*2.3.2 VMH*

The VMH is known as the satiety center. Indeed, activation of VMH neurons expressing the transcription factor SF1 (steroidogenic factor 1) reduces food intake and increases energy expenditure in mice [33]. VMH neurons including some SF1 neurons express MC4R or MC3R, suggesting that NPY/AgRP neurons and POMC neurons in the ARC regulate VMH neurons. We recently showed that activation of SF1-expressing neurons in the VMH by DREADD (designer receptors exclusively activated by designer drugs) technology not only reduces food intake and increases energy expenditure but also increases glucose uptake in certain peripheral tissues including interscapular brown adipose tissue, skeletal muscle, and the heart [33]. We have also shown that leptin increases insulin sensitivity in peripheral tissues as well as glucose utilization by the whole body through the VMH [34, 35]. Furthermore, we revealed that the hypothalