Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells

Metabolic syndrome (MetS) poses considerable toxicological risks due to its association with an increased likelihood of metabolic dysfunction-associated steatotic liver disease (MASLD), and is characterized by hypertension, hyperglycemia, dyslipidemia, and obesity. This study aimed to investigate th...

Full description

Saved in:
Bibliographic Details
Main Authors: Hui-Hsuan Lin, Pei-Rong Yu, Chiao-Yun Tseng, Ming-Shih Lee, Jing-Hsien Chen
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/14/5/595
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850127530225303552
author Hui-Hsuan Lin
Pei-Rong Yu
Chiao-Yun Tseng
Ming-Shih Lee
Jing-Hsien Chen
author_facet Hui-Hsuan Lin
Pei-Rong Yu
Chiao-Yun Tseng
Ming-Shih Lee
Jing-Hsien Chen
author_sort Hui-Hsuan Lin
collection DOAJ
description Metabolic syndrome (MetS) poses considerable toxicological risks due to its association with an increased likelihood of metabolic dysfunction-associated steatotic liver disease (MASLD), and is characterized by hypertension, hyperglycemia, dyslipidemia, and obesity. This study aimed to investigate the therapeutic potential of flavonoid-rich lotus seedpod extract (LSE) in alleviating MetS and MASLD-related hepatic disturbances. In vivo, mice subjected to a high-fat diet (HFD) and streptozotocin (STZ) injection were supplemented with LSE or simvastatin for 6 weeks. Obesity indicators included body weight and epididymal fat, while insulin resistance was measured by fasting serum glucose, serum insulin, homeostasis model assessment–insulin resistance index (HOMA-IR), and oral glucose tolerance (OGTT). Also, the levels of serum lipid profiles and blood pressure were evaluated. Adipokines, proinflammatory cytokines, liver fat droplets, and peri-portal fibrosis were analyzed to clarify the mechanism of MetS. LSE significantly reduced the HFD/STZ-induced MetS markers better than simvastatin, as demonstrated by hypoglycemic, hypolipidemic, antioxidant, and anti-inflammatory effects. In vitro, LSE improved oleic acid (OA)-triggered phenotypes of MASLD in hepatocyte HepG2 cells by reducing lipid accumulation and enhancing cell viability. This effect might be mediated through proteins involved in lipogenesis that are downregulated by adenosine monophosphate-activated protein kinase (AMPK). In addition, LSE reduced reactive oxygen species (ROS) generation and glycogen levels, as demonstrated by enhancing insulin signaling involving reducing insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation and increasing glycogen synthase kinase 3 beta (GSK3β) and protein kinase B (PKB) expression. These benefits were dependent on AMPK activation, as confirmed by the AMPK inhibitor compound C. These results indicate that LSE exhibits protective effects against MetS-caused toxicological disturbances in hepatic carbohydrate and lipid metabolism, potentially contributing to its efficacy in preventing MASLD or MetS.
format Article
id doaj-art-2a667a43ecc34e099594fd36309313ea
institution OA Journals
issn 2076-3921
language English
publishDate 2025-05-01
publisher MDPI AG
record_format Article
series Antioxidants
spelling doaj-art-2a667a43ecc34e099594fd36309313ea2025-08-20T02:33:39ZengMDPI AGAntioxidants2076-39212025-05-0114559510.3390/antiox14050595Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 CellsHui-Hsuan Lin0Pei-Rong Yu1Chiao-Yun Tseng2Ming-Shih Lee3Jing-Hsien Chen4Department of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung City 40201, TaiwanDepartment of Nutrition, Chung Shan Medical University, Taichung City 40201, TaiwanDepartment of Nutrition, Chung Shan Medical University, Taichung City 40201, TaiwanDepartment of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung City 40201, TaiwanClinical Laboratory, Chung Shan Medical University Hospital, Taichung City 40201, TaiwanMetabolic syndrome (MetS) poses considerable toxicological risks due to its association with an increased likelihood of metabolic dysfunction-associated steatotic liver disease (MASLD), and is characterized by hypertension, hyperglycemia, dyslipidemia, and obesity. This study aimed to investigate the therapeutic potential of flavonoid-rich lotus seedpod extract (LSE) in alleviating MetS and MASLD-related hepatic disturbances. In vivo, mice subjected to a high-fat diet (HFD) and streptozotocin (STZ) injection were supplemented with LSE or simvastatin for 6 weeks. Obesity indicators included body weight and epididymal fat, while insulin resistance was measured by fasting serum glucose, serum insulin, homeostasis model assessment–insulin resistance index (HOMA-IR), and oral glucose tolerance (OGTT). Also, the levels of serum lipid profiles and blood pressure were evaluated. Adipokines, proinflammatory cytokines, liver fat droplets, and peri-portal fibrosis were analyzed to clarify the mechanism of MetS. LSE significantly reduced the HFD/STZ-induced MetS markers better than simvastatin, as demonstrated by hypoglycemic, hypolipidemic, antioxidant, and anti-inflammatory effects. In vitro, LSE improved oleic acid (OA)-triggered phenotypes of MASLD in hepatocyte HepG2 cells by reducing lipid accumulation and enhancing cell viability. This effect might be mediated through proteins involved in lipogenesis that are downregulated by adenosine monophosphate-activated protein kinase (AMPK). In addition, LSE reduced reactive oxygen species (ROS) generation and glycogen levels, as demonstrated by enhancing insulin signaling involving reducing insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation and increasing glycogen synthase kinase 3 beta (GSK3β) and protein kinase B (PKB) expression. These benefits were dependent on AMPK activation, as confirmed by the AMPK inhibitor compound C. These results indicate that LSE exhibits protective effects against MetS-caused toxicological disturbances in hepatic carbohydrate and lipid metabolism, potentially contributing to its efficacy in preventing MASLD or MetS.https://www.mdpi.com/2076-3921/14/5/595metabolic syndromelotus seedpod extractlipid dysmetabolisminsulin resistance
spellingShingle Hui-Hsuan Lin
Pei-Rong Yu
Chiao-Yun Tseng
Ming-Shih Lee
Jing-Hsien Chen
Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
Antioxidants
metabolic syndrome
lotus seedpod extract
lipid dysmetabolism
insulin resistance
title Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
title_full Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
title_fullStr Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
title_full_unstemmed Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
title_short Protective Effects of Lotus Seedpod Extract on Hepatic Lipid and Glucose Metabolism via AMPK-Associated Mechanisms in a Mouse Model of Metabolic Syndrome and Oleic Acid-Induced HepG2 Cells
title_sort protective effects of lotus seedpod extract on hepatic lipid and glucose metabolism via ampk associated mechanisms in a mouse model of metabolic syndrome and oleic acid induced hepg2 cells
topic metabolic syndrome
lotus seedpod extract
lipid dysmetabolism
insulin resistance
url https://www.mdpi.com/2076-3921/14/5/595
work_keys_str_mv AT huihsuanlin protectiveeffectsoflotusseedpodextractonhepaticlipidandglucosemetabolismviaampkassociatedmechanismsinamousemodelofmetabolicsyndromeandoleicacidinducedhepg2cells
AT peirongyu protectiveeffectsoflotusseedpodextractonhepaticlipidandglucosemetabolismviaampkassociatedmechanismsinamousemodelofmetabolicsyndromeandoleicacidinducedhepg2cells
AT chiaoyuntseng protectiveeffectsoflotusseedpodextractonhepaticlipidandglucosemetabolismviaampkassociatedmechanismsinamousemodelofmetabolicsyndromeandoleicacidinducedhepg2cells
AT mingshihlee protectiveeffectsoflotusseedpodextractonhepaticlipidandglucosemetabolismviaampkassociatedmechanismsinamousemodelofmetabolicsyndromeandoleicacidinducedhepg2cells
AT jinghsienchen protectiveeffectsoflotusseedpodextractonhepaticlipidandglucosemetabolismviaampkassociatedmechanismsinamousemodelofmetabolicsyndromeandoleicacidinducedhepg2cells