A team of scientists from the Genomics Research Centre, Academia Sinica demonstrated the enzymatic activity of Naa10p on fat tissue.
Diet-induced obesity (DIO) is a serious public health issue worldwide, increasing the risk of various chronic diseases such as Type 2 Diabetes, cardiovascular disease, stroke, and some cancers.
In a study published in the Journal Mol Cell by a team led by Dr. Li-Jung Juan of the Genomics Research Centre, Academia Sinica showed that the mammalian N-α-acetyltransferase 10 protein (Naa10p) enzyme activity may provide a potential strategy for treating obesity.
Naa10p physiologically functions in the early development of an infant. Mutations in human Naa10p have been associated with severe developmental defects including Ogden syndrome where patients typically rarely survive beyond the age of one and a half years.
The study reports that inactivation of Naa10p gene in mice prevents high fat diet-induced obesity, promotes formation of beige fats, and increases energy expenditure and thermogenesis. Specifically switching off adipose Naa10p gene further confirmed the role Naa10p in preventing formation of fat.
In their experiments, the adipose-specific Naa10p gene deactivated in adult mice not only shows no signs of developmental defects, but also has no symptoms of diet-induced obesity. Inhibiting Naa10p enzymatic activity in adult adipose tissues might just be a potential new cure for obesity.
The study was primarily corresponded by Dr. Li-Jung Juan. Most experiments were carried out by the first and co-corresponding author Dr. Chen-Cheng Lee, an Academia Sinica Postdoctoral Scholar at Juan Lab, with critical help from Yi-Chun Shih, Ming-Lun Kang and Ramanan Devaraj from the same lab. Collaborators include Dr. Yi-Cheng Chang and Lee-Ming Chuang from Department of Internal Medicine, National Taiwan University Hospital. [APBN]