ArticleScientific reports2022
Cinnamon extract improves abnormalities in glucose tolerance by decreasing Acyl-CoA synthetase long-chain family 1 expression in adipocytes.
Article in Scientific reports, 2022. 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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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Trial
- A review on the role of functional foods and derivatives for diabetes management.Journal of food science and technology · 2025Review
- Molecular, cellular, and metabolic insights of cinnamon (Cinnamomum zeylanicum) advantages in diabetes and related complications: condiment or medication?Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exploring the Antioxidative Effects of Ginger and Cinnamon: A Comprehensive Review of Evidence and Molecular Mechanisms Involved in Polycystic Ovary Syndrome (PCOS) and Other Oxidative Stress-Related Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Natural activators of AMPK signaling: potential role in the management of type-2 diabetes.Journal of diabetes and metabolic disorders · 2023Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
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.
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