Liu ZT, Yang GW, Zhao X, Dong SH, Jiao Y, Ge Z, Yu A, Zhang XQ, Xu XZ, Cheng ZQ, Zhang X, Wang KX. Growth hormone improves insulin resistance in visceral adipose tissue after duodenal-jejunal bypass by regulating adiponectin secretion. World J Diabetes 2024; 15(6): 1340-1352 [PMID: 38983805 DOI: 10.4239/wjd.v15.i6.1340]
Corresponding Author of This Article
Ke-Xin Wang, Doctor, Doctor, Department of General Surgery, Qilu Hospital of Shandong University, No. 107 Wenhua West Road, Jinan 250012, Shandong Province, China. wkx3726@163.com
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. Jun 15, 2024; 15(6): 1340-1352 Published online Jun 15, 2024. doi: 10.4239/wjd.v15.i6.1340
Growth hormone improves insulin resistance in visceral adipose tissue after duodenal-jejunal bypass by regulating adiponectin secretion
Zi-Tian Liu, Guang-Wei Yang, Xiang Zhao, Shuo-Hui Dong, Yang Jiao, Zheng Ge, Ao Yu, Xi-Qiang Zhang, Xin-Zhen Xu, Zhi-Qiang Cheng, Xiang Zhang, Ke-Xin Wang
Zi-Tian Liu, Guang-Wei Yang, Xiang Zhao, Shuo-Hui Dong, Zheng Ge, Ao Yu, Xi-Qiang Zhang, Xin-Zhen Xu, Zhi-Qiang Cheng, Xiang Zhang, Ke-Xin Wang, Department of General Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong Province, China
Yang Jiao, Department of General Surgery, Shandong University of Qilu Hospital (Qingdao), Qingdao 266000, Shandong Province, China
Author contributions: Zhang X and Cheng ZQ designed the study; Liu ZT performed the research; Yang GW, Zhao X, Dong SH performed data collection and analysis; Liu ZT analyzed the data and wrote the manuscript; Jiao Y, Ge Z, Yu A, Zhang XQ, Xu XZ provided data curation; Wang KX provided funding acquisition and supervision; all authors have read and approve the final manuscript.
Supported byNational Natural Science Foundation of China (General Program), No. 82070852 and No. 82270901.
Institutional animal care and use committee statement: The study was conducted according to the guidelines of the Declaration of Helsinki, and approved by the Application Format for Ethical Approval for Research Involving Animals, Qilu Hosipital of Shandong University (protocol code DWLL-2021-033, The application was passed in July 2021).
Conflict-of-interest statement: The authors declare no conflict of interest.
Data sharing statement: The data presented in this study are openly available in GEO (accession number: GSE243812).
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ke-Xin Wang, Doctor, Doctor, Department of General Surgery, Qilu Hospital of Shandong University, No. 107 Wenhua West Road, Jinan 250012, Shandong Province, China. wkx3726@163.com
Received: February 19, 2024 Revised: March 12, 2024 Accepted: April 15, 2024 Published online: June 15, 2024 Processing time: 113 Days and 6.7 Hours
Abstract
BACKGROUND
The mechanism of improvement of type 2 diabetes after duodenal-jejunal bypass (DJB) surgery is not clear.
AIM
To study the morphological and functional changes in adipose tissue after DJB and explore the potential mechanisms contributing to postoperative insulin sensitivity improvement of adipose tissue in a diabetic male rat model.
METHODS
DJB and sham surgery was performed in a-high-fat-diet/streptozotocin-induced diabetic rat model. All adipose tissue was weighed and observed under mi-croscope. Use inguinal fat to represent subcutaneous adipose tissue (SAT) and mesangial fat to represent visceral adipose tissue. RNA-sequencing was utilized to evaluate gene expression alterations adipocytes. The hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction, western blot, and enzyme-linked immunosorbent assay were used to study the changes. Insulin resistance was evaluated by immunofluorescence.
RESULTS
After DJB, whole body blood glucose metabolism and insulin sensitivity in adipose tissue improved. Fat cell volume in both visceral adipose tissue (VAT) and SAT increased. Compared to SAT, VAT showed more significantly functional alterations after DJB and KEGG analysis indicated growth hormone (GH) pathway and downstream adiponectin secretion were involved in metabolic regulation. The circulating GH and adiponectin levels and GH receptor and adiponectin levels in VAT increased. Cytological experiment showed that GH stimulated adiponectin secretion and improve insulin sensitivity.
CONCLUSION
GH improves insulin resistance in VAT in male diabetic rats after receiving DJB, possibly by increasing adiponectin secretion.
Core Tip: Our results provide focused insight into the effects of duodenal-jejunal bypass (DJB) on adipose tissue function and insulin resistance in diabetic male rats. Unlike previous studies that often focused on broader metabolic improvements after DJB, this study focused on adipocytes and their molecular changes. Establishing a link between growth hormone (GH), adiponectin, and insulin sensitivity by identifying alterations in the GH pathway.
