T-cell Metabolism as Interpreted in Obesity-associated Inflammation

被引:1
作者
Bharath, Leena P. [1 ]
Hart, Samantha N. [2 ,3 ]
Nikolajczyk, Barbara S. [2 ,3 ,4 ,5 ]
机构
[1] Merrimack Coll, Dept Nutr & Publ Hlth, N Andover, MA 01845 USA
[2] Univ Kentucky, Dept Mol, Lexington, KY 40536 USA
[3] Univ Kentucky, Dept Cellular Biochem, Lexington, KY 40536 USA
[4] Univ Kentucky, Pharmacol & Nutr Sci, Lexington, KY 40536 USA
[5] Univ Kentucky, Barnstable Brown Diabet Ctr, Lexington, KY 40536 USA
关键词
type; 2; diabetes; prediabetes; human; mitochondria; INSULIN-RESISTANT SUBJECTS; HUMAN SKELETAL-MUSCLE; NECROSIS-FACTOR-ALPHA; ADIPOSE-TISSUE; MITOCHONDRIAL DYNAMICS; REGULATORY T; RISK-FACTORS; PPAR-GAMMA; DYSFUNCTION; ACTIVATION;
D O I
10.1210/endocr/bqac124
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The appreciation of metabolic regulation of T-cell function has exploded over the past decade, as has our understanding of how inflammation fuels comorbidities of obesity, including type 2 diabetes. The likelihood that obesity fundamentally alters T-cell metabolism and thus chronic obesity-associated inflammation is high, but studies testing causal relationships remain underrepresented. We searched PubMed for key words including mitochondria, obesity, T cell, type 2 diabetes, cristae, fission, fusion, redox, and reactive oxygen species to identify foundational and more recent studies that address these topics or cite foundational work. We investigated primary papers cited by reviews found in these searches and highlighted recent work with >100 citations to illustrate the state of the art in understanding mechanisms that control metabolism and thus function of various T-cell subsets in obesity. However, "popularity" of a paper over the first 5 years after publication cannot assess long-term impact; thus, some likely important work with fewer citations is also highlighted. We feature studies of human cells, supplementing with studies from animal models that suggest future directions for human cell research. This approach identified gaps in the literature that will need to be filled before we can estimate efficacy of mitochondria-targeted drugs in clinical trials to alleviate pathogenesis of obesity-associated inflammation.
引用
收藏
页数:11
相关论文
共 115 条
[1]   Targeting T-cell oxidative metabolism to improve influenza survival in a mouse model of obesity [J].
Alwarawrah, Yazan ;
Nichols, Amanda G. ;
Green, William D. ;
Eisner, William ;
Kiernan, Kaitlin ;
Warren, Jonathan ;
Hale, Laura P. ;
Beck, Melinda A. ;
MacIver, Nancie J. .
INTERNATIONAL JOURNAL OF OBESITY, 2020, 44 (12) :2419-2429
[2]   Adipose macrophage infiltration is associated with insulin resistance and vascular endothelial dysfunction in obese subjects [J].
Apovian, Caroline M. ;
Bigornia, Sherman ;
Mott, Melanie ;
Meyers, Melissa R. ;
Ulloor, Jagadish ;
Gagua, Manana ;
McDonnell, Marie ;
Hess, Donald ;
Joseph, Lija ;
Gokce, Noyan .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2008, 28 (09) :1654-1659
[3]   Chronic enrichment of hepatic endoplasmic reticulum-mitochondria contact leads to mitochondrial dysfunction in obesity [J].
Arruda, Ana Paula ;
Pers, Benedicte M. ;
Parlakguel, Guenes ;
Gueney, Ekin ;
Inouye, Karen ;
Hotamisligil, Goekhan S. .
NATURE MEDICINE, 2014, 20 (12) :1427-1435
[4]   Expression of Mfn2, the Charcot-Marie-Tooth neuropathy type 2A gene, in human skeletal muscle -: Effects of type 2 diabetes, obesity, weight loss, and the regulatory role of tumor necrosis factor α, and interleukin-6 [J].
Bach, D ;
Naon, D ;
Pich, S ;
Soriano, FX ;
Vega, N ;
Rieusset, J ;
Laville, M ;
Guillet, C ;
Boirie, Y ;
Wallberg-Henriksson, H ;
Manco, M ;
Calvani, M ;
Castagneto, M ;
Palacín, M ;
Mingrone, G ;
Zierath, JR ;
Vidal, H ;
Zorzano, A .
