Neutral (WGPN) and acidic (WGPA) polysaccharides were fractionated from ginseng polysaccharide. WGPN and WGPA decreased fasting blood glucose by different manners of administration. Intra-gastric administration of WGPA showed a marked hypoglycemic effect, which may be related to its anti-oxidative activity. The results indicated that WGPA may have anti-diabetic potential.

Skin ulcers were one of the serious complications of diabetes. Diabetic patients always suffer from the vascular lesions and complications of peripheral neuritis, peripheral vascular lesions and collagen abnormalities, which result in skin wounds that were refractory and often develop into chronic ulcers. Healing of diabetic skin ulcers mainly involves an inflammatory reaction, wound proliferation, remodeling regulation and control of stem cells. Since 2005, the development of molecular biology has allowed for a more in-depth study of diabetic skin ulcers. The Wnt/β-catenin pathway is a classic highly conserved signal transduction pathway involved in a variety of biological processes such as cell proliferation, apoptosis, and differentiation. It is considered as one of the important pathways involved in the healing of skin wounds. This article not only summarizes the mechanism of Wnt/β-catenin pathway in the inflammatory response of diabetic ulcer wounds, wound proliferation, wound remodeling, and stem cells, but also discusses the existence of interactions between the Wnt signal pathway and other pathways.

Insulin stimulates lipogenesis but insulin resistance is also associated with increased hepatic lipogenesis in obesity. However, the underlying mechanism remains poorly characterized. Here, we show a noncanonical insulin-Snail1 pathway that suppresses lipogenesis. Insulin robustly upregulates zinc-finger protein Snail1 in a PI 3-kinase-dependent manner. In obesity, the hepatic insulin-Snail1 cascade is impaired due to insulin resistance. Hepatocyte-specific deletion of Snail1 enhances insulin-stimulated lipogenesis in hepatocytes, exacerbates dietary NAFLD in mice, and attenuates NAFLD-associated insulin resistance. Liver-specific overexpression of Snail1 has the opposite effect. Mechanistically, Snail1 binds to the fatty acid synthase promoter and recruits HDAC1/2 to induce deacetylation of H3K9 and H3K27, thereby repressing fatty acid synthase promoter activity. Our data suggest that insulin pathways bifurcate into canonical (lipogenic) and noncanonical (anti-lipogenesis by Snail1) two arms. The noncanonical arm counterbalances the canonical arm through Snail1-elicited epigenetic suppression of lipogenic genes. Impairment in the insulin-Snail1 arm may contribute to NAFLD in obesity.