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المؤلفSampath, Chethan
المؤلفRashid, Muhammed
المؤلفSang, Shengmin
المؤلفAhmedna, Mohamed
تاريخ الإتاحة2017-02-13T09:29:32Z
تاريخ النشر2017-01-16
اسم المنشورFood Chemistry
المعرّفhttp://dx.doi.org/10.1016/j.foodchem.2017.01.056
الاقتباسSampath, Chethan. Rashid, Muhammed. Sang, Shengmin. Ahmedna, Mohamed. "Specific bioactive compounds in ginger and apple alleviate hyperglycemia in mice with high fat diet-induced obesity via Nrf2 mediated pathway", Food Chemistry, Vol. 226, pp. 79-88
الرقم المعياري الدولي للكتاب0308-8146
معرّف المصادر الموحدhttp://hdl.handle.net/10576/5245
الملخصProlonged hyperglycemia activates the formation of advanced glycation end-products (AGEs). Major dicarbonyl compounds such as methylglyoxal or glyoxal are found to be the main precursors of AGEs and N(e)-(carboxymethyl)lysine (CML) found to be predominantly higher in the diabetic population. We hypothesized that phloretin from apple and [6]-gingerol from ginger inhibit formation of AGEs and suppress the receptor for advanced glycation end products (RAGE) via nuclear factor erythroid-2- related-factor-2 (Nrf2)-dependent pathway. Phloretin and [6]-gingerol were supplemented at two different doses to C57BL/6 mice on high fat diet or standard diet for a period of 17 weeks. Phloretin or [6]- gingerol supplementation significantly reduced plasma glucose, alanine aminotransferase, aspartate aminotransferase, AGEs and insulin levels. Phloretin and [6]-gingerol also decreased the levels of AGEs and CML levels, via Nrf2 pathway, enhancing GSH/GSSG ratio, heme oxygenase-1 and glyoxalase 1 in liver tissue. These results suggest that phloretin and [6]-gingerol are potential dietary compounds that can alleviate diabetes-induced complications.
راعي المشروعQatar National research Fund
اللغةen
الناشرElsevier
الموضوعAdvance glycation end-products
Phloretin
[6]-Gingerol
Nrf2
RAGE
GSH
العنوانSpecific bioactive compounds in ginger and apple alleviate hyperglycemia in mice with high fat diet-induced obesity via Nrf2 mediated pathway
النوعArticle
الصفحات79-88
رقم المجلد226
dc.accessType Abstract Only


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