| First Author | Ste Marie L | Year | 2005 |
| Journal | Obes Res | Volume | 13 |
| Issue | 9 | Pages | 1518-22 |
| PubMed ID | 16222052 | Mgi Jnum | J:114434 |
| Mgi Id | MGI:3688991 | Doi | 10.1038/oby.2005.185 |
| Citation | Ste Marie L, et al. (2005) Norepinephrine- and epinephrine-deficient mice gain weight normally on a high-fat diet. Obes Res 13(9):1518-22 |
| abstractText | OBJECTIVE: Signaling through adrenergic receptors (ARs) by norepinephrine (NE) and epinephrine (Epi) regulates weight gain when mice are fed a high-fat diet (HFD) by controlling diet-induced thermogenesis. Thus, one would predict that mice unable to make NE/Epi because of inactivation of the dopamine beta-hydroxylase gene (Dbh-null mice) would have a propensity to become obese. We characterized the response of Dbh-null and control mice to a HFD. RESEARCH METHODS AND PROCEDURES: Dbh-null and control mice were fed an HFD or a regular diet (RD) for 2 months. Body weight, adiposity, muscle triglyceride levels, and adipocyte size were measured, as were circulating leptin, adiponectin, triglyceride, glucose, and insulin levels. A glucose tolerance test was also preformed. RESULTS: Dbh-null mice gain weight normally on an HFD and have the same adiposity. Their serum triglyceride and leptin levels are normal, but adipocytes are approximately 30% smaller than controls. Dbh-null mice maintain low blood glucose levels and glucose tolerance when exposed to the HFD in contrast to controls. DISCUSSION: Complete lack of NE/Epi does not predispose to obesity. Because mice lacking all three betaARs become obese on an HFD, an imbalance of signaling through alpha- and betaARs seems to be responsible for obesity. Surprisingly, Dbh-null mice maintain glucose tolerance. |
