Receptor for ADIPOQ, an essential hormone secreted by adipocytes that regulates glucose and lipid metabolism (PubMed:17327425, PubMed:17268472, PubMed:24742672). Required for normal glucose and fat homeostasis and for maintaining a normal body weight (PubMed:17327425, PubMed:24742672). ADIPOQ-binding activates a signaling cascade that leads to increased AMPK activity, and ultimately to increased fatty acid oxidation, increased glucose uptake and decreased gluconeogenesis (PubMed:12802337, PubMed:17327425, PubMed:17268472, PubMed:24742672). Has high affinity for globular adiponectin and low affinity for full-length adiponectin (PubMed:12802337). May form homooligomers and heterooligomers with ADIPOR2 (By similarity). Interacts with APPL2 (via BAR domain); hinders the accessibility of APPL1 to ADIPOR1; negatively regulates adiponectin signaling; ADIPOQ dissociates this interaction and facilitates the recruitment of APPL1 to ADIPOR1 (PubMed:19661063). Interacts with APPL1; ADIPOQ enhances this interaction; inhibites adiponectin-stimulated binding of APPL2 to ADIPOR1 (PubMed:19661063). Localized to the cell membrane and intracellular organelles. Detected in brain and quadriceps muscle (at protein level) (PubMed:17327425). Widely expressed (PubMed:12802337). Expressed in heart, kidney, liver, lung, skeletal muscle, white adipose tissue, brown adipose tissue, aorta and spleen (PubMed:12802337, PubMed:24742672). Weakly expressed in brain and testis (PubMed:12802337). 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, but display defects in glucose and lipid homeostasis. The precise phenotype may depend on experimental details and genetic background. Mutant mice have normal body weight, but increased plasma glucose and insulin levels (PubMed:17268472). Mutant male mice, but not female mice, display increased body weight gain on standard chow, in spite of similar food intake as wild-type (PubMed:17327425). Mutant mice display increased body weight, both on standard chow and on high fat and high sucrose diet (PubMed:24742672). Male mice have increased total body fat mass after 15 weeks, and have increased weights of both white and brown adipose tissue (PubMed:17327425, PubMed:24742672). Mutant mice have impaired glucose tolerance (PubMed:24742672). Male mice have decreased glucose tolerance, but no significant change in the insulin response (PubMed:17327425). Female mice display increased fasting glucose levels, but unchanged fasting insulin levels (PubMed:17327425). Male and female mice display increased levels of liver triglycerides relative to wild-type (PubMed:17327425, PubMed:24742672). Male mice display decreased locomotor activity and decreased energy expenditure relative to wild-type (PubMed:17327425). Mutant mice display normal revascularization after chronic limb ischemia caused by severing of blood vessels (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. Truncated C-terminus. This frameshift abolishes the stop codon.