Gpat3, or glycerol-3-phosphate acyltransferase 3, is a key rate-limiting enzyme regulating triglyceride synthesis [1]. It is involved in lipid metabolic pathways and plays important roles in various biological processes, such as adipogenesis [4]. Genetic models, like gene knockout mouse models, are valuable for studying its functions.

In mouse models, GPAT3 deficiency attenuates corticosterone-caused hepatic steatosis and oxidative stress through the GSK3β/Nrf2 signals [1]. In Seipin -/-Gpat3 -/- mice, there is a significant improvement in liver steatosis and insulin sensitivity, suggesting a functional link between seipin and GPAT3 [3]. In addition, GPAT3 -/- mice show reduced Kupffer cell inflammation reaction, accompanied by improved mitochondrial function and decreased production of lysophosphatidic acid (LPA) [2].

In conclusion, GPAT3 is crucial in lipid metabolism, especially in triglyceride synthesis. Studies using KO mouse models have revealed its roles in diseases like hepatic steatosis, insulin resistance, and inflammation-related liver diseases, providing insights into potential therapeutic strategies targeting GPAT3 for these conditions.