RESUMEN
Distinctive indigenous duck (Anas platyrhynchos) populations of Guangxi, China, evolved due to the geographical, cultural, and environmental variability of this region. To investigate the genetic diversity and population structure of the indigenous ducks of Guangxi, 78 individuals from eight populations were collected and sequenced by whole-genome resequencing with an average depth of â¼9.40×. The eight indigenous duck populations included four breeds and four resource populations. Moreover, the genome data of 47 individuals from two typical meat-type breeds and two native egg-type breeds were obtained from a public database. Calculation of heterozygosity, nucleotide diversity (π), Tajima's D, and FST indicated that the Guangxi populations were characterized by higher genetic diversity and lower differentiation than meat-type breeds. The highest diversity was observed in the Xilin-Ma ducks. Principal component, structure, and phylogenetic tree analyses revealed the relationship between the indigenous duck populations of Guangxi. A mild degree of differentiation was observed among the Guangxi populations, although three populations were closer to the meat or egg breeds. Indigenous populations are famous for their special flavor, small body size, and slow growth rates. Selective sweep analysis revealed the candidate genes and pathways associated with these growth traits. Our findings provide a valuable source of information regarding genetic diversity, population conservation, and genome-associated breeding of ducks.
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Patos , Genoma , Animales , Cruzamiento , China , Patos/genética , Variación Genética , Humanos , Filogenia , Polimorfismo de Nucleótido SimpleRESUMEN
BACKGROUND/AIMS: Recent studies have suggested a crucial role for PI3K-Akt-mTOR pathway in regulating cell proliferation, so we hypothesize that insulin acts goose hepatocellular growth by PI3K-Akt-mTOR signal pathway. Because the physiological status of liver cells in vitro is different from that in vivo, a simplified cell model in vitro was established. METHODS: Goose primary hepatocytes were isolated and incubated in either no addition as a control or insulin or PI3K-Akt-mTOR pathway inhibitors or co-treatment with glucose and PI3K-Akt-mTOR pathway inhibitors; Then, cell DNA synthesis and cell cycle analysis were detected by BrdU-incorporation Assay and Flow cytometric analysis; the mRNA expression and protein expression of factors involved in the cell cycle were determined by Real-Time RT-PCR, ELISA, and western blot. RESULTS: Here we first showed that insulin evidently increased the cell DNA synthesis, the mRNA level and protein content of factors involved in the cell proliferation of goose primary hepatocytes. Meanwhile, insulin evidently increased the mRNA level and protein content of factors involved in PI3K-Akt-mTOR pathway. However, the up-regulation of insulin on cell proliferation was decreased significantly by the inhibitors of PBK-Akt-mTOR pathway, LY294002, rapamycin or NVP-BEZ235. CONCLUSION: These findings suggest that PI3K-Akt-mTOR pathway plays an essential role in insulin-regulated cell proliferation of goose hepatocyte.
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Proliferación Celular , Hepatocitos/citología , Insulina/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Serina-Treonina Quinasas TOR/metabolismo , Animales , Proliferación Celular/efectos de los fármacos , Células Cultivadas , Gansos , Hepatocitos/efectos de los fármacos , Hepatocitos/metabolismo , Insulina/farmacología , Hígado/citología , Hígado/efectos de los fármacos , Hígado/metabolismo , Transducción de Señal/efectos de los fármacosRESUMEN
BACKGROUND: We previously showed that the fatty liver formations observed in overfed geese are accompanied by the activation of the PI3K-Akt-mTOR pathway and an increase in plasma insulin concentrations. Recent studies have suggested a crucial role for the PI3K-Akt-mTOR pathway in regulating lipid metabolism; therefore, we hypothesized that insulin affects goose hepatocellular lipid metabolism through the PI3K-Akt-mTOR signaling pathway. METHODS: Goose primary hepatocytes were isolated and treated with serum-free media supplemented with PI3K-Akt-mTOR pathway inhibitors (LY294002, rapamycin, and NVP-BEZ235, respectively) and 50 or 150 nmol/L insulin. RESULTS: Insulin induced strong effects on lipid accumulation as well as the mRNA and protein levels of genes involved in lipogenesis, fatty acid oxidation, and VLDL-TG assembly and secretion in primary goose hepatocytes. The stimulatory effect of insulin on lipogenesis was significantly decreased by treatment with PI3K-Akt-mTOR inhibitors. These inhibitors also rescued the insulin-induced down-regulation of fatty acid oxidation and VLDL-TG assembly and secretion. CONCLUSION: These findings suggest that the stimulatory effect of insulin on lipid deposition is mediated by PI3K-Akt-mTOR regulation of lipogenesis, fatty acid oxidation, and VLDL-TG assembly and secretion in goose hepatocytes.
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Hepatocitos/metabolismo , Insulina/farmacología , Lipogénesis , Lipoproteínas VLDL/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Animales , Células Cultivadas , Ácidos Grasos/metabolismo , Gansos , Hepatocitos/efectos de los fármacos , Inhibidores de las Quinasa Fosfoinosítidos-3 , Inhibidores de Proteínas Quinasas/farmacología , Transducción de Señal , Triglicéridos/metabolismoRESUMEN
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Authors. It has come to the attention of the corresponding author that there are two errors in Section 3.1 of the Results section titled "Effect of overfeeding on gene expression and enzyme activity of several genes in liver". The first error is that the article contains the wrong number of overfeeding days. The second error is that there are incorrect correlations between liver weight, lipids content in live and plasma metabolic substrates because of the wrong overfeeding days. The authors take responsibility for them and apologize to the readership of Molecular and Cellular Endocrinology.