Obesity induces a chronic low-grade inflammation that originates from the adipose tissue and plays a crucial role in the development of obesity-driven metabolic complications, including insulin resistance and type 2 diabetes. Chronic inflammation is partly a consequence of failing to actively resolve inflammation, e.g. due to a local lack of so-called "specialized proresolving lipid mediators" (SPMs). SPMs, like resolvins, protectins and lipoxins derive from the long-chain n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic and docosahexaenoic acid (EPA and DHA) or the n-6 PUFA arachidonic acid and promote resolution i.e. active termination of inflammation. Possible obesity-induced changes of SPMs and/or SPM precursors in adipose tissue could trigger obesity-driven chronic inflammation and thus provide a rationale for potential therapeutic treatment options. First, the impact of obesity on SPM and SPM precursor levels in adipose tissue was investigated in two mouse models of obesity, namely a diet-induced and genetic (db/db) obesity model applying HPLC-tandem mass spectrometry. Besides, I assessed whether dietary treatment with SPM precursors (n-3 and n-6 PUFA) or direct application of SPMs and their precursors attenuates adipose tissue inflammation and metabolic dysregulation in obesity. Obesity significantly reduced levels of DHA-derived 17-hydroxy-DHA (17-HDHA, resolvin D1 precursor and protectin D1 pathway biomarker) and protectin D1, and AA-derived 15-hydroxyeicosatetraenoic acid (lipoxin precursor) in murine adipose tissue. Dietary treatment with the n-3 PUFA EPA and DHA enhanced endogenous synthesis of n-3 PUFA-derived SPMs and their precursors in obesity while decreasing adipose tissue inflammation and enhancing insulin sensitivity. Of note, direct 17-HDHA application attenuated adipose tissue inflammation probably by reducing NF-kappaB activation, and increased glucose tolerance and insulin sensitivity in obese mice. These findings provide evidence that an obesity-induced deficit of certain SPMs and their precursors contributes to chronic adipose tissue inflammation in obesity. Moreover, 17-HDHA could represent a novel strategy to treat obesity-derived complications.