Review
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Jul 27, 2022; 14(7): 1291-1306
Published online Jul 27, 2022. doi: 10.4254/wjh.v14.i7.1291
Hepatogenous diabetes: Knowledge, evidence, and skepticism
Ramesh Kumar, Diego García-Compeán, Tanmoy Maji
Ramesh Kumar, Tanmoy Maji, Department of Gastroenterology, All India Institute of Medical Sciences, Patna 801507, Bihar, India
Diego García-Compeán, Department of Gastroenterology, University Hospital, Universidad Autónoma de Nuevo León, México, Monterrey 64700, México
Author contributions: Kumar R contributed in concept and design of manuscript, data collection and manuscript writing; García-Compeán D and Maji T contributed in concept, data collection and manuscript writing.
Conflict-of-interest statement: The authors declare that they have no conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ramesh Kumar, MD, Associate Professor, Department of Gastroenterology, All India Institute of Medical Sciences, Phulwari Sharif, Patna 801507, Bihar, India. docrameshkr@gmail.com
Received: January 13, 2022
Peer-review started: January 13, 2022
First decision: April 16, 2022
Revised: April 27, 2022
Accepted: July 5, 2022
Article in press: July 5, 2022
Published online: July 27, 2022
Abstract

The diabetogenic potential of liver cirrhosis (LC) has been known for a long time, and the name "hepatogenous diabetes" (HD) was coined in 1906 to define the condition. Diabetes mellitus (DM) that develops as a consequence of LC is referred to as HD. In patients with LC, the prevalence rates of HD have been reported to vary from 21% to 57%. The pathophysiological basis of HD seems to involve insulin resistance (IR) and pancreatic β-cell dysfunction. The neurohormonal changes, endotoxemia, and chronic inflammation of LC initially create IR; however, the toxic effects eventually lead to β-cell dysfunction, which marks the transition from impaired glucose tolerance to HD. In addition, a number of factors, including sarcopenia, sarcopenic obesity, gut dysbiosis, and hyperammonemia, have recently been linked to impaired glucose metabolism in LC. DM is associated with complications and poor outcomes in patients with LC, although the individual impact of each type 2 DM and HD is unknown due to a lack of categorization of diabetes in most published research. In fact, there is much skepticism within scientific organizations over the recognition of HD as a separate disease and a consequence of LC. Currently, T2DM and HD are being treated in a similar manner although no standardized guidelines are available. The different pathophysiological basis of HD may have an impact on treatment options. This review article discusses the existence of HD as a distinct entity with high prevalence rates, a strong pathophysiological basis, clinical and therapeutic implications, as well as widespread skepticism and knowledge gaps.

Keywords: Cirrhosis, Diabetes, Hepatogenous diabetes, Glucose intolerance, Insulin resistance, Metabolism

Core Tip: Hepatogenous diabetes appears to be the most prevalent form of diabetes in patients with liver cirrhosis. It is linked to the pathophysiological alterations and severity of cirrhosis. However, it is still an underappreciated problem and is not recognized as a distinct entity by scientific organizations. This article discusses the current state of knowledge about hepatogenous diabetes, including evidence of its existence and clinical implications.