Na
| Autor: | Leo K Y, Chan, Yi, Wang, Enders K W, Ng, Po Sing, Leung |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Glucose Transporter Type 2
Male Dose-Response Relationship Drug Sodium-Hydrogen Exchanger 3 Down-Regulation Protein Serine-Threonine Kinases Postprandial Period Immediate-Early Proteins Amiloride Mice Inbred C57BL Glucose Sodium-Glucose Transporter 1 Diabetes Mellitus Type 2 Intestinal Absorption Gene Knockdown Techniques Hyperglycemia Glucose Intolerance Intestine Small Epithelial Sodium Channel Blockers Animals Humans Caco-2 Cells Intestinal Mucosa |
| Zdroj: | Diabetes, obesitymetabolism. 20(3) |
| ISSN: | 1463-1326 |
| Popis: | To elucidate the role of NaHuman jejunal samples were obtained from patients undergoing gastrectomy.NHE3 expression was upregulated in db/db mouse jejunal BBM and high-glucose-treated Caco2 cells. NHE3 blockade impaired SGLT1-mediated glucose absorption in human jejunum, m+/db and db/db mouse jejunums, and Caco2 cells, via serum/glucocorticoid-regulated kinase 1 (SGK1). NHE3 knockdown suppressed SGLT1-mediated glucose uptake and reduced mRNA and protein levels of SGK1 and SGLT1, which were conversely enhanced by NHE3 overexpression. Chronic S3226 treatment diminished postprandial glucose levels and ameliorated glucose intolerance in db/db mice.NHE3 is essential in the modulation of small intestinal BBM glucose absorption. Our findings provide a rationale for future possible clinical application of NHE3 for treatment of T2DM through reducing intestinal glucose uptake and counteracting postprandial hyperglycaemia. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text