| First Author | Kim ER | Year | 2017 |
| Journal | JCI Insight | Volume | 2 |
| Issue | 14 | PubMed ID | 28724789 |
| Mgi Jnum | J:288592 | Mgi Id | MGI:6407505 |
| Doi | 10.1172/jci.insight.93367 | Citation | Kim ER, et al. (2017) Red blood cell beta-adrenergic receptors contribute to diet-induced energy expenditure by increasing O2 supply. JCI Insight 2(14) |
| abstractText | Diet-induced obesity (DIO) represents the major cause for the current obesity epidemic, but the mechanism underlying DIO is unclear. beta-Adrenergic receptors (beta-ARs) play a major role in sympathetic nervous system-mediated (SNS-mediated) diet-induced energy expenditure (EE). Rbc express abundant beta-ARs; however, a potential role for rbc in DIO remains untested. Here, we demonstrated that high-fat, high-caloric diet (HFD) feeding increased both EE and blood O2 content, and the HFD-induced increases in blood O2 level and in body weight gain were negatively correlated. Deficiency of beta-ARs in rbc reduced glycolysis and ATP levels, diminished HFD-induced increases in both blood O2 content and EE, and resulted in DIO. Importantly, specific activation of cAMP signaling in rbc promoted HFD-induced EE and reduced HFD-induced tissue hypoxia independent of obesity. Both HFD and pharmacological activation cAMP signaling in rbc led to increased glycolysis and ATP levels. These results identify a previously unknown role for rbc beta-ARs in mediating the SNS action on HFD-induced EE by increasing O2 supply, and they demonstrate that HFD-induced EE is limited by blood O2 availability and can be augenmented by increased O2 supply. |