DIABETES, 2005, 54 (09) :2685-2693
[5]   Distinct modes of mitochondrial metabolism uncouple T cell differentiation and function [J].
Bailis, Will ;
Shyer, Justin A. ;
Zhao, Jun ;
Canaveras, Juan Carlos Garcia ;
Al Khazal, Fatimah J. ;
Qu, Rihao ;
Steach, Holly R. ;
Bielecki, Piotr ;
Khan, Omair ;
Jackson, Ruaidhri ;
Kluger, Yuval ;
Maher, Louis J., III ;
Rabinowitz, Joshua ;
Craft, Joe ;
Flavell, Richard A. .
NATURE, 2019, 571 (7765) :403-+
[6]   Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8+ T Cells [J].
Bantug, Glenn R. ;
Fischer, Marco ;
Grahlert, Jasmin ;
Balmer, Maria L. ;
Unterstab, Gunhild ;
Develioglu, Leyla ;
Steiner, Rebekah ;
Zhang, Lianjun ;
Costa, Ana S. H. ;
Gubser, Patrick M. ;
Burgener, Anne-Valerie ;
Sauder, Ursula ;
Loliger, Jordan ;
Belle, Reka ;
Dimeloe, Sarah ;
Lotscher, Jonas ;
Jauch, Annaise ;
Recher, Mike ;
Honger, Gideon ;
Hall, Michael N. ;
Romero, Pedro ;
Frezza, Christian ;
Hess, Christoph .
IMMUNITY, 2018, 48 (03) :542-+
[7]   Depletion of fat-resident Treg cells prevents age-associated insulin resistance [J].
Bapat, Sagar P. ;
Suh, Jae Myoung ;
Fang, Sungsoon ;
Liu, Sihao ;
Zhang, Yang ;
Cheng, Albert ;
Zhou, Carmen ;
Liang, Yuqiong ;
LeBlanc, Mathias ;
Liddle, Christopher ;
Atkins, Annette R. ;
Yu, Ruth T. ;
Downes, Michael ;
Evans, Ronald M. ;
Zheng, Ye .
NATURE, 2015, 528 (7580) :137-+
[8]   Tregs facilitate obesity and insulin resistance via a Blimp-1/IL-10 axis [J].
Beppu, Lisa Y. ;
Mooli, Raja Gopal Reddy ;
Qu, Xiaoyao ;
Marrero, Giovanni J. ;
Finley, Christopher A. ;
Fooks, Allen N. ;
Mullen, Zachary P. ;
Frias, Adolfo B., Jr. ;
Sipula, Ian ;
Xie, Bingxian ;
Helfrich, Katherine E. ;
Watkins, Simon C. ;
Poholek, Amanda C. ;
Ramakrishnan, Sadeesh K. ;
Jurczak, Michael J. ;
D'Cruz, Louise M. .
JCI INSIGHT, 2021, 6 (03)
[9]   De novo fatty acid synthesis controls the fate between regulatory T and T helper 17 cells [J].
Berod, Luciana ;
Friedrich, Christin ;
Nandan, Amrita ;
Freitag, Jenny ;
Hagemann, Stefanie ;
Harmrolfs, Kirsten ;
Sandouk, Aline ;
Hesse, Christina ;
Castro, Carla N. ;
Baehres, Heike ;
Tschirner, Sarah K. ;
Gorinski, Nataliya ;
Gohmert, Melanie ;
Mayer, Christian T. ;
Huehn, Jochen ;
Ponimaskin, Evgeni ;
Abraham, Wolf-Rainer ;
Mueller, Rolf ;
Lochner, Matthias ;
Sparwasser, Tim .
NATURE MEDICINE, 2014, 20 (11) :1327-1333
[10]   BCR-Induced Ca2+ Signals Dynamically Tune Survival, Metabolic Reprogramming, and Proliferation of Naive B Cells [J].
Berry, Corbett T. ;
Liu, Xiaohong ;
Myles, Arpita ;
Nandi, Satabdi ;
Chen, Youhai H. ;
Hershberg, Uri ;
Brodsky, Igor E. ;
Cancro, Michael P. ;
Lengner, Christopher J. ;
May, Michael J. ;
Freedman, Bruce D. .
CELL REPORTS, 2020, 31 (02)