Azgp1, also known as Zinc-alpha2-glycoprotein (ZAG), is a multifunctional secreted glycoprotein involved in various biological processes. It has been implicated in pathways related to metabolism, inflammation, and cancer-related processes such as epithelial-mesenchymal transition (EMT) and angiogenesis. Understanding its function is crucial as it may offer insights into energy homeostasis, disease development, and potential therapeutic targets [1,2,3,4].

In POMC neuron-specific Azgp1 knockout (KO) mice, an increase in susceptibility to diet-induced obesity was observed, while overexpression of Azgp1 in these neurons under high-fat diet conditions led to reduced energy intake, increased energy expenditure, and improved metabolic phenotypes. This indicates that Azgp1 in POMC neurons plays a crucial role in controlling whole-body metabolism [1].

In periodontitis, Azgp1-/-mice showed reduced periodontal inflammation and alveolar bone loss compared to those with adeno-associated virus-mediated overexpression of Azgp1, suggesting that Azgp1 aggravates periodontitis by promoting macrophage M1 polarization and pyroptosis [2].

In prostate cancer, AZGP1 knockout mice had higher blood vessel density in the prostate, and in vitro studies showed that AZGP1 inhibits angiogenesis, indicating that loss of AZGP1 promotes angiogenesis in prostate cancer [4].

In conclusion, Azgp1 plays essential roles in regulating energy homeostasis, metabolism, and inflammation, as well as in cancer-related processes such as angiogenesis. The use of Azgp1 KO mouse models has significantly contributed to understanding its functions in diseases like obesity, periodontitis, and prostate cancer, providing potential therapeutic targets for these conditions.