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Oleanolic acid and moderate drinking increase the pancreatic GLP-1R expression of the β -cell mass deficiency induced hyperglycemia.

Authors :
Xu L
Hu R
Jois SV
Zhang L
Source :
PeerJ [PeerJ] 2023 Jul 24; Vol. 11, pp. e15705. Date of Electronic Publication: 2023 Jul 24 (Print Publication: 2023).
Publication Year :
2023

Abstract

Background: Oleanolic acid (OA) and moderate drinking have been reported to attenuate diabetes. However, the underlying mechanism of OA and moderate drinking alone or in combination on the islet β -cell deficiency induced diabetes is not fully elucidated.<br />Methods: Male Sprague Dawley (SD) rats were intraperitoneally injected with 55 mg/kg streptozotocin (STZ) to induce β -cell deficiency. OA, 5% ethanol (EtOH), or a mixture of OA in 5% ethanol (OA+EtOH) were applied to three treatment groups of hyperglycemia rats for 6 weeks.<br />Results: STZ caused the increase of fast blood glucose (FBG) level.OA and EtOH treatment alone or in combination decreased the STZ increased FBG level during the 6 weeks of treatment. In addition, OA treatment also significantly increased the β -cell to total islet cell ratio. Both EtOH and OA+EtOH treatments promoted the increase of total islet cell number and α -cell to β -cell ratio when compared to OA group. STZ induced hyperglycemia dramatically reduced the glucagon-like peptide-1 receptor (GLP-1R) positive cells in islets, all the three treatments significantly increased the pancreatic GLP-1R positive cell number. In the meantime, STZ induced hyperglycemia suppressed the insulin mRNA expression and boosted the glucagon mRNA expression. EtOH and OA+EtOH treatments increased the insulin mRNA expression, but none of the 3 treatments altered the elevated glucagon level.<br />Conclusion: GLP-1R positive cell ratio in islets is crucial for the blood glucose level of diabetes. OA and 5% ethanol alone or in combination suppresses the blood glucose level of β -cell deficiency induced diabetes by increasing islet GLP-1R expression.<br />Competing Interests: The authors declare there are no competing interests.<br /> (©2023 Xu et al.)

Details

Language :
English
ISSN :
2167-8359
Volume :
11
Database :
MEDLINE
Journal :
PeerJ
Publication Type :
Academic Journal
Accession number :
37520251
Full Text :
https://doi.org/10.7717/peerj.15705