Glucose Regulation Effect by the Functional Bitter Melon Compound BmpP® in Palmitic Acid-Induced Insulin Resistance HepG2 Cells

Background: Insulin resistance is one of the major causes and manifestations of diabetes. Previous studies have demonstrated the glucose-regulating effects of bitter melon. Therefore, this study employs a PA-induced insulin-resistant cell model to investigate the potential of functional bitter melon compound BmpP® in glycemic regulation. Methods: Insulin resistance was induced in HepG2 cells by exposure to 0.25 mM palmitic acid (PA) for 18 hours. The effects of BmpP® on cellular glucose oxidase activity, glycogen accumulation, and ono-esterified fatty acid (NEFA) levels were then evaluated. Results: BmpP® reversed the PA-induced reduction in glucose oxidase activity and glycogen accumulation in HepG2 cells. Additionally, PA-induced NEFA accumulation was alleviated following BmpP® treatment. Conclusion: These findings suggest that BmpP® enhances glucose utilization and exhibits potential as a functional food supplement for glycemic regulation.

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Publication Details

Journal
Universal library of medical and health sciences.
Published
2025-04-23
DOI
https://doi.org/10.70315/uloap.ulmhs.2025.0302006
Primary Topic
Natural Antidiabetic Agents Studies
Type
article
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article

Glucose Regulation Effect by the Functional Bitter Melon Compound BmpP® in Palmitic Acid-Induced Insulin Resistance HepG2 Cells

Ching-Di Chang
Universal library of medical and health sciences.
Natural Antidiabetic Agents Studies
article

Glucose Regulation Effect by the Functional Bitter Melon Compound BmpP® in Palmitic Acid-Induced Insulin Resistance HepG2 Cells

Ching-Di Chang
article en

Abstract

Background: Insulin resistance is one of the major causes and manifestations of diabetes. Previous studies have demonstrated the glucose-regulating effects of bitter melon. Therefore, this study employs a PA-induced insulin-resistant cell model to investigate the potential of functional bitter melon compound BmpP® in glycemic regulation. Methods: Insulin resistance was induced in HepG2 cells by exposure to 0.25 mM palmitic acid (PA) for 18 hours. The effects of BmpP® on cellular glucose oxidase activity, glycogen accumulation, and ono-esterified fatty acid (NEFA) levels were then evaluated. Results: BmpP® reversed the PA-induced reduction in glucose oxidase activity and glycogen accumulation in HepG2 cells. Additionally, PA-induced NEFA accumulation was alleviated following BmpP® treatment. Conclusion: These findings suggest that BmpP® enhances glucose utilization and exhibits potential as a functional food supplement for glycemic regulation.

Universal library of medical and health sciences.Vol. 03(02)
Openalex Percentile: Top 89%
Natural Antidiabetic Agents Studies
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