. Glucose uptake was significantly reduced by 12.0%. FCE50 significantly reduced mRNA expression of acetyl-CoA carboxylase in 3T3-L1 cells. These results indicate that the anti-adipogenic effect of FCE50 might be due to its radical scavenging activity and anti-oxidant potential.

Arachidonic acid has a dominant effect to regulate lipogenic genes in 3T3-L1 adipocytes compared to omega-3 fatty acids

BackgroundThe effects of long-chain n-3 and n-6 polyunsaturated fatty acids (PUFA) on the regulation of adipocytes metabolism are well known. These fatty acids are generally consumed together in our diets; however, the metabolic regulation of adipocytes in the presence of these fatty acids when given together is not known.ObjectiveTo investigate the effects of n-3 PUFA and arachidonic acid (AA), an n-6 PUFA, on the regulation of adipogenic and lipogenic genes in mature 3T3-L1 adipocytes.Methods3T3-L1 adipocytes were incubated in the presence or absence of 100 µM of eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA; docosapentaenoic acid, DPA and AA, either alone or AA+n-3 PUFA; control cells received bovine serum albumin alone. The mRNA expression of adipogenic and lipogenic genes was measured. The fatty acid composition of adipocytes was analyzed using gas chromatography.ResultsIndividual n-3 PUFA or AA had no effect on the mRNA expression of peroxisome-proliferator-activated receptor-γ; however, AA+EPA and AA+DPA significantly increased (P<0.05) the expression compared to control cells (38 and 42%, respectively). AA and AA+EPA increased the mRNA expression of acetyl-CoA carboxylase 1 (P<0.05). AA treatment decreased the mRNA expression of stearoyl-CoA desaturase (SCD1) (P<0.01), while n-3 PUFA, except EPA, had no effect compared to control cells. AA+DHA and AA+DPA inhibited SCD1 gene expression (P<0.05) suggesting a dominant effect of AA. Fatty acids analysis of adipocytes revealed a higher accretion of AA compared to n-3 PUFA.ConclusionsOur findings reveal that AA has a dominant effect on the regulation of lipogenic genes in adipocytes.

Dietary CLA‐induced Lipolysis Is Delayed in Soy Oil‐Fed Mice Compared to Coconut Oil‐Fed Mice

Conjugated linoleic acid (CLA) has been shown to cause a reduction in obesity in several species. CLA-induced body fat loss is enhanced when mice are fed coconut oil (CO) and involves increased lipolysis. The objective of this paper was to determine if the CLA-induced lipolysis in mice fed with different oil sources was time-dependent. Mice were fed 7% soybean oil (SO) or CO diets for 6week and then supplemented with 0 or 0.5% CLA for 3, 7, 10 or 14days. Body fat and ex-vivo lipolysis was determined. Body fat was reduced by CO on day 7 (P<0.01) and in both CO and SO-fed mice (P<0.05) in response to CLA on d14. Lipolysis was increased by CLA in CO-fed mice (P<0.01) but not in SO-fed mice on day 7 and 10, but on day 14 CLA increased lipolysis in both CO- and SO-fed mice (P<0.001). Expression and activation level of proteins involved in lipolysis and lipogenesis was determined by western blotting and real-time PCR, respectively. No significant differences were detected in protein expression. CO-fed mice had greater fatty acid synthase and stearyl CoA desaturase 1 mRNA expression and less acetyl CoA carboxylase mRNA expression (P<0.01). Sterol regulatory binding protein 1c was decreased by CLA in CO-fed mice and increased in SO-fed mice (P<0.05). Malic enzyme expression was increased by CLA (P<0.001) and CO (P<0.01). Therefore, CLA-induced lipolysis occurs more rapidly in CO vs SO-fed mice and lipogenesis is decreased in CO-fed mice with CLA supplementation.