Regulation Of Adiponectin On Chicken Fat Metabolism And Its Molecular Mechanism

The present study was conducted to investigate the effect of adiponectin on fat deposition and muscle quality of broiler chicken in vivo and lipid metabolism of chicken adipocyte in vitro, mean while, the mechanism of the action of adiponectin was also observed. Rosiglitazone and dexamethasone were used to treat broilers in vivo for three weeks; over-expression and interference vectors targeting of chicken adiponectin gene were constructed and transfected into chicken preadipocytes;200μg/mL recombinant globular adiponectin was used to treat chicken preadipocyte. At last, recombinant adenovirus vector targeting chicken adiponectin was constructed and treated chicken preadipocytes to clarify the effect of adiponectin on mitochondria development and its function in chicken adipocyte. Results showed that:1.(1) Rosiglitazone increased serum adiponectin concentration in a time-dependent manner, while dexamethasone increased serum adiponectin;(2) Rosiglitazone up-regulated the expression levels of adiponectin and adipoRl in tissues, while dexamethasone decreased adiponectin and adipoRl mRNA levels;(3) Rosiglitazone decreased the levels of serum lipids, while dexamethasone increased serum lipids;(4) Rosiglitazone decreased abdominal fat, neck subcutaneous fat deposition and lipids in muscle, while dexamethasone increased abdominal fat, neck subcutaneous fat, leg subcutaneous fat, abdominal subcutaneous fat and lipids in muscle;(5) Rosiglitazone down-regulated total FA, SFA and MUFA in muscle, while dexamethasone increased the deposition of total FA,SFA and MUFA in muscle;(6) Rosiglitazone increased the expression of ATGL in tissues and inhibited CEBPa and FAS, while dexamethasone have the opposite effect.2.(1) overexpression adiponectin inhibited the differentiation of chicken preadipocyte;(2) adiponectin decreased the expression of CEBPa and FAS, while increased ATGL expression;(3) over-expression of adiponectin could activate p38MAPK/ATF-2pathway and also repaired the suppression of p38MAPK and ATF-2activation by SB253580;(4) over-expression of adiponectin suppressed TOR/p70S6Kinase pathway in chicken adipocytes and may further reduce the phosphorylation level of the TOR and p70S6Kinase based on the inhibitory effect of TOR.3.(1) globular adiponectin inhibited the differentiation of chicken preadipocyte;(2) globular adiponectin decreased the expression of CEBPa and FAS, while increased ATGL expression;(3) globular adiponectin could activate p38MAPK/ATF-2pathway and also repaired the suppression of p38MAPK and ATF-2activation by SB253580;(4) globular adiponectin suppressed TOR/p70S6Kinase pathway in chicken adipocytes and may further reduce the phosphorylation level of the TOR and p70S6Kinase based on the inhibitory effect of TOR.4.(1) over-expression of adiponectin inhibited chicken adipocyte differentiation, increased the expression of CEBPa, LPL and ATGL, while decreased the expression of FAS, A-FABP and ACC;(2) over-expression of adiponectin promoted glucose uptake and FFA release in medium during24h;(3) over-expression of adiponectin promoted mitochondria development and increased the expression of glucose and lipid metabolism marker genes in the mitochondria;(4) over-expression of adiponectin increased mitochondrial membrane potential;(5) over-expression of adiponectin activated p38MAPK and ERK pathway, while inhibited the activation of TOR pathway.In summary, in our studies, we proved that rosiglitazone and dexamethasone could regulate the levels of serum adiponectin and analyzed the impact of serum adiponectin on fat deposition and meat quality. Over-expression of full length of adiponectin and globular adiponectin had the same impact on the inhibitory of chicken preadipocyte differentiation. Over-expression of adiponectin promoted mitochondria development and also stimulated glucose and lipid metabolism in mitochondria. p38MAPK, ERK and TOR signaling pathways involved in the regulation of adiponectin on mitochondrial function.