Sanyal D. Exploring the genetic basis of childhood monogenic diabetes. World J Diabetes 2024; 15(9): 1829-1832 [DOI: 10.4239/wjd.v15.i9.1829]
Corresponding Author of This Article
Debmalya Sanyal, FACE, FRCP, MBBS, MD, MRCP, Professor, Department of Endocrinology, KPC Medical College, 1F Raja Subodh Chandra Mullick Road, Kolkata Pin 700032, West Bengal, India. drdebmalyasanyal@gmail.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Sep 15, 2024; 15(9): 1829-1832 Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1829
Exploring the genetic basis of childhood monogenic diabetes
Debmalya Sanyal
Debmalya Sanyal, Department of Endocrinology, KPC Medical College, Kolkata Pin 700032, West Bengal, India
Debmalya Sanyal, Department of Endocrinology, NH RTIICS, Kolkata Pin 700099, West Bengal, India
Debmalya Sanyal, School of Medicine, University of New Castle, Callaghan NSW 2308, Australia
Author contributions: Sanyal D contributed to manuscript development.
Conflict-of-interest statement: All the authors report no relevant 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: Debmalya Sanyal, FACE, FRCP, MBBS, MD, MRCP, Professor, Department of Endocrinology, KPC Medical College, 1F Raja Subodh Chandra Mullick Road, Kolkata Pin 700032, West Bengal, India. drdebmalyasanyal@gmail.com
Received: December 18, 2023 Revised: May 29, 2024 Accepted: June 28, 2024 Published online: September 15, 2024 Processing time: 253 Days and 5.1 Hours
Abstract
Monogenic diabetes is caused by one or even more genetic variations, which may be uncommon yet have a significant influence and cause diabetes at an early age. Monogenic diabetes affects 1% to 5% of children, and early detection and genetically focused treatment of neonatal diabetes and maturity-onset diabetes of the young can significantly improve long-term health and well-being. The etiology of monogenic diabetes in childhood is primarily attributed to genetic variations affecting the regulatory genes responsible for beta-cell activity. In rare instances, mutations leading to severe insulin resistance can also result in the development of diabetes. Individuals diagnosed with specific types of monogenic diabetes, which are commonly found, can transition from insulin therapy to sulfonylureas, provided they maintain consistent regulation of their blood glucose levels. Scientists have successfully devised materials and methodologies to distinguish individuals with type 1 or 2 diabetes from those more prone to monogenic diabetes. Genetic screening with appropriate findings and interpretations is essential to establish a prognosis and to guide the choice of therapies and management of these interrelated ailments. This review aims to design a comprehensive literature summarizing genetic insights into monogenetic diabetes in children and adolescents as well as summarizing their diagnosis and management.
Core Tip: Monogenic diabetes, a rare yet impactful condition in childhood, results from genetic variations, causing early-onset diabetes. Affecting 1%-5% of children, early detection and tailored genetic treatments can enhance long-term health. Culprits include genetic variations in beta-cell regulatory genes and severe insulin resistance. Identifying specific types allows transitioning to sulfonylureas while maintaining glucose control. Tools to differentiate diabetes types underscore genetic screening's importance for prognosis and treatment guidance. This review delves into genetic insights into childhood monogenic diabetes, offering diagnosis and management guidance for affected youth's better health.
