Twenty castrated Boer crossbred goats were used in the present study with two treatments to examine the effect of dietary replacement of ordinary rice with red yeast rice on nutrient utilization, enteric methane emission and ruminal archaea structure and composition. Two treatment diets contained (DM basis) 70.0% of forage, 21.8% of concentrates and 8.2% of either ordinary rice (control) or red yeast rice (RYR). Nutrient utilization was measured and enteric methane emissions were determined in respiration chambers. Results showed that RYR had significantly lower digestibility of N and organic matter compared to control group. However, feeding red yeast rice did not affect N retention as g/d or a proportion of N intake, and reduced heat production as MJ/d or as a proportion of metabolizable energy intake, thus leading to a higher proportion of metabolizable energy intake to be retained in body tissue. RYR also had significantly lower methane emissions either as g/d, or as a proportion of feed intake. Although feeding red yeast rice had no negative effect on any rumen fermentation variables, it decreased serum contents of total cholesterol, triglycerides, HDL-cholesterol and LDL-cholesterol. In the present study, 75616 archaeal sequences were generated and clustered into 2364 Operational Taxonomic Units. At the genus level, the predominant archaea in the rumen of goats was Methanobrevibacter, which was significantly inhibited with the supplementation of red yeast rice. In conclusion, red yeast rice is a potential feed ingredient for mitigation of enteric methane emissions of goats. However, caution should be taken when it is used because it may inhibit the digestibility of some nutrients. Further studies are required to evaluate its potential with different diets and animal species, as well as its effects on animal health and food safety.
To investigate how cholesterol induces hepatocytic steatosis, we investigated the effect of cholesterol on hepatic lipogenesis and the assembly and secretion of very-low-density lipoprotein-triglycerides (VLDL-TGs) in goose primary hepatocytes. We found that cholesterol at 20 μg/ml increased the concentrations of extracellular VLDL, intracellular cholesterol, and intracellular TGs, while cholesterol at 30 μg/ml had a reduced effect (p < 0.05). Additionally, cholesterol at 20 μg/ml, but not at 10 or 30 μg/ml, increased the extracellular TG concentration. Cholesterol increased the fatty acid synthase (FAS) enzyme activity in a dose-dependent manner. Incubation with cholesterol increased the mRNA level of genes involved in lipogenesis, including sterol regulatory element-binding proteins (SREBPs), FAS, acetyl-CoA carboxylase-α (ACCα), and liver X receptors. The mRNA level of the acyl-CoA: diacylglycerol acyltransferase 1 (DGAT1) gene changed in response to cholesterol treatment in a dose-dependent manner. Similar to the regulation of extracellular VLDL and intracellular TG accumulation, the mRNA levels of the microsomal triglyceride transfer protein, forkhead box O1, and DGAT2 increased with treatment with 10 or 20 μg/ml of cholesterol, but decreased with treatment with 30 μg/ml of cholesterol (p < 0.05). Cholesterol had no evident effect on the mRNA level of the apolipoprotein B gene. Incubation with cholesterol at 20 and 30 μg/ml increased the nuclear SREBP-1 protein level (p < 0.05) and the binding affinity of the nuclear SREBP-1 to ACCα SRE probes. In conclusion, cholesterol not only activates the transcription of genes involved in fatty acid synthesis and TG accumulation, but also activates the transcription of genes involved in the assembly and secretion of VLDL-TG in goose primary hepatocytes.
The objective of the current research was to investigate the pattern of subcutaneous adipose tissue growth during Peking duck (Anas platyrhynchos) early development and to determine the reasons for regional differences. The morphological characteristics in 5 regions of subcutaneous tissue, including the neck area (NSF), chest area (CSF), lower abdomen area (ASF), back area (BSF), and leg area (LSF), were analyzed by comparing the morphology of the sections, adipocyte volume and number, and lipid content from wk 1 to 8. Moreover, the mRNA expression of several molecular marker genes, including 47-kDa tail interacting protein (TIP47), adipose differentiation-related protein (ADRP), and perilipin, were detected from wk 1 to 8 using quantitative real-time PCR. Our results revealed that the average cell number declined greatly as fattening proceeded (except in the NSF) and changed very little after wk 4 in all 5 regions. In contrast, the average cell volume and triglyceride content per cell increased gradually during early duck growth. The BSF and LSF lipid content had a different pattern of change than the other regions. The NSF, CSF, and ASF regions had the highest lipid content values at all stages, the BSF was intermediate, and the LSF was the lowest at all weeks except wk 3. The highest TIP47 expression level was found in the NSF from wk 1 to 2 and BSF at wk 1. The relative expression level of TIP47 was higher in the CSF than in the ASF and BSF at wk 4, and was higher in the NSF than in the ASF at wk 6. The highest levels of ADRP and perilipin were detected in the LSF. These results suggest that a combination of adipocyte hyperplasia and hypertrophy is mainly responsible for the development of duck adipose tissue before wk 4, after which adipose expansion is accomplished by adipocyte hypertrophy only. Adipocyte hyperplastic and hypertrophic capacity, fat storage capacity, and metabolic activity may be partial explanations for the regional differences during duck growth.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.