369 Investigating the impact of bariatric surgery on metabolic mechanisms that promote obesity-associated inflammation in subjects with and without Type 2 Diabetes
OBJECTIVES/GOALS: This project will provide novel insights into mechanism(s) by which differences in inflammation develop & resolve, or fail to resolve, in metabolically different groups of bariatric surgery patients determined by Type 2 Diabetes status. My work may uncover unique differences be...
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Published in | Journal of clinical and translational science Vol. 8; no. s1; p. 111 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Cambridge
Cambridge University Press
01.04.2024
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Abstract | OBJECTIVES/GOALS: This project will provide novel insights into mechanism(s) by which differences in inflammation develop & resolve, or fail to resolve, in metabolically different groups of bariatric surgery patients determined by Type 2 Diabetes status. My work may uncover unique differences between cohorts, encouraging development of personalized medicine. METHODS/STUDY POPULATION: I analyzed human blood samples collected before and 3, 6, & 12 months after bariatric surgery at the University of Kentucky through an established tissue bank. Subjects hadnormal glucose tolerance, pre-diabetes, or Type 2 Diabetes, based on HbA1c%. Iisolated peripheral blood mono nuclear cells & will comparecytokine profiles among cohorts across all time points. I will define & perturbmetabolic differencesin immune cells among cohorts & across time via isotope tracing, fuel source limitation, and metabolite inhibition. This will determine causal relationships between cytokine profiles & immune cell metabolism. RESULTS/ANTICIPATED RESULTS: I anticipatecytokine profiles, a functional output of immune cells, will differ among cohorts pre-surgery, and that this difference will diminish post-surgery. Differencesmay be insignificant by the 12 month time point. I also anticipate differences in fuel usage and metabolite productionin immune cells among cohorts pre-surgery, and that these differences only partially resolve post-surgery to poise immune cells for continued chronic inflammatory action. I hypothesize that T2D status has a lasting impact on immune cell function and fuel usage patterns, and will continue to supportchronic inflammation following short term T2D remission and longer-term weight loss. DISCUSSION/SIGNIFICANCE: There has been an alarming increase in obesity and its comorbidities over recent decades, and inflammation is a known supporter of T2D. The anticipated rewiring of immune cell metabolism post-surgery, if incomplete, may poise subjects forweight regain and T2D recurrence. |
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AbstractList | OBJECTIVES/GOALS: This project will provide novel insights into mechanism(s) by which differences in inflammation develop & resolve, or fail to resolve, in metabolically different groups of bariatric surgery patients determined by Type 2 Diabetes status. My work may uncover unique differences between cohorts, encouraging development of personalized medicine. METHODS/STUDY POPULATION: I analyzed human blood samples collected before and 3, 6, & 12 months after bariatric surgery at the University of Kentucky through an established tissue bank. Subjects hadnormal glucose tolerance, pre-diabetes, or Type 2 Diabetes, based on HbA1c%. Iisolated peripheral blood mono nuclear cells & will comparecytokine profiles among cohorts across all time points. I will define & perturbmetabolic differencesin immune cells among cohorts & across time via isotope tracing, fuel source limitation, and metabolite inhibition. This will determine causal relationships between cytokine profiles & immune cell metabolism. RESULTS/ANTICIPATED RESULTS: I anticipatecytokine profiles, a functional output of immune cells, will differ among cohorts pre-surgery, and that this difference will diminish post-surgery. Differencesmay be insignificant by the 12 month time point. I also anticipate differences in fuel usage and metabolite productionin immune cells among cohorts pre-surgery, and that these differences only partially resolve post-surgery to poise immune cells for continued chronic inflammatory action. I hypothesize that T2D status has a lasting impact on immune cell function and fuel usage patterns, and will continue to supportchronic inflammation following short term T2D remission and longer-term weight loss. DISCUSSION/SIGNIFICANCE: There has been an alarming increase in obesity and its comorbidities over recent decades, and inflammation is a known supporter of T2D. The anticipated rewiring of immune cell metabolism post-surgery, if incomplete, may poise subjects forweight regain and T2D recurrence. |
Author | Johnson, Lance Hart, Samantha Steiner, Joshua Nikolajczyk, Barbara |
AuthorAffiliation | University of Kentucky |
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Copyright | The Author(s), 2024. The Association for Clinical and Translational Science. This work is licensed under the Creative Commons Attribution – Non-Commercial – No Derivatives License This is an Open Access article, distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is unaltered and is properly cited. The written permission of Cambridge University Press must be obtained for commercial re-use or in order to create a derivative work. (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Association for Clinical and Translational Science 2024 2024 The Association for Clinical and Translational Science |
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SubjectTerms | Comorbidity Diabetes Diabetes mellitus (non-insulin dependent) Gastrointestinal surgery Glucose tolerance Immunological tolerance Inflammation Metabolism Metabolites Obesity Other Peripheral blood Population studies Precision medicine Remission Surgery Weight control |
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Title | 369 Investigating the impact of bariatric surgery on metabolic mechanisms that promote obesity-associated inflammation in subjects with and without Type 2 Diabetes |
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