| First Author | Zhou QL | Year | 2018 |
| Journal | Mol Cell Biol | Volume | 38 |
| Issue | 8 | PubMed ID | 29378832 |
| Mgi Jnum | J:284780 | Mgi Id | MGI:6391842 |
| Doi | 10.1128/MCB.00153-17 | Citation | Zhou QL, et al. (2018) Membrane Trafficking Protein CDP138 Regulates Fat Browning and Insulin Sensitivity through Controlling Catecholamine Release. Mol Cell Biol 38(8) |
| abstractText | CDP138 is a calcium- and lipid-binding protein that is involved in membrane trafficking. Here, we report that mice without CDP138 develop obesity under normal chow diet (NCD) or high-fat diet (HFD) conditions. CDP138(-/-) mice have lower energy expenditure, oxygen consumption, and body temperature than wild-type (WT) mice. CDP138 is exclusively expressed in adrenal medulla and is colocalized with tyrosine hydroxylase (TH), a marker of sympathetic nervous terminals, in the inguinal fat. Compared with WT controls, CDP138(-/-) mice had altered catecholamine levels in circulation, adrenal gland, and inguinal fat. Adrenergic signaling on cyclic AMP (cAMP) formation and hormone-sensitive lipase (HSL) phosphorylation induced by cold challenge but not by an exogenous beta3 adrenoceptor against CL316243 were decreased in adipose tissues of CDP138(-/-) mice. Cold-induced beige fat browning, fatty acid oxidation, thermogenesis, and related gene expression were reduced in CDP138(-/-) mice. CDP138(-/-) mice are also prone to HFD-induced insulin resistance, as assessed by Akt phosphorylation and glucose transport in skeletal muscles. Our data indicate that CDP138 is a regulator of stress response and plays a significant role in adipose tissue browning, energy balance, and insulin sensitivity through regulating catecholamine secretion from the sympathetic nervous terminals and adrenal gland. |
