Obesity and obesity-related pathologies (such as diabetes, cardiac ischaemia and stroke) represent an important health issue in developed countries. Fibrosis has a crucial role in adipose tissue dysfunction; thus, elucidating its underlying mechanisms could aid the identification of potential therapeutic targets for obesity. The enzymatic activity of lysyl oxidase (LOX) is required for tissue fibrosis and remodelling, but its involvement in adipose tissue dysfunction is still unclear. Here, Victoria Cachofeiro's and Cristina Rodríguez's groups tried to clarify this. They found an increase in LOX expression in tissue samples from morbidly obese individuals and they replicated this finding in obese rats fed a high-fat diet. Interestingly, in these animals the LOX inhibitor β-aminopropionitrile (BAPN) reduces adipose tissue fibrosis, counteracts the increase in body weight and fat mass, and normalises multiple metabolic parameters (including glucose, insulin and triglyceride levels). Moreover, BAPN ameliorates the obesity-related dysfunction of several proteins involved in the control of insulin sensitivity (such as adiponectin, glucose transporter 4 and suppressor of cytokine signalling 3) both in obese rats and in 3T3-L1 adipocytes, an in vitro model of insulin resistance. These results suggest that targeting LOX and tissue fibrosis is a promising strategy to treat adipose tissue dysfunction in obesity. Page 543

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