Decaffeinated green tea and coffee extracts and metabolic syndrome

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J. Pharm. Pharmacogn. Res., vol. 11, no. 3, pp. 414-425, May-June 2023. DOI: https://doi.org/10.56499/jppres23.1593_11.3.414 Original Article Decaffeinated green tea and green coffee extracts as metformin's add-on enhance metabolic syndrome risk factors and improve the cardiac insulin-gene-related pathway [Extractos de té verde y café verde descafeinados como complemento de la metformina mejoran los factores de riesgo del … Continue reading Decaffeinated green tea and coffee extracts and metabolic syndrome

J. Pharm. Pharmacogn. Res., vol. 11, no. 3, pp. 414-425, May-June 2023.

DOI: https://doi.org/10.56499/jppres23.1593_11.3.414

Original Article

Decaffeinated green tea and green coffee extracts as metformin's add-on enhance metabolic syndrome risk factors and improve the cardiac insulin-gene-related pathway

[Extractos de té verde y café verde descafeinados como complemento de la metformina mejoran los factores de riesgo del síndrome metabólico y la vía cardiaca relacionada con los genes de la insulina]

Indah Nur Chomsy1*, Mohammad Saifur Rohman2*, Husnul Khotimah3, Nashi Widodo4, Nur Ida Panca Nugrahini5

1Doctoral Program in Medical Science, Faculty of Medicine, Universitas Brawijaya, Malang, 65145, Indonesia.

2Department of Cardiology and Vascular Medicine, Saiful Anwar General Hospital, Faculty of Medicine, Universitas Brawijaya, Malang, 65145, Indonesia.

3Laboratory of Pharmacology, Faculty of Medicine, Universitas Brawijaya, Malang, 65145, Indonesia.

4Biology Department, Faculty of Mathematics and Natural Sciences, Universitas Brawijaya, Malang, East Java, 65145, Indonesia.

5Doctoral Program of Food Sciences, Department of Food Science and Biotechnology, Faculty of Agricultural Technology, Universitas Brawijaya, Malang, 65145, Indonesia.

*E-mail: ippoenk@ub.ac.id

Abstract

Context: Dysregulation of glucose metabolism in metabolic syndrome (METS) is allegedly due to the disruption of insulin as the main pathway in cellular metabolism. Green tea and green coffee are known to have potential benefit in METS therapy.

Aims: To evaluate the effect of therapy using decaffeinated green tea-green coffee extract as metformin's add-on in the risk factors of METS and its effect on the cardiac insulin-gene-related pathway, such as IRS1, PI3Kr1, and GLUT4.

Methods: METS model rats were divided into five groups. The rats' level of body weight (BW), fasting blood glucose (FBG), triglycerides (TG), high-density lipoprotein (HDL), insulin (INS), and homeostatic model assessment for insulin resistance (HOMA-IR) were measured periodically. After nine weeks of treatment, the rats were euthanized, and the heart was isolated for measurement of IRS1, PI3Kr1, and GLUT4 gene expression by reverse-transcriptase polymerase chain reaction.

Results: This study found that there was a decrease in BW, FBG, TG and an increase in HDL in METS model rats given therapy with metformin and green tea-green coffee extract (COMB) (p<0.0001). There is also improvement in insulin resistance by reducing HOMA-IR in the COMB group (p = 0.0434 for INS and p<0.0001 for HOMA-IR). This study found that IRS1, PI3K, and GLUT4 gene expression increased in the COMB group. The five groups differ significantly, with a p = 0.000.

Conclusions: Therapy using a combination of decaffeinated green tea and green coffee extract as an add-on of metformin improved METS risk factor via a significant reduction in BW, FBG, TG, increasing HDL and improving insulin resistance. It also increased the IRS1, PI3Kr1, and GLUT4 gene expression as markers of cardiac insulin-gene-related pathways.

Keywords: green tea; green coffee; insulin signalling; metabolic syndrome; metformin.

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Resumen

Contexto: La desregulación del metabolismo de la glucosa en el síndrome metabólico (METS) se debe supuestamente a la alteración de la insulina como vía principal en el metabolismo celular. Se sabe que el té verde y el café verde tienen beneficios potenciales en la terapia del METS.

Objetivos: Evaluar el efecto de la terapia con extracto descafeinado de té verde y café verde como complemento de la metformina en los factores de riesgo del METS y su efecto en la vía cardiaca relacionada con los genes de la insulina, como IRS1, PI3Kr1 y GLUT4.

Métodos: Las ratas del modelo METS se dividieron en cinco grupos. Se midieron periódicamente el peso corporal (PC), la glucemia en ayunas (GSA), los triglicéridos (TG), las lipoproteínas de alta densidad (HDL), la insulina (INS) y el modelo homeostático de evaluación de la resistencia a la insulina (HOMA-IR) de las ratas. Tras nueve semanas de tratamiento, se practicó la eutanasia a las ratas y se aisló el corazón para medir la expresión de los genes IRS1, PI3Kr1 y GLUT4 mediante la reacción en cadena de la polimerasa con transcriptasa inversa.

Resultados: En este estudio se observó una disminución del BW, FBG, TG y un aumento de HDL en ratas modelo METS tratadas con metformina y extracto de té verde y café (COMB) (p<0,0001). También se observa una mejora de la resistencia a la insulina mediante la reducción del HOMA-IR en el grupo COMB (p = 0,0434 para INS y p<0,0001 para HOMA-IR). Este estudio descubrió que la expresión de los genes IRS1, PI3K y GLUT4 aumentaba en el grupo COMB. Los cinco grupos difieren significativamente, con una p = 0,000.

Conclusiones: La terapia con una combinación de té verde descafeinado y extracto de café verde como complemento de la metformina mejoró el factor de riesgo METS a través de una reducción significativa de BW, FBG, TG, aumentando HDL y mejorando la resistencia a la insulina. También aumentó la expresión de los genes IRS1, PI3Kr1 y GLUT4 como marcadores de las vías cardíacas relacionadas con los genes de la insulina.

Palabras Clave: café verde; metformina; señalización de la insulina; síndrome metabólico; té verde.

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Citation Format: Chomsy IN, Rohman MS, Khotimah H, Widodo N, Nugrahini NIP (2023) Decaffeinated green tea and green coffee extracts as metformin's add-on enhance metabolic syndrome risk factors and improve the cardiac insulin-gene-related pathway. J Pharm Pharmacogn Res 11(3): 414–425. https://doi.org/10.56499/jppres23.1593_11.3.414
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