Aging is the greatest risk factor for perturbations in metabolism including insulin resistance, dyslipidemia, and inflammation. Lipocalin 2 (Lcn2) is a circulating factor secreted from adipose tissue in response to obesity, inflammation, and nutrient/growth signals. Deis, Guo, et al. found that overexpression of Lcn2 in adipose tissue led to improved cold adaptation, altered whole-body energy expenditure with a trend towards fat oxidation, increased oxidative gene expression, decreased adipose tissue weight and adipocyte size, and decreased glucose/TG levels. Their results also suggest that overexpression of Lcn2 preserves adipose tissue function and prevents age-related glucose intolerance and liver lipid accumulation.