Highlights of IMMUNOLOGY2026™ - Invited Program Recordings-Mechanisms that support obesity-associated inflammation in human prediabetes

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The speaker thanked sponsors and collaborators before presenting research on inflammation in human obesity, prediabetes, and aging. She argued that a major modern health issue is that people are now aging while already obese, unlike past generations when obesity developed later in life. Her studies showed that aging-related inflammation differs depending on body weight and metabolic status.<br /><br />In lean, healthy adults, age-related immune inflammation was dominated by a Th17 cytokine profile. In people with obesity, however, the inflammatory pattern changed and was not driven by the same Th17 cytokines. Metformin also behaved differently depending on context: in lean cells it reduced inflammation and improved autophagy, but in obese individuals its effects were weaker in vitro and in clinical trial samples it appeared to help mainly in people with obesity and prediabetes, not those who were normoglycemic. Preliminary single-cell data suggested metformin may increase regulatory T cells and transitional T cells.<br /><br />The speaker also described unexpected mitochondrial findings. Older cells from people with obesity had more networked mitochondria and higher oxidative metabolism, but were less metabolically flexible. A mitochondrial probe altered mitochondrial structure and increased inflammatory cytokines in older cells, but did not restore youthful immune behavior.<br /><br />Overall, obesity strongly modifies aging-related immune inflammation, and mitochondrial changes alone may not explain the full biology.

Keywords

obesity

aging

inflammation

prediabetes

metformin

mitochondria

immune cells