Ghrelin treatment alleviates appetite-related receptor expressions and oxidative stress in fructose-streptozotocin-induced diabetic rat duodenum

Please use this identifier to cite or link to this item: http://nopr.niscpr.res.in/handle/123456789/65485

metadata.dc.identifier.doi: https://doi.org/10.56042/ijeb.v63i03.11585Title: Ghrelin treatment alleviates appetite-related receptor expressions and oxidative stress in fructose-streptozotocin-induced diabetic rat duodenumAuthors: YAZICI, Zeynep Mine COSKUN
BEYDOGAN, Alisa Bahar
BILGE, Bilge Nur
BOLKENT, SemaKeywords: Cannabinoid receptor 1;Gastric peptide;Immunohistochemistry;Biochemistry;Type 2 diabetesIssue Date: Mar-2025Publisher: NIScPR-CSIR, IndiaAbstract: Ghrelin (GHR), a peptide that regulates appetite and energy balance, is important for type 2 diabetes (T2D). Glucagon-like peptide-1 receptor (GLP-1R) and cannabinoid receptor 1 (CB-1R) are two receptors associated with energy and food metabolism. Understanding the effects of GHR on GLP-1R and CB-1R may help develop treatments for weight regulation in T2D. We investigated the effects of GHR supplementation on both appetite-related receptor expression and oxidative stress in the duodenum of a rat model of diabetes. Rats (n=21) were divided into control (CO), T2D, and T2D+GHR groups. The number and intensity of GLP-1R and CB-1R immunopositive cells were detected by immunohistochemistry. Expression levels of GLP-1R and CB-1R mRNAs were analyzed by qPCR in the duodenum. Oxidative stress parameters were measured in duodenal tissues. During the third and fourth weeks of the experiment, body weight in the T2D+GHR group was significantly reduced compared to the T2D group. The number and intensity of CB-1R and GLP-1R immunopositive cells were significantly lower in the T2D+GHR group than in the T2D group. The results of GLP-1R and CB-1R mRNA expression paralleled the immunohistochemical staining. According to our findings, GHR supplementation may contribute to healing in the duodenum of a diabetic rat model by suppressing appetite-related receptors.Page(s): 192-199ISSN: ISSN: 0975-1009 (Online) ; ISSN: 0019-5189 (Print)Appears in Collections:IJEB Vol.63(03) [March 2025]

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