ArticleJournal of food science and technology2014
Dietary coconut kernel protein beneficially modulates NFκB and RAGE expression in streptozotocin induced diabetes in rats.
Article in Journal of food science and technology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Role of TLR4/MyD88/NF-κB signaling in heart and liver-related complications in a rat model of type 2 diabetes mellitus.The Journal of international medical research · 2021Article
- Role of HMGB1 signaling in the inflammatory process in diabetic retinopathy.Cellular signalling · 2020Review
- Effects ofAntioxidants (Basel, Switzerland) · 2019Article
- Gamma-tocopherol supplementation ameliorated hyper-inflammatory response during the early cutaneous wound healing in alloxan-induced diabetic mice.Experimental biology and medicine (Maywood, N.J.) · 2017Article
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4 authors at 2 institutions in 1 country.
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Abstract
Previous studies showed that arginine rich coconut kernel protein (CKP) maintains glucose homeostasis in experimental diabetic rats. But the mechanism of this effect was not clear. This study investigated the effect of CKP on the expression of liver receptor for advance glycated end products (RAGE), inducible nitric oxide synthase (iNOS) and NFkB. Diabetes was induced by injecting a single dose of streptozotocin (75 mg/kg body weight) intraperitoneally. After inducing diabetes, CKP was administered to rats orally for 45 days. After the experimental period, serum glucose, insulin, liver glycogen, glucose metabolizing enzyme activities and the expression of liver RAGE, iNOS and NFkB was evaluated. The results showed that CKP beneficially modulated the levels of glucose and insulin as well as the metabolizing enzyme activities. Expression of RAGE and NFkB was found to be over expressed in diabetic rats but was found to be down regulated in CKP fed diabetic rats. iNOS expression was down regulated in diabetic rats, which was expressed normally in CKP fed diabetic rats. These results clearly demonstrated that anti diabetic activity of CKP is mediated through NFkB pathway.
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