Cinnamon extract improves abnormalities in glucose tolerance by decreasing Acyl-CoA synthetase long-chain family 1 expression in adipocytes.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
22 07 2022
Historique:
received: 03 12 2021
accepted: 24 05 2022
entrez: 22 7 2022
pubmed: 23 7 2022
medline: 27 7 2022
Statut: epublish

Résumé

We previously demonstrated that cinnamon extract (CE) alleviates streptozotocin-induced type 1 diabetes in rats. The present study aimed to elucidate the detailed molecular target of cinnamon in cultured adipocytes and epididymal adipose tissue of type 2 diabetes model mice. Two-dimensional gel electrophoresis was employed to determine the molecular target of cinnamon in adipocytes. The function of Acyl-CoA synthetase long-chain family-1 (ACSL1), a molecular target of cinnamon that was identified in this study, was further investigated in 3T3-L1 adipocytes using specific inhibitors. Type 2 diabetes model mice (KK-Ay/TaJcl) were used to investigate the effect of CE on glucose tolerance, ACSL1 expression, and related signal molecules in vivo. CE decreased ACSL1 mRNA and protein expression in 3T3-L1 adipocytes but increased glucose uptake and AMPK signaling activation; moreover, a similar effect was observed with an ACSL1 inhibitor. CE improved glucose tolerance and downregulated ACSL1 in mice adipose tissue in vivo. ACSL1 was demonstrated as a molecular target of CE in type 2 diabetes both in a cell culture system and diabetic mouse model.

Identifiants

pubmed: 35869105
doi: 10.1038/s41598-022-13421-9
pii: 10.1038/s41598-022-13421-9
pmc: PMC9307619
doi:

Substances chimiques

Insulin 0
Plant Extracts 0
Coenzyme A Ligases EC 6.2.1.-
Glucose IY9XDZ35W2
Coenzyme A SAA04E81UX

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

12574

Informations de copyright

© 2022. The Author(s).

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Auteurs

Tsubame Nishikai-Shen (T)

Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Kanagawa, 252-0880, Japan.
Department of Applied Life Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, 252-0880, Japan.
Intractable Disease Research Center, Juntendo University School of Medicine, Tokyo, 113-8421, Japan.
Division of Regenerative Therapy, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.

Tomomi Hosono-Fukao (T)

Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Kanagawa, 252-0880, Japan.
Department of Applied Life Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, 252-0880, Japan.

Toyohiko Ariga (T)

Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Kanagawa, 252-0880, Japan.
Department of Applied Life Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, 252-0880, Japan.

Takashi Hosono (T)

Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Kanagawa, 252-0880, Japan.
Department of Applied Life Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, 252-0880, Japan.

Taiichiro Seki (T)

Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Kanagawa, 252-0880, Japan. seki.taiichirou@nihon-u.ac.jp.
Department of Applied Life Sciences, Nihon University Graduate School of Bioresource Sciences, Kanagawa, 252-0880, Japan. seki.taiichirou@nihon-u.ac.jp.

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