Abstract
In this study, we investigated the impact of bariatric surgery on the adipose proteome to better understand the metabolic and cellular mechanisms underlying weight loss following the procedure. A total of 46 patients with severe obesity were included, with samples collected both before and after bariatric surgery. In addition, 15 healthy individuals without obesity who did not undergo surgery served as controls and were studied once. We utilized quantitative liquid chromatography-tandem mass spectrometry analysis to conduct a large-scale proteomic study on abdominal subcutaneous biopsies obtained from the study participants. Our proteomic profiling revealed that among the 2,254 compared proteins, 46 were upregulated and 34 were downregulated 6 months post surgery compared with baseline [false discovery rate (FDR) < 0.01]. We observed a downregulation of proteins associated with mitochondrial integrity, amino acid catabolism, and lipid metabolism in the patients with severe obesity compared with the controls. Bariatric surgery was associated with an upregulation in pathways related to mitochondrial function, protein synthesis, folding and trafficking, actin cytoskeleton regulation, and DNA binding and repair. These findings emphasize the significant changes in metabolic and cellular pathways following bariatric surgery, highlighting the potential mechanisms underlying the observed health improvements postbariatric surgery. The data provided alongside this paper will serve as a valuable resource for the development of targeted therapeutic strategies for obesity and related metabolic complications.
| Original language | English |
|---|---|
| Pages (from-to) | E311-E324 |
| Journal | American Journal of Physiology - Endocrinology and Metabolism |
| Volume | 328 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 2025 |
| MoE publication type | A1 Journal article-refereed |
Funding
This work was supported by the Academy of Finland (Grant No. 307402 to P.N.), the University of Turku, University Hospital, Åbo Akademi University (Finland). P.D. received funding from the Finnish Medical Association, the Finnish Diabetes Research Foundation, Finnish Cultural Foundation, Finnish-Norwegian Medical Foundation, Instrumentarium Science Foundation, Pa€ivikki and Sakari Sohlberg Foundation, the Onni and Hilja Tuovinen Foundation, Jalmari and Rauha Ahokas Foundation, and Aarne Koskelo Foundation. M.-J.H. was supported by the Finnish Diabetes Research Foundation and the Academy of Finland (Grant 332151). A. Roivainen and S.P. were supported by the Academy of Finland (Grant 335975). P.J. received a Finnish Distinguished Professorship from TEKES and the Academy of Finland. The Turku Proteomics Facility is supported by Biocenter Finland. The group of V.M.O. was supported by the Academy of Finland (Grant 322647), the Sigrid Jusélius Foundation, the Liv och Ha€lsa Foundation, the Finnish Diabetes Research Foundation, Diabetes Wellness Finland, the Magnus Ehrnrooth Foundation, Finnish Society of Sciences and Letters and Jane and Aatos Erkko Foundation. L.L.E. reports grants from the European Research Council ERC (677943), European Union’s Horizon 2020 research and innovation programme (955321), Academy of Finland (310561, 314443, 329278, 335434, 335611, and 341342), and Sigrid Juselius Foundation during the conduct of the study. Our research is also supported by Biocenter Finland and ELIXIR Finland. This work was conducted within the Finnish Centre of Excellence in Molecular Imaging in Cardiovascular and Metabolic Research. Mass spectrometry analysis was performed at the Turku Proteomics Facility, University of Turku, and Åbo Akademi University. This work was supported by the Academy of Finland (Grant No. 307402 to P.N.), the University of Turku, University Hospital, Åbo Akademi University (Finland). P.D. received funding from the Finnish Medical Association, the Finnish Diabetes Research Foundation, Finnish Cultural Foundation, Finnish-Norwegian Medical Foundation, Instrumentarium Science Foundation, Paivikki € and Sakari Sohlberg Foundation, the Onni and Hilja Tuovinen Foundation, Jalmari and Rauha Ahokas Foundation, and Aarne Koskelo Foundation. M.-J.H. was supported by the Finnish Diabetes Research Foundation and the Academy of Finland (Grant 332151). A. Roivainen and S.P. were supported by the Academy of Finland (Grant 335975). P.J. received a Finnish Distinguished Professorship from TEKES and the Academy of Finland. The Turku Proteomics Facility is supported by Biocenter Finland. The group of V.M.O. was supported by the Academy of Finland (Grant 322647), the Sigrid Jusélius Foundation, the Liv och Halsa € Foundation, the Finnish Diabetes Research Foundation, Diabetes Wellness Finland, the Magnus Ehrnrooth Foundation, Finnish Society of Sciences and Letters and Jane and Aatos Erkko Foundation. L.L.E. reports grants from the European Research Council ERC (677943), European Union’s Horizon 2020 research and innovation programme (955321), Academy of Finland (310561, 314443, 329278, 335434, 335611, and 341342), and Sigrid Juselius Foundation during the conduct of the study. Our research is also supported by Biocenter Finland and ELIXIR Finland.
Keywords
- adipose tissue
- metabolic and cellular pathways
- metabolic bariatric surgery
- proteomics
- severe obesity
Fingerprint
Dive into the research topics of 'Proteomic profiling reveals alterations in metabolic and cellular pathways in severe obesity and following metabolic bariatric surgery'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver