Receptor for ADIPOQ, an essential hormone secreted by adipocytes that regulates glucose and lipid metabolism (PubMed:17327425, PubMed:17068142, PubMed:17268472, PubMed:24742672). Required for normal body fat and glucose homeostasis (PubMed:17327425, PubMed:17068142, PubMed:17268472, PubMed:24742672). ADIPOQ-binding activates a signaling cascade that leads to increased PPARA activity, and ultimately to increased fatty acid oxidation and glucose uptake (PubMed:12802337, PubMed:17268472, PubMed:24742672). Has intermediate affinity for globular and full-length adiponectin (PubMed:12802337). Required for normal revascularization after chronic ischemia caused by severing of blood vessels (PubMed:24742672). May form homooligomers and heterooligomers with ADIPOR1 (By similarity). Interacts with APPL2 (via BAR domain); ADIPOQ dissociates this interaction (PubMed:19661063). Localized to the cell membrane and intracellular organelles. Detected in liver and quadriceps muscle (at protein level) (PubMed:17327425). Highly expressed in liver (PubMed:12802337). Highly expressed in white adipose tissue, and at intermediate levels in brown adipose tissue (PubMed:24742672). Expressed at intermediate level in heart, kidney, lung and skeletal muscle. Weakly expressed in brain, spleen and testis. The N-terminus is cytoplasmic and the C-terminus is extracellular, contrary to what is observed for G-protein coupled receptors. Unlike G-protein coupled receptors, transmembrane helices are not kinked or tilted relative to the plane of the membrane. Mutant mice are viable and fertile, and display increased glucose tolerance (PubMed:17327425, PubMed:17068142, PubMed:17268472, PubMed:24742672). On a high fat diet, they have lower fasting insulin levels than wild-type (PubMed:17327425, PubMed:24742672). Mutant mice have lower plasma cholesterol levels on a high fat diet, and possibly also on normal chow (PubMed:17327425, PubMed:17068142). The precise phenotype may depend on the experimental details and on genotype. Male and female mutant mice are somewhat leaner than wild-type on standard chow and do not display increased weight gain on a high fat diet (PubMed:17327425, PubMed:24742672). Mutant mice have normal body weight on standard chow, but decreased weight gain on a high-fat diet (PubMed:17068142). Female mutant mice display lower total body fat than wild-type on a high fat diet (PubMed:17327425). Both male and female mice have reduced levels of white and brown adipose tissue relative to wild-type (PubMed:17327425). Mutant male mice display decreased testis weight, atrophy of the seminiferous tubules and aspermia (PubMed:17327425). Both male and female mice display increased brain weight relative to wild-type (PubMed:17327425). Mutant mice have increased locomotor activity and increased energy expenditure on a high fat diet (PubMed:17327425). Mutant mice display impaired revascularization, limb retraction, atrophy and necrosis in response to limb ischemia caused by severing the femoral artery (PubMed:24742672). Hepatocytes from mice lacking both Adipor1 and Adipor2 show loss of adiponectin binding and lack of adiponectin-mediated activation of AMPK and Ppara (PubMed:17268472). Mice lacking both Adipor1 and Adipor2 display elevated glucose and insulin levels in blood plasma, indicative of glucose intolerance and insulin resistance (PubMed:17268472). Belongs to the ADIPOR family.