| Literature DB >> 36166181 |
Guoqing Tang1, Chengxin Ma1, Liangkui Li2, Shaoyan Zhang1, Fengsheng Li1, Jin Wu1, Yesheng Yin1, Qing Zhu1, Yan Liang1, Ru Wang3, He Huang1, Tong-Jin Zhao1,4, Hongyuan Yang5, Peng Li1,2,4, Feng-Jung Chen6,7.
Abstract
Brown adipose tissue (BAT) plays an essential role in non-shivering thermogenesis. The phosphatidylinositol transfer protein, cytoplasmic 1 (PITPNC1) is identified as a lipid transporter that reciprocally transfers phospholipids between intracellular membrane structures. However, the physiological significance of PITPNC1 and its regulatory mechanism remain unclear. Here, we demonstrate that PITPNC1 is a key player in thermogenesis of BAT. While Pitpnc1-/- mice do not differ with wildtype mice in body weight and insulin sensitivity on either chow or high-fat diet, they develop hypothermia when subjected to acute cold exposure at 4°C. The Pitpnc1-/- brown adipocytes exhibit defective β-oxidation and abnormal thermogenesis-related metabolism pathways in mitochondria. The deficiency of lipid mobilization in Pitpnc1-/- brown adipocytes might be the result of excessive accumulation of phosphatidylcholine and a reduction of phosphatidic acid. Our findings have uncovered significant roles of PITPNC1 in mitochondrial phospholipid homeostasis and BAT thermogenesis.Entities:
Keywords: PITPNC1; acute cold exposure; lipid homeostasis; thermogenesis; β-oxidation
Year: 2022 PMID: 36166181 DOI: 10.1007/s11427-022-2157-y
Source DB: PubMed Journal: Sci China Life Sci ISSN: 1674-7305 Impact factor: 10.372