Chronic oxidative stress is a hallmark of obesity, yet the mechanisms by which specific redox events alter adipose tissue function remain poorly understood. Although reactive oxygen species are often viewed as damaging byproducts of metabolic dysfunction, they can also function as regulatory signals through reversible oxidation of specific amino acid residues within proteins. Here, we identify methionine sulfoxide reductase A (MSRA), an enzyme that controls the redox state of methionine residues, as a key regulator of adipose homeostasis during metabolic stress. Using complementary models, we show that loss of MSRA promotes adipose dysfunction under conditions including aging, nutrient excess, and thermogenic challenge. These findings support a model in which methionine redox control constitutes a previously underappreciated layer of adipose regulation, linking oxidative stress to adipocyte plasticity and systemic metabolic balance. Together, this work identifies MSRA as a candidate mediator of obesity-associated adipose dysfunction and suggests that methionine-based redox signaling may represent a broader mechanism in metabolic disease.