| First Author | Martí-Pàmies Í | Year | 2020 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 319 |
| Issue | 2 | Pages | E363-E375 |
| PubMed ID | 32603262 | Mgi Jnum | J:296843 |
| Mgi Id | MGI:6469136 | Doi | 10.1152/ajpendo.00362.2019 |
| Citation | Marti-Pamies I, et al. (2020) Deficiency of bone morphogenetic protein-3b induces metabolic syndrome and increases adipogenesis. Am J Physiol Endocrinol Metab 319(2):E363-E375 |
| abstractText | Bone morphogenetic protein (BMP) receptor signaling is critical for the regulation of the endocrine system and cardiovascular structure and function. The objective of this study was to investigate whether Bmp3b, a glycoprotein synthetized and secreted by adipose tissue, is necessary to regulate glucose and lipid metabolism, adipogenesis, and cardiovascular remodeling. Over the course of 4 mo, Bmp3b-knockout (Bmp3b(-/-)) mice gained more weight than wild-type (WT) mice. The plasma levels of cholesterol and triglycerides were higher in Bmp3b(-/-) mice than in WT mice. Bmp3b(-/-) mice developed insulin resistance and glucose intolerance. The basal heart rate was higher in Bmp3b(-/-) mice than in WT mice, and echocardiography revealed eccentric remodeling in Bmp3b(-/-) mice. The expression of adipogenesis-related genes in white adipose tissue was higher in Bmp3b(-/-) mice than in WT control mice. In vitro studies showed that Bmp3b modulates the activity of the C/ebpalpha promoter, an effect mediated by Smad2/3. The results of this study suggest that Bmp3b is necessary for the maintenance of homeostasis in terms of age-related weight gain, glucose metabolism, and left ventricular (LV) remodeling and function. Interventions that increase the level or function of BMP3b may decrease cardiovascular risk and pathological cardiac remodeling. |
