Diabetes mellitus is a systemic metabolic disease characterized by disrupted glucose and lipid metabolism. With an alarming rise of incidence each year, there is therefore a pressing need to find more efficient medicines and methods for its treatment. Using the obese type 2 diabetes db/db mouse model, in our pervious work we found that a new type of nanomaterial could inhibit the formation of insulin resistance. The underlying mechanisms of its therapeutic effect in the glucose and lipid metabolism are further investigated in the present study. Compared with the control mice, the blood glucose of the mice decreased significantly after the nanomaterial injection, accompanied by a dose-dependent hypoglycemic effect. The impaired glucose tolerance and insulin resistance were significantly improved in mice treated with the material. We found that the expression of PCK1 and G6Pc were reduced at both RNA and protein levels, whilst p-AKT was stimulated at the protein level after the nanomaterial injection, which indicated its positive impact on glucose metabolism. Reductions in total, adipose and liver weight were also present in db/db mice treated with the material, compared with the control. In the aspect of lipid metabolism, H and E and oil red O staining of liver tissue revealed an amelioration of fatty liver symptoms in mice injected with the material. Consistent with the observed phenotype, the mRNA expression of the FA synthesis enzymes ACC and FAS were decreased significantly after the treatment, as confirmed by q-PCR analysis. Meanwhile, an observably lower nucleus abundance of SREBP1c, the important transcriptional regulator of ACC and FAS, was detected following the treatment, using immunohistochemical approach. These results demonstrate the striking effects of the nanomaterial on the glucose and lipid metabolism. Taken together, our data implies the significance of this novel type of nanomaterial as the next-generation therapy for diabetes and fatty liver, yet the relevant mechanisms are to be further examined.
J. Wu: None. Y. Chen: None. L. Liu: None. Q. Yao: None. X. Liu: None. Y. Wu: None.