Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes

Type 2 diabetes is characterized by insulin resistance, which contributes to dysregulated glucose and lipid metabolism and is associated with chronic inflammation. While previous studies have examined the effects of myricitrin in streptozotocin-induced diabetic models, its impact on the <i>db&...

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Main Authors: Sang Ryong Kim, Young-Je Kim, HwiCheol Kim, Sojeong Park, Un Ju Jung
Format: Article
Language:English
Published: MDPI AG 2025-03-01
Series:Molecules
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Online Access:https://www.mdpi.com/1420-3049/30/7/1460
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author Sang Ryong Kim
Young-Je Kim
HwiCheol Kim
Sojeong Park
Un Ju Jung
author_facet Sang Ryong Kim
Young-Je Kim
HwiCheol Kim
Sojeong Park
Un Ju Jung
author_sort Sang Ryong Kim
collection DOAJ
description Type 2 diabetes is characterized by insulin resistance, which contributes to dysregulated glucose and lipid metabolism and is associated with chronic inflammation. While previous studies have examined the effects of myricitrin in streptozotocin-induced diabetic models, its impact on the <i>db</i>/<i>db</i> mouse, a model that better reflects insulin resistance-associated metabolic disturbances, remains unclear. In this study, mice were divided into three groups (<i>db</i>/+, <i>db</i>/<i>db</i>, and <i>db</i>/<i>db</i> + 0.02% myricitrin) and were fed their respective diets for five weeks. Myricitrin supplementation reduced fat mass, adipocyte size, and plasma leptin levels, which were elevated in <i>db</i>/<i>db</i> mice. Although myricitrin did not affect fasting blood glucose levels, it lowered plasma insulin, hemoglobin A1c, postprandial glucose levels, and the homeostasis model assessment of insulin resistance, suggesting improvements in insulin sensitivity and glucose homeostasis. Enhanced pancreatic insulin expression, along with reduced hepatic gluconeogenic enzyme activities and mRNA expression, contributed to the improved glucose homeostasis observed in myricitrin-supplemented mice. Additionally, myricitrin reduced hepatic triglyceride levels and lipid droplet accumulation by inhibiting hepatic fatty acid synthase activity. It also decreased plasma inflammatory marker levels and their mRNA expression in adipose tissue. These findings suggest that myricitrin may be a promising therapeutic candidate for type 2 diabetes.
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spelling doaj-art-0afe2b064e4f48eaafcae1eecddc24b62025-08-20T02:09:22ZengMDPI AGMolecules1420-30492025-03-01307146010.3390/molecules30071460Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 DiabetesSang Ryong Kim0Young-Je Kim1HwiCheol Kim2Sojeong Park3Un Ju Jung4School of Life Science and Biotechnology, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of KoreaDepartment of Food Science and Nutrition, Kyungpook National University, 80 Daehak-ro, Buk-gu, Daegu 41566, Republic of KoreaDepartment of Food Science and Nutrition, Pukyong National University, 45 Yongso-ro, Nam-gu, Busan 48513, Republic of KoreaDepartment of Food Science and Nutrition, Pukyong National University, 45 Yongso-ro, Nam-gu, Busan 48513, Republic of KoreaDepartment of Food Science and Nutrition, Pukyong National University, 45 Yongso-ro, Nam-gu, Busan 48513, Republic of KoreaType 2 diabetes is characterized by insulin resistance, which contributes to dysregulated glucose and lipid metabolism and is associated with chronic inflammation. While previous studies have examined the effects of myricitrin in streptozotocin-induced diabetic models, its impact on the <i>db</i>/<i>db</i> mouse, a model that better reflects insulin resistance-associated metabolic disturbances, remains unclear. In this study, mice were divided into three groups (<i>db</i>/+, <i>db</i>/<i>db</i>, and <i>db</i>/<i>db</i> + 0.02% myricitrin) and were fed their respective diets for five weeks. Myricitrin supplementation reduced fat mass, adipocyte size, and plasma leptin levels, which were elevated in <i>db</i>/<i>db</i> mice. Although myricitrin did not affect fasting blood glucose levels, it lowered plasma insulin, hemoglobin A1c, postprandial glucose levels, and the homeostasis model assessment of insulin resistance, suggesting improvements in insulin sensitivity and glucose homeostasis. Enhanced pancreatic insulin expression, along with reduced hepatic gluconeogenic enzyme activities and mRNA expression, contributed to the improved glucose homeostasis observed in myricitrin-supplemented mice. Additionally, myricitrin reduced hepatic triglyceride levels and lipid droplet accumulation by inhibiting hepatic fatty acid synthase activity. It also decreased plasma inflammatory marker levels and their mRNA expression in adipose tissue. These findings suggest that myricitrin may be a promising therapeutic candidate for type 2 diabetes.https://www.mdpi.com/1420-3049/30/7/1460myricitrin<i>db</i>/<i>db</i> miceinsulin resistancehepatic steatosisinflammation
spellingShingle Sang Ryong Kim
Young-Je Kim
HwiCheol Kim
Sojeong Park
Un Ju Jung
Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
Molecules
myricitrin
<i>db</i>/<i>db</i> mice
insulin resistance
hepatic steatosis
inflammation
title Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
title_full Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
title_fullStr Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
title_full_unstemmed Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
title_short Therapeutic Potential of Myricitrin in a <i>db</i>/<i>db</i> Mouse Model of Type 2 Diabetes
title_sort therapeutic potential of myricitrin in a i db i i db i mouse model of type 2 diabetes
topic myricitrin
<i>db</i>/<i>db</i> mice
insulin resistance
hepatic steatosis
inflammation
url https://www.mdpi.com/1420-3049/30/7/1460
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