Role of fibrosis in human white adipose tissue expansion in obesity
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Elisa Giannetta | Tutor di riferimento |
Obesity has been declared the largest global chronic health problem in adults by World Health Organization, considering all the associated cardiovascular, orthopedic, reproductive and metabolic complications. It is nowadays clear that visceral adipose tissue accumulation is strictly related to metabolic complications. In recent years, new evidences in mouse models demonstrated that the correct expansion of adipose tissue is able to prevent metabolic complication even in obese animals. The main characteristics of this "healthy" adipose tissue accumulation are smaller and more abundant adipocytes, high blood vessels density, low fibrosis and high adiponectin synthesis. Studies on mouse models demonstrated that adipocyte precursor could differentiate into functional white adipocytes or into fibrogenic progenitors, not able to differentiate in mature adipocytes. Fibrogenic progenitors express collagen and PDGFRb, inducing fibrosis, produce inflammatory cytokines and promote macrophage infiltration and activation. The importance of increased fibrosis at the expend of functional adipogenesis in human white adipose tissue dysfunctional expansion has not been completely clarified.
The aim of this study is to evaluate, through real time PCR, the expression of a panel of genes involved in adipogenesis, lipid function and storage trough the synthesis of triglycerides and adipokines, inflammatory pathway and fibrogenesis in human visceral and subcutaneous adipose tissue specimens, already collected in the context of Chiasm study, comparing metabolically healthy obese and morbid obese patients.