Search

BACKGROUND: The present study was designed to investigate the effect of albusin B on lipid metabolism and antioxidant defense in broiler chickens by a proteomic approach. The bacteriocin, albusin B of Ruminococcus albus 7, expressed by yeast was applied in this study. Three dietary treatments, consisting of the basal diet (control), basal diet + albusin B (2.5 g kg−1), and basal diet + nosiheptide (2.5 mg kg−1) were randomly fed to 90 broiler chickens from 1 to 35 days of age, respectively. After 35 days of supplementation, the growth performance, lipid metabolism and antioxidant proteins in the jejunum and liver, intestinal protein profile, and plasma lipid profile were analyzed. RESULTS: Broilers with albusin B supplementation had greater body weight than the control broilers. Compared with the control broilers, lower triglyceride and higher high-density lipoprotein concentration in the blood were observed in both broilers with albusin B and nosiheptide supplementation. In addition, albusin B suppressed the mRNA expression of fatty acid binding protein 2 and ATP binding cassette transporter G 5 in the jejunum. In the jejunal protein profiles, four antioxidant proteins were upregulated by albusin B and nosiheptide treatments. The jejunal antioxidant gene expression had a concordant pattern. Hepatic genes related to lipid metabolism, 3-hydroxy-3-methyl-glutaryl CoA reductase, and superoxide dismutase were upregulated by albusin B supplementation. CONCLUSION: Albusin B supplementation modulated lipid metabolism and activated systemic antioxidant defense, which might partially contribute to the performance of broiler chickens. Copyright © 2012 Society of Chemical Industry

Studies show that adiponectin and its receptors (AdipoR1 and 2) play important roles in regulating glucose and lipid metabolism in mice. Obesity, type II diabetes and cardiovascular disease are highly correlated with downregulated adiponectin signaling; however, research has not clarified the functions of AdipoR1 in vivo.In this study, mice were induced to overexpress the AdipoR1 transgene so that its functions could be studied in relation to hypertrophic cardiomyopathy. Wild-type and AdipoR1-transgenic male mice were fed ad libitum with a standard chow diet or else a high-fat/sucrose diet (HFSD) for 24 weeks, beginning at 6-7 weeks of age.After receiving the 24-week HFSD, AdipoR1-transgenic mice did not become obese, nor did they develop heart hypertrophy. The AdipoR1 transgene decreased the elevating cardiac troponin I expression caused by the HFSD. While the HFSD induced mRNA expression of CD36 and CPTI, AdipoR1 reversed it. Suppression of cardiac SOD mRNA expression by the HFSD was improved by the AdipoR1 transgene. The HFSD caused a higher autophagic gene expression of Beclin 1 and Lamp 2 A in the heart, whereas the AdipoR1 transgene ameliorated them.The AdipoR1 transgene enabled mice to resist diet-induced obesity while decreasing lipid accumulation, oxidative stress and autophagic damage. These effects might contribute to the improvement of heart functions in diet-induced obese mice.

Hepatic lipid overloading induces lipotoxicity which can cause hepatocyte damage, fibrosis, and eventually progress to cirrhosis, which is associated with nonalcoholic fatty liver disease. Adiponectin receptors play important roles in regulating lipid metabolism. In this study, we used a lentivirus system to overexpress the adiponectin receptor 1 (AdipoR1) in HepG2 cells to define the role of adiponectin and its receptor 1 in the development of fatty liver syndrome. Exposure of human hepatocytes, HepG2 cells, to palmitate (0.2 or 0.4 mM) for 16 h resulted in elevated apoptosis, whereas AdipoR1 decreased the palmitate-induced apoptosis. Transgene AdipoR1 increased the expression of FATP2, acyl-coA oxidase, and carnitine palmitoyltransferase I in palmitate-treated HepG2 cells. The transcript level of acetyl-CoA carboxylase and fatty acid synthase was upregulated by palmitate treatment, while AdipoR1 reversed the effect induced by palmitate. AdipoR1 increased the gene expression of cytochrome C oxidase, peroxisome proliferator-activated receptor α, and decreased the gene expression of PGC1α and AMPKα in HepG2 cells under palmitate treatment. Palmitate suppressed ATP production, while transgene AdipoR1 reversed the decreased ATP production by palmitate. Transgene AdipoR1 enhanced AKT phosphorylation in HepG2 cells both with and without palmitate treatment. When PI3 kinase inhibitor was applied, the protective effect of AdipoR1 was absent, such that palmitate again decreased ATP production while also reducing cell viability. AdipoR1 enhances fatty acid metabolism and cell viability in palmitate-treated HepG2 cells partially by activating AKT signaling. Therefore, AdipoR1 has therapeutic potential in the treatment of nonalcoholic fatty liver disease.

The present study was designed to investigate the effect of albusin B on lipid metabolism and antioxidant defense in broiler chickens by a proteomic approach. The bacteriocin, albusin B of Ruminococcus albus 7, expressed by yeast was applied in this study. Three dietary treatments, consisting of the basal diet (control), basal diet + albusin B (2.5 g kg⁻¹), and basal diet + nosiheptide (2.5 mg kg⁻¹) were randomly fed to 90 broiler chickens from 1 to 35 days of age, respectively. After 35 days of supplementation, the growth performance, lipid metabolism and antioxidant proteins in the jejunum and liver, intestinal protein profile, and plasma lipid profile were analyzed.Broilers with albusin B supplementation had greater body weight than the control broilers. Compared with the control broilers, lower triglyceride and higher high-density lipoprotein concentration in the blood were observed in both broilers with albusin B and nosiheptide supplementation. In addition, albusin B suppressed the mRNA expression of fatty acid binding protein 2 and ATP binding cassette transporter G 5 in the jejunum. In the jejunal protein profiles, four antioxidant proteins were upregulated by albusin B and nosiheptide treatments. The jejunal antioxidant gene expression had a concordant pattern. Hepatic genes related to lipid metabolism, 3-hydroxy-3-methyl-glutaryl CoA reductase, and superoxide dismutase were upregulated by albusin B supplementation.Albusin B supplementation modulated lipid metabolism and activated systemic antioxidant defense, which might partially contribute to the performance of broiler chickens.