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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.

Energy imbalance alters Ca 2+ handling and excitability of POMC neurons