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. 2019 Sep 19;10(4):237–244. doi: 10.1007/s13340-019-00409-6

Fig. 2.

Fig. 2

Scheme illustrating the mechanisms by which a typical AdipoR agonist increases insulin sensitivity and glucose tolerance leading to healthy longevity. In the liver, AdipoRon is shown to suppress the expression of genes involved in gluconeogenesis, increase fatty acid oxidation, and reduce oxidative stress and inflammation [18]. In the muscle, a typical AdipoR agonists is assumed to increase mitochondrial biogenesis leading to increased exercise endurance, while at the same time increasing the levels of expression of genes involved in fatty acid combustion, oxidative phosphorylation, and oxidative stress reduction [18]. In white adipose tissue (WAT), AdipoRon is shown to reduce oxidative stress and inflammation as well as inhibit the accumulation of M1 macrophages. Enhanced activation of the AdipoR pathways is assumed to improve insulin resistance and normalize lipid metabolism [18]. Drugs targeted at the AdipoR pathways may have beneficial effects on obesity-linked diseases and healthy longevity