Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation

Abstract Statins, the first‐line medication for dyslipidemia, are linked to an increased risk of type 2 diabetes. But exactly how statins cause diabetes is yet unknown. In this study, a developed short‐term statin therapy on hyperlipidemia mice show that hepatic insulin resistance is a cause of stat...

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Main Authors: Yijun Lin, Shuying Wang, Zixuan Li, Yuling Zhou, Ruiying Wang, Yan Wang, Yan Chen
Format: Article
Language:English
Published: Wiley 2024-09-01
Series:Advanced Science
Subjects:
Online Access:https://doi.org/10.1002/advs.202403451
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author Yijun Lin
Shuying Wang
Zixuan Li
Yuling Zhou
Ruiying Wang
Yan Wang
Yan Chen
author_facet Yijun Lin
Shuying Wang
Zixuan Li
Yuling Zhou
Ruiying Wang
Yan Wang
Yan Chen
author_sort Yijun Lin
collection DOAJ
description Abstract Statins, the first‐line medication for dyslipidemia, are linked to an increased risk of type 2 diabetes. But exactly how statins cause diabetes is yet unknown. In this study, a developed short‐term statin therapy on hyperlipidemia mice show that hepatic insulin resistance is a cause of statin‐induced diabetes. Statin medication raises the expression of progesterone and adiponectin receptor 9 (PAQR9) in liver, which inhibits insulin signaling through degradation of protein phosphatase, Mg2+/Mn2+ dependent 1 (PPM1α) to activate ERK pathway. STIP1 homology and U‐box containing protein 1 (STUB1) is found to mediate ubiquitination of PPM1α promoted by PAQR9. On the other hand, decreased activity of hepatocyte nuclear factor 4 alpha (HNF4α) seems to be the cause of PAQR9 expression under statin therapy. The interventions on PAQR9, including deletion of PAQR9, caloric restriction and HNF4α activation, are all effective treatments for statin‐induced diabetes, while liver specific over‐expression of PPM1α is another possible tactic. The results reveal the importance of HNF4α‐PAQR9‐STUB1‐PPM1α axis in controlling the statin‐induced hepatic insulin resistance, offering a fresh insight into the molecular mechanisms underlying statin therapy.
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publishDate 2024-09-01
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spelling doaj-art-c508dd08f8d04ec8a47e1a7ff2910fb82025-08-20T01:55:19ZengWileyAdvanced Science2198-38442024-09-011134n/an/a10.1002/advs.202403451Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT PhosphorylationYijun Lin0Shuying Wang1Zixuan Li2Yuling Zhou3Ruiying Wang4Yan Wang5Yan Chen6Xiamen Cardiovascular Hospital School of Medicine Xiamen University Xiamen 361016 ChinaCAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and Health University of Chinese Academy of Sciences Chinese Academy of Sciences Shanghai 200031 ChinaCAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and Health University of Chinese Academy of Sciences Chinese Academy of Sciences Shanghai 200031 ChinaXiamen Cardiovascular Hospital School of Medicine Xiamen University Xiamen 361016 ChinaXiamen Cardiovascular Hospital School of Medicine Xiamen University Xiamen 361016 ChinaXiamen Cardiovascular Hospital School of Medicine Xiamen University Xiamen 361016 ChinaCAS Key Laboratory of Nutrition Metabolism and Food Safety Shanghai Institute of Nutrition and Health University of Chinese Academy of Sciences Chinese Academy of Sciences Shanghai 200031 ChinaAbstract Statins, the first‐line medication for dyslipidemia, are linked to an increased risk of type 2 diabetes. But exactly how statins cause diabetes is yet unknown. In this study, a developed short‐term statin therapy on hyperlipidemia mice show that hepatic insulin resistance is a cause of statin‐induced diabetes. Statin medication raises the expression of progesterone and adiponectin receptor 9 (PAQR9) in liver, which inhibits insulin signaling through degradation of protein phosphatase, Mg2+/Mn2+ dependent 1 (PPM1α) to activate ERK pathway. STIP1 homology and U‐box containing protein 1 (STUB1) is found to mediate ubiquitination of PPM1α promoted by PAQR9. On the other hand, decreased activity of hepatocyte nuclear factor 4 alpha (HNF4α) seems to be the cause of PAQR9 expression under statin therapy. The interventions on PAQR9, including deletion of PAQR9, caloric restriction and HNF4α activation, are all effective treatments for statin‐induced diabetes, while liver specific over‐expression of PPM1α is another possible tactic. The results reveal the importance of HNF4α‐PAQR9‐STUB1‐PPM1α axis in controlling the statin‐induced hepatic insulin resistance, offering a fresh insight into the molecular mechanisms underlying statin therapy.https://doi.org/10.1002/advs.202403451AKT phosphorylationhepatic insulin resistanceprogesterone and adiponectin receptor 9 (PAQR9)statinstype 2 diabetes
spellingShingle Yijun Lin
Shuying Wang
Zixuan Li
Yuling Zhou
Ruiying Wang
Yan Wang
Yan Chen
Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
Advanced Science
AKT phosphorylation
hepatic insulin resistance
progesterone and adiponectin receptor 9 (PAQR9)
statins
type 2 diabetes
title Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
title_full Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
title_fullStr Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
title_full_unstemmed Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
title_short Short‐Term Statin Therapy Induces Hepatic Insulin Resistance Through HNF4α/PAQR9/PPM1α Axis Regulated AKT Phosphorylation
title_sort short term statin therapy induces hepatic insulin resistance through hnf4α paqr9 ppm1α axis regulated akt phosphorylation
topic AKT phosphorylation
hepatic insulin resistance
progesterone and adiponectin receptor 9 (PAQR9)
statins
type 2 diabetes
url https://doi.org/10.1002/advs.202403451
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