Metformin regulates hepatic lipid metabolism through activating AMP-activated protein kinase and inducing ATGL in laying hens.

Although many clinical trials have showed that metformin improves non-alcoholic fatty liver disease, which is a common liver disease associated with hepatic enzyme abnormalities, an animal model is required to investigate the effects of altered gene expression and post-translational processing (proteins) in mediating the observed responses. Laying hens appear to develop fatty livers, as in the case in human beings, when ingesting energy in excess of maintenance, and they can be used as an animal model for observing hepatic steatosis. The aim of this study was to investigate whether metformin could improve the non-alcoholic fatty liver of laying hens and to examine the possible mechanisms of lipid-lowering effects. Forty-eight Leghorn laying hens of Hy-Line variety W-36 - 44 weeks with 64.8% hen-day egg production - were randomly assigned into 4 treatments, each receiving 0, 10, 30, or 100mg of metformin with saline per kg body weight by daily wing vein injection. Results showed that, compared with the control, significant decreases existed in the laying rates; plasma triglyceride, cholesterol, and insulin levels; body weights; abdominal fat weights; hepatic lipid contents; and hepatic fatty acid synthase expression of layers receiving 30 or 100mg per kg body weight, whereas significant increases in their hepatic 5'adenosine monophosphate-activated protein kinase, acyl-CoA carboxylase phosphorylation, adipose triglyceride lipase, and carnitine palmitoyl transferase-1 expression were observed. These data suggest that metformin could reduce lipid deposits in the liver and that the laying hen is a valuable animal model for studying hepatic steatosis.

Development of an automated immunoassay for advanced glycosylation end products in human serum.

OBJECTIVE: Nonenzymatic reaction of protein and carbohydrate produce a series of brown fluorescent advanced glycosylation end products (AGEs). However, a convenient and rapid assay for serum AGEs level is currently unavailable. METHODS: We raised AGEs-specific polyclonal antibodies, which were used to develop a fully automated, noncompetitive, homogeneous, light-scattering immunoassay for serum AGEs. RESULTS: The assay requires a sample volume of 2 microL and takes a reaction time of 2 min. The coefficient of variation range from 1.8 to 6.1%, and the mean recovery rate was 98.6%. Comparative analysis shows moderate correlation with competitive ELISA (r = 0.8209, n = 52). The mean +/- SD concentration of AGEs in young and in older healthy subjects were 4.6 +/- 1.5 (n = 39) and 4.9 +/- 1.4 (n = 40), respectively. The level of AGEs was significantly higher in serum from patients with type II DM 7.8 +/- 4.8 (n = 89) than that from the normal subjects (p < 0.05). CONCLUSIONS: The automatic immunoassay for AGEs is appropriate for clinical use.