| First Author | Paeger L | Year | 2017 |
| Journal | Elife | Volume | 6 |
| PubMed ID | 28762947 | Mgi Jnum | J:257939 |
| Mgi Id | MGI:6141835 | Doi | 10.7554/eLife.25641 |
| Citation | Paeger L, et al. (2017) Energy imbalance alters Ca(2+) handling and excitability of POMC neurons. Elife 6:e25641 |
| abstractText | Satiety-signaling, pro-opiomelanocortin (POMC)-expressing neurons in the arcuate nucleus of the hypothalamus play a pivotal role in the regulation of energy homeostasis. Recent studies reported altered mitochondrial dynamics and decreased mitochondria- endoplasmic reticulum contacts in POMC neurons during diet-induced obesity. Since mitochondria play a crucial role in Ca(2+) signaling, we investigated whether obesity alters Ca(2+) handling of these neurons in mice. In diet-induced obesity, cellular Ca(2+) handling properties including mitochondrial Ca(2+) uptake capacity are impaired, and an increased resting level of free intracellular Ca(2+) is accompanied by a marked decrease in neuronal excitability. Experimentally increasing or decreasing intracellular Ca(2+) concentrations reproduced electrophysiological properties observed in diet-induced obesity. Taken together, we provide the first direct evidence for a diet-dependent deterioration of Ca(2+) homeostasis in POMC neurons during obesity development resulting in impaired function of these critical energy homeostasis-regulating neurons. |
