Figure 7.

Schematic diagram of the molecular pathways activated in adipocytes upon limited nutrient delivery. Ageing is associated with reduced vascularization of visceral AT. Resident adipocytes suffer from limited nutrient delivery and metabolically adapt to this condition to prevent energetic catastrophe. Upon nutrient starvation ATGL upregulation is crucial in preventing adipocytes death and AT inflammation via the increase of mitochondrial lipid oxidation. ROS produced by mitochondrial proline oxidase are the upstream mediators of the FoxO1-dependent ATGL expression. ATGL represents a stress resistance mediator in adipocytes, restraining AT dysfunction typical of age-related metabolic disorders. AT, visceral adipose tissue; ATGL, adipose triglyceride lipase; CPT1b, carnitine palmitoyltransferase 1b; FoxO1, forkhead box protein O1; FoxO1RE, FoxO1-responsive element; OXPHOS, oxidative phosphorylation; pnpla2, patatin-like phospholipase domain containing 2; POX, proline oxidase; PRO, proline; P5C, pyrroline 5 carboxylate; ROS, reactive oxygen species; TG, triglycerides