Age-associated insulin resistance (IR) and obesity-associated IR are physiologically distinct forms of adult-onset diabetes. Although macrophage-driven inflammation drives the obesity-associated condition, the mechanisms for age-associated IR are not known. Ronald Evans and colleagues show that fat-resident regulatory T cells (fTregcells) accumulate in adipose tissue as a function of age, but not obesity. Mice lacking fTreg cells are protected against age-associated IR, yet remain susceptible to obesity-associated IR and metabolic disease. Depletion of fTreg cells via anti-ST2 antibody treatment increases adipose tissue insulin sensitivity. Although not the main topic of this study, these findings do not support a role for fTreg cells in obesity-associated insulin resistance or in the therapeutic actions of thiazolidinedione or ‘glitazone’ antidiabetics. This contradicts claims that Treg cells were beneficial and necessary for restoration of insulin sensitivity in obese mice by the thiazolidinedione drug pioglitazone.
- Inflammation keeps old mice healthy (News & Views p44, doi: 10.1038/nature15648)
- Depletion of fat-resident Treg cells prevents age-associated insulin resistance (Letter p137, doi: 10.1038/nature16151)
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