Vipin VA, Blesson CS, Yallampalli C. Maternal low protein diet and fetal programming of lean type 2 diabetes. World J Diabetes 2022; 13(3): 185-202 [PMID: 35432755 DOI: 10.4239/wjd.v13.i3.185]
Corresponding Author of This Article
Chellakkan Selvanesan Blesson, MPhil, MSc, PhD, Assistant Professor, Department of Obstetrics and Gynecology, Baylor College of Medicine, One Baylor Plaza MS: BCM 610, Houston, TX 77030, United States. selvanes@bcm.edu
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
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/
Vidyadharan Alukkal Vipin, Chellakkan Selvanesan Blesson, Chandra Yallampalli, Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX 77030, United States
Chellakkan Selvanesan Blesson, Family Fertility Center, Texas Children's Hospital, Houston, TX 77030, United States
Author contributions: Author Contribution: Vipin VA, Yallampalli C and Blesson CS had substantial contributions to conception, synthesis and survey of literature, and contributed to draft the manuscript.
Supported bythe National Institutes of Health Grants, No. HL102866, HL58144 and DK114689.
Conflict-of-interest statement: Authors have no conflict of interest.
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: Chellakkan Selvanesan Blesson, MPhil, MSc, PhD, Assistant Professor, Department of Obstetrics and Gynecology, Baylor College of Medicine, One Baylor Plaza MS: BCM 610, Houston, TX 77030, United States. selvanes@bcm.edu
Received: September 28, 2021 Peer-review started: September 28, 2021 First decision: December 4, 2021 Revised: December 30, 2021 Accepted: February 10, 2022 Article in press: February 10, 2022 Published online: March 15, 2022
Abstract
Maternal nutrition is found to be the key factor that determines fetal health in utero and metabolic health during adulthood. Metabolic diseases have been primarily attributed to impaired maternal nutrition during pregnancy, and impaired nutrition has been an immense issue across the globe. In recent years, type 2 diabetes (T2D) has reached epidemic proportion and is a severe public health problem in many countries. Although plenty of research has already been conducted to tackle T2D which is associated with obesity, little is known regarding the etiology and pathophysiology of lean T2D, a variant of T2D. Recent studies have focused on the effects of epigenetic variation on the contribution of in utero origins of lean T2D, although other mechanisms might also contribute to the pathology. Observational studies in humans and experiments in animals strongly suggest an association between maternal low protein diet and lean T2D phenotype. In addition, clear sex-specific disease prevalence was observed in different studies. Consequently, more research is essential for the understanding of the etiology and pathophysiology of lean T2D, which might help to develop better disease prevention and treatment strategies. This review examines the role of protein insufficiency in the maternal diet as the central driver of the developmental programming of lean T2D.
