To do one and to get more - Part II - Diabetes and metabolic dysfunction-associated fatty liver diseases

Sep 29, 2026

Uploaded by James

Type 2 diabetes mellitus (DM) involves impaired pancreatic β-cell insulin secretion and/or reduced peripheral insulin sensitivity, leading to hyperglycemia and insulin resistance. As a chronic systemic inflammatory disorder, DM arises from dysregulated interactions among ethnic, genetic, epigenetic, immunoregulatory, hormonal, and environmental factors. Given the strong link between DM and metabolic dysfunction-associated fatty liver disease (MAFLD) and their high comorbidity, dual targeting using antidiabetic agents may improve glycemic control and liver outcomes.

LanguageEnglish

CategoryHealthcare

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Reading Time28 min

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INTRODUCTION

Diabetes mellitus and comorbid complications

Rationale for targeting diabetes and MAFLD together

J Chin MedAssoc Review ARticle To do one and to get more: Part II. Diabetes and metabolic dysfunction-associated fatty liver diseases Wen-Ling Leea,b,c, Peng-Hui Wangb,d,e,f,*, Szu-Ting Yangb,d, Chia-Hao Liub,d, Wen-Hsun Changd,g, Fa-Kung Leeh aDepartment of Medicine, Cheng-Hsin General Hospital, Taipei, Taiwan, ROC; bInstitute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, ROC; cDepartment of Nursing, Oriental Institute of Technology, New Taipei City, Taiwan, ROC; dDepartment of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; eDepartment of Medical Research, China Medical University Hospital, Taichung, Taiwan, ROC; fFemale Cancer Foundation, Taipei, Taiwan, ROC; gDepartment of Nursing, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; hDepartment of Obstetrics and Gynecology, Cathy General Hospital, Taipei, Taiwan, ROC Abstract Type 2 diabetes mellitus (DM) is characterized by inability of faulty pancreatic β-cells to secret a normal amount of insulin to maintain normal body consumption, and/or peripheral tissue has a decreased susceptibility to insulin, resulting in hyperglycemia and insulin resistance. Similar to other chronic systemic inflammatory diseases, DM is a result from dysregulated interactions between ethnic, genetic, epigenetic, immunoregulatory, hormonal, and environmental factors. Therefore, it is rational to suppose the concept as “To do one and to get more”, while using antidiabetic agents (ADA), a main pharmacologic agent for the treatment of DM, can provide an extraglycemia effect on comorbidities or concomittent comorbidities to DM. In this review, based on the much strong correlation between DM and metabolic dysfunction-associated fatty liver diseases (MAFLD) shown by similar pathophysiological mechanisms and a high prevalence of DM in MAFLD and its vice versa (a high prevalence of MAFLD in DM), it is possible to use the strategy to target both diseases simultaneously. We focus on a new classification of ADA, such as glucagon-like peptide-1 receptor (GLP1R) agonist and sodium-glucose cotransporter-2 (SGLT-2) inhibitors to show the potential benefits of extraglycemic effect on MAFLD. We conclude that the management of DM patients, especially for those who need ADA as adjuvant therapy should include healthy lifestyle modification to overcome the metabolic syndrome, contributing to the urgent need of an effective weight-reduction strategy. GLP1R agonist is one of effective body weight-lowering medications, which may be a better choice for DM complicated with MAFLD or its-associated severe form as metabolic associated steatohepatitis (MASH), although the role of SGLT-2 inhibitors is also impressive. The prescription of these two classes of ADA may satisfy the concept “To do one and to get more”, based on successful sugar-lowering effect for controlling DM and extraglycemia benefits of hepatoprotective activity in DM patients. Keywords: Anidiabetic agents; Diabetes mellitus (DM); Extraglycemic effects; Fatty liver 1. INTRODUCTION Diabetes mellitus (DM), a complex chronic systemic inflammatory disease, is a heavy socio-economic burden resulting from the severe morbidity and mortality imposed by direct * Address Correspondence. Dr. Peng-Hui Wang, Department of Obstetricsand Gynecology, Taipei Veterans General Hospital, 201, Section 2, Shi-Pai Road, Taipei 112, Taiwan, [ROC. E-mail addresses: phwang@vghtpe.gov.tw](ROC. E-mail addresses: phwang@vghtpe.gov.tw); [pongpongwang@gmail.com](pongpongwang@gmail.com) (P.-H. Wang). Conflicts of interest: Dr Peng-Hui, an editorial board member at Journal of the Chinese Medical Association, had no role in the peer review process of or decision to publish this article. The other authors declare that they have no conflicts of interest related to the subject matter or materials discussed in this article. Journal of Chinese Medical Association. (2022) 85: 1109-1119. Received August 1

FAQs

Why is diabetes mellitus described as a complex chronic inflammatory disease?

The document explains that DM results from dysregulated interactions among ethnic, genetic, epigenetic, immunoregulatory, hormonal, and environmental factors, producing systemic inflammation and long-term organ risks.

What is the relationship between DM and metabolic dysfunction-associated fatty liver disease (MAFLD)?

The review highlights strong correlation and bidirectional prevalence: DM is common in MAFLD, and MAFLD is also highly prevalent in DM, sharing similar pathophysiological mechanisms.

Which antidiabetic agent classes are emphasized for potential benefits beyond glucose lowering?

The article focuses on glucagon-like peptide-1 receptor (GLP-1R) agonists and sodium-glucose cotransporter-2 (SGLT-2) inhibitors, emphasizing possible extraglycemic effects relevant to MAFLD and related liver injury.

Sep 29, 2026

Uploaded by James