Zc3h10 controls mitochondrial function during adipogenesis M. Audano1, S. Pedretti1, D. Caruso1, E. De Fabiani1 and N. Mitro1 1Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milano, Italy.
The rising incidence of obesity has become a major public health problem worldwide. Numerous studies have demonstrated that obesity is associated with raising of metabolic disorders such as hypertension, insulin resistance, diabetes and cardiovascular diseases. Brown (BAT) and white (WAT) adipose tissues are important organs involved in lipid homeostasis. Metabolic impairment due to mitochondrial dysfunction in BAT and WAT is tightly associated with alterations of adipose tissue development, metabolic disorders and obesity. Nevertheless, the molecular circuits linking mitochondrial biology and adipose tissue development still need to be fully understood. Using a functional high-throughput screening, we isolated the newly characterized mitochondrial regulator zinc finger CCCH-type containing 10 (Zc3h10). Our results indicate that Zc3h10 is a nuclear RNA binding protein (RBP) and that its expression increases during murine adipocyte differentiation. Further, Zc3h10 silencing in preadipocytes impairs mitochondrial function and alters metabolic profile in preadipocytes and decreases adipogenic potential in differentiated adipocytes. Taken together, these data help to better characterize the role of mitochondria during adipogenesis and annotate Zc3h10 as a novel regulator of mitochondrial function in adipocytes.
This work is supported by European Foundation for the Study of Diabetes (EFSD)/Lilly European Diabetes Research Programme 2015.
Credits: None available.
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