Jaiswal AK, Sadasivam M, Aja S, Hamad ARA. Lack of Syndecan-1 produces significant alterations in whole-body composition, metabolism and glucose homeostasis in mice. World J Diabetes 2020; 11(4): 126-136 [PMID: 32313611 DOI: 10.4239/wjd.v11.i4.126]
Corresponding Author of This Article
Abdel Rahim A Hamad, PhD, Associate Professor, Department of Pathology, Johns Hopkins University School of Medicine, Ross 66G, 720 Rutland Ave, Baltimore, MD 21205, United States. ahamad@jhmi.edu
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Basic Study
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. Apr 15, 2020; 11(4): 126-136 Published online Apr 15, 2020. doi: 10.4239/wjd.v11.i4.126
Lack of Syndecan-1 produces significant alterations in whole-body composition, metabolism and glucose homeostasis in mice
Anil Kumar Jaiswal, Mohanraj Sadasivam, Susan Aja, Abdel Rahim A Hamad
Anil Kumar Jaiswal, Department of Pathobiology, Johns Hopkins University, Baltimore, MD 21205, United States
Mohanraj Sadasivam, Abdel Rahim A Hamad, Department of Pathology, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, United States
Susan Aja, Department of Neuroscience, Johns Hopkins University, Baltimore, MD 21205, United States
Author contributions: Jaiswal AK and Sadasivam M participated equally in the design, execution of the experiments and analysis of the data; Jaiswal AK, Sadasivam M, Aja S and Hamad ARA interpreted the data, and wrote the paper.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Johns Hopkins University Animal Care and Use Committee, in compliance with the Animal Welfare Act and principles set forth in the Guide for the Care and Use of Laboratory Animals.
Conflict-of-interest statement: Authors declare no conflict of interest.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
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: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Abdel Rahim A Hamad, PhD, Associate Professor, Department of Pathology, Johns Hopkins University School of Medicine, Ross 66G, 720 Rutland Ave, Baltimore, MD 21205, United States. ahamad@jhmi.edu
Received: October 23, 2019 Peer-review started: October 23, 2019 First decision: December 12, 2019 Revised: December 20, 2019 Accepted: February 8, 2020 Article in press: February 8, 2020 Published online: April 15, 2020 Processing time: 165 Days and 10.8 Hours
Core Tip
Core tip: Obesity is a disease state with serious adverse metabolic complications that currently has no cure. Identifying key modulators is required for developing effective cures. Here we investigated Syndecan-1 (Sdc1), a member of the heparan sulfate proteoglycan family for its roles in regulating obesity and glucose homeostasis. Sdc1 knockout (Sdc1 KO) mice have reduced body weight with decreases in fat and lean masses under both chow and high fat diet conditions. The reduced body weight was not due to changes in food intakes, but Sdc1 KO mice exhibited altered feeding behavior as they ate more during the dark phase and less during the light phase than wild type mice. In addition, Sdc1 KO mice suffered from high rate of energy expenditure, glucose intolerance and insulin resistance. Our results reveal critical multisystem and opposing roles for Sdc1 in regulating normal energy balance and glucose homeostasis.
