Research Paper Volume 6, Issue 8 pp 690—704

Figure 6. Schematic model for increased survival and lifespan in hNAG-1 mice. Overexpression of hNAG-1 in female mice lowers serum levels of IGF-1 and insulin and thus reduces IGF-1/insulin (IIS)/mTOR signaling. Circulating hNAG-1 also increases lipolysis, thermogenesis, and metabolism in hNAG-1 mice [14], and reduces macrophage infiltration into WAT and reduces inflammation in hNAG-1 mice [15, 16]. hNAG-1 mice are thus resistant to obesity, have increased energy metabolism and increased insulin sensitivity, which leads to increased lifespan, and reduced age- or dietary-induced pathological lesions.