Inhibition of dipeptidyl peptidase-4 averts Free Fatty acids deposition in the hearts of oral estrogen-progestin contraceptive-induced hyperinsulinemic female rats.

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dc.contributor.authorAdegoke, T.E.
dc.contributor.authorSabinari, I.W.
dc.contributor.authorAreola, E.D.
dc.contributor.authorAjao, F.O.
dc.contributor.authorAsafa, O.O.
dc.contributor.authorSoluoku, T.K.
dc.contributor.authorBello, A.
dc.contributor.authorAdesanmi, A.M.
dc.contributor.authorYusuf, S.O.
dc.contributor.authorOmoleye, A.O.
dc.contributor.authorAyinla M.T
dc.contributor.authorOlatunji, L.A.
dc.date.accessioned2025-05-03T16:08:53Z
dc.date.available2025-05-03T16:08:53Z
dc.date.issued2021
dc.description.abstractFree fatty acid (FFA) deposition in non-adipose tissues such as the heart is a characteristic of insulin resistant states which feature hyperinsulinemia and dipeptidyl peptidase-4 (DPP-4) activation. Estrogen–progestin oral contraceptives (OC) treatment reportedly increased DPP-4 activity in rat tissue, and DPP-4 inhibitors have anti-diabetic and anti-inflammatory properties. This study aims to investigate the effects of DPP-4 inhibition on cardiac FFA deposition in estrogen–progestin-treated female rats. From our data, estrogen–progestin OC exposure in female rats led to elevated plasma insulin, cardiac DPP-4 activity, FFA and triglyceride (TG) accumulation, TG/high-density lipoprotein cholesterol (TG/HDL-C) ratio, adenosine deaminase/xanthine oxidase/uric acid pathway (ADA/XO/UA), lipid peroxidation, glycogen synthase activity, and alanine phosphatase; whereas cardiac glucose-6-phosphate dehydrogenase, Na+/K+-ATPase and nitric oxide (NO) were decreased. However, DPP-4 inhibition resulted in decreased plasma insulin, cardiac DPP-4 activity, FFA, TG, TG/HDL-C ratio, and alkaline phosphatase. These were accompanied by reduced ADA/XO/UA pathway, lipid peroxidation, and augmented NO and Na+/K+-ATPase in estrogen–progestin OC-treated rats. DPP-4 inhibition attenuated cardiac lipid deposition accompanied by reduced activity in the ADA/XO/UA pathway in estrogen–progestin OC-treated female rats. DPP-4 is therefore a plausible therapeutic target in cardiometabolic disorders.
dc.identifier.citationAdegoke, T.E., Sabinari, I.W., Areola, E.D., Ajao, F.O., Asafa, O.O., Soluoku, T.K., Bello, A., Adesanmi, A.M., Yusuf, S.O., Omoleye, A.O., Ayinla, M.T. & Olatunji, L.A. (2021). Inhibition of dipeptidyl peptidase-4 averts Free Fatty acids deposition in the hearts of oral estrogen-progestin contraceptive-induced hyperinsulinemic female rats. Canadian Journal of Physiology and Pharmacology. 99(12); 1216-1323, Published by Canadian Science Publishing. Available online at https://cdnsciencepub.com/toc/cjpp/99/12
dc.identifier.issn0008-4212
dc.identifier.issn1205-7541.
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/15995
dc.language.isoen
dc.publisherCanadian Science Publishing.
dc.relation.ispartofseriesvol 99 no. 12; 1216-1323
dc.subjectCardiac lilid accumulation
dc.subjectCardiac metabolic disorders
dc.subjectDipeptidyl peptidase-4
dc.subjectHormonal contraceptive
dc.subjectHyperinsulinemia
dc.titleInhibition of dipeptidyl peptidase-4 averts Free Fatty acids deposition in the hearts of oral estrogen-progestin contraceptive-induced hyperinsulinemic female rats.
dc.typeArticle

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