mProX™ Human GCGR Stable Cell Line

Liu D, et al. "Alpinia katsumadai Hayata Volatile Oil Is Effective in Treating ." Journal of agricultural and food chemistry, 2023.
The aim of this study was to investigate the therapeutic effects and mechanisms of AKHO, a potential treatment for 5-fluorouracil-induced intestinal mucositis in mice. Using measures such as mouse body weight, diarrhea score, and H&E staining, the therapeutic effects of AKHO were evaluated. 16S rDNA and nontargeted metabolomics were used to examine the underlying mechanism, while WB, ELISA, and immunohistochemistry were utilized to validate potential mechanisms. The results showed that AKHO significantly reduced diarrhea scores and intestinal damage induced by 5-FU, and also lowered serum levels of LD and DAO while upregulating the expressions of ZO-1 and occludin in the ileum. AKHO also demonstrated an increase in the abundance of Lactobacillus in the gut and a suppression of KEGG pathways, including cortisol synthesis and secretion and arachidonic acid metabolism. Further validation studies showed that AKHO downregulated the expressions of prostaglandin E2 (PGE2), microsomal prostaglandin E synthase-1 (mPGES-1), and PGE2 receptor EP4, while upregulating the expression of glucocorticoid (GC) receptor (GR), resulting in an improvement in intestinal epithelial barrier function. In conclusion, this study suggests that AKHO may have protective effects against 5-FU-induced mucositis by regulating tight junction proteins through modulation of the GC/GR and mPGES-1/PGE2/EP4 pathway, providing valuable insights into the potential uses of this pharmaceutical/food resource.
Pubmed: 37800952   DOI: 10.1021/acs.jafc.3c05051

Peng J, et al. "Hepatic sialic acid synthesis modulates glucose homeostasis in both liver and ." Molecular metabolism, 2023.
Sialic acid, as a terminal monosaccharide of glycans in glycoproteins and glycolipids, plays an important role in regulating glucose metabolism. The rate-limiting enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is responsible for converting glucose into sialic acid. However, the impact of sialic acid synthesis and sialylation in the liver on glucose homeostasis is still unclear. To address this gap in knowledge, a study was conducted using a hepatocyte-specific GNE knockdown mouse model to decrease sialic acid production and sialylation in hepatocytes. Results showed that liver GNE deletion led to impaired insulin suppression of glucose production and blunted glucagon receptor function due to changes in sialylation. This, in turn, enhanced peripheral insulin sensitivity and improved glucose tolerance. These findings reveal the role of hepatic sialic acid synthesis in modulating glucose homeostasis in both the liver and skeletal muscle.
Pubmed: 37777009   DOI: 10.1016/j.molmet.2023.101812