[Effect of chlorogenic acid on disordered glucose and lipid metabolism in db/db mice and its mechanism].

To explore the effect of chlorogenic acid on disordered glucose and lipid metabolism in db/db mice and its mechanism.Thirteen 5-6-week-old male db/db mice were randomly divided into db/db-CGA group (n=7) and db/db-CON group (n=6), and thirteen 5-6-week-old male db/m mice were randomly divided into db/m-CGA group (n=6) and db/m-CON group (n=7). Mice in the CGA groups were administrated with CGA 80 mg/(kg·d)by gavage, and mice in the CON groups were administrated with PBS in the same volume by gavage. Twelve weeks later, the level of biomedical parameters in plasma, liver, and skeletal muscle were determined, the concentrations of adiponectin and visfatin in visceral adipose, and the mRNA expression of glucose-6-phosphatase (G-6-Pase) and peroxisome proliferators-activated receptor-α (PPAR-α) as well as the protein level of PPAR-α in liver were detected.Twelve weeks after CGA administration, the levels of triglycerides in plasma, liver, and skeletal muscle and the fasting plasma glucose in db/db-CGA group were significantly lower than those in db/db-CON group(P<0.05). The muscle glycogen level was significantly higher than that in db/db-CON group (P<0.05), and the adiponectin concentration was significantly higher than that in db/db-CON group ( P<0.01) and lower than that in db/m-CGA group(P<0.05). The visfatin concentration in db/db-CGA group was significantly lower than that in db/db-CON group (P<0.01) and significantly higher than that in db/m-CGA group(P<0.05). The mRNA expression level of G-6-Pase was significantly down-regulated in db/db-CGA group when compared with db/db-CON group (P<0.05). Both the mRNA and the protein expression levels of PPAR-α were significantly up-regulated in db/db-CGA group(P<0.05) compared with in db/db-CON group.CGA improves the disordered glucose/lipid metabolism in db/db mice, which is speculated to be related with its role in modulating the adipokines secretion, up-regulating hepatic PPAR-α, and inhibiting G-6-Pase expression.