AdipoR1, the receptor of adiponectin secreted by adipose tissue, is crucial in regulating glucose and lipid metabolism. It initiates signal transduction events upon binding to adiponectin, including phosphorylation of adenosine monophosphate (AMPK) and p38 mitogen-activated protein kinase (p38 MAPK), and increased peroxisome proliferator-activated receptor alpha (PPARα) ligand activity. These processes are regulated by APPL1, which binds to AdipoR1's intracellular region. AdipoR1 also has ceramidase activity, reducing intracellular ceramide, and is involved in whole-body energy homeostasis and anti-inflammatory responses [1].

In a study on obesity-induced male infertility, AdipoR1 knockout mice showed decreased testes weight, sperm count, sperm motility, and sperm fertilizing ability. Also, the phosphorylation of AMPK was decreased, and the expression of pro-apoptotic genes, caspase-6 activity, and pathologically apoptotic seminiferous tubules were increased in their testes. Oral administration of AdipoRon, an adiponectin receptor agonist, decreased caspase-6 activity and apoptotic seminiferous tubules, thus improving sperm motility in high-fat diet-fed male mice. This indicates that decreased AdipoR1/AMPK signaling may lead to male infertility [2].

In conclusion, AdipoR1 is essential for maintaining normal physiological functions, especially in metabolism and anti-inflammation. The use of AdipoR1 knockout mouse models has revealed its significance in obesity-induced male infertility, providing insights into the underlying mechanisms and potential therapeutic targets for this disease.