Therefore, the results of the present study indicated that treatment with TW mitigated hyperglycemia-induced upregulated Wnt-1 and β-catenin expression in kidney tissues and ameliorated diabetes-induced kidney injury in rats.
The decreased hepatic expression of IRS1 and β-catenin in NAFLD is linked to histological progression such as ballooning, and might lead to diabetes as a result of impaired glucose metabolism.
We investigated the changes in adherens junction proteins, such as vascular endothelial-cadherin and β-catenin, of skeletal muscle and vessels in patients with or without diabetes in the setting of cardiopulmonary bypass and cardiac operation.
Increasing evidence supported that semaphorin 3A (Sema3A), insulin-like growth factor (IGF)-1 and β-catenin were involved in the development of osteoporosis and diabetes.
In addition to known driver mutations in TP53 and CTNNB1, our mutation analysis identified non-synonymous mutations in genes implicated in metabolic diseases, i.e. diabetes and obesity: IRS1, HMGCS1, ATP8B1, PRMT6 and CLU, suggesting a common molecular etiology for HCC of alternative pathogenic origin.
Our results reveal a mechanism by which high glucose enhances signaling through the cancer-associated Wnt/β-catenin pathway and may explain the increased frequency of cancer associated with obesity and diabetes.
Our objective was to extend these findings by using therapeutic agents to determine whether the regulation of glycogen synthase kinase-3 (GSK-3)/beta-catenin and mTOR signaling represent key components necessary for effecting a positive impact on human beta-cell mass relevant to type 1 and 2 diabetes.
Significantly, this mutation does not affect phosphorylation of "nonprimed" substrates in the Wnt-signaling pathway (Axin and beta-catenin), suggesting new approaches to design more selective GSK3 inhibitors for the treatment of diabetes.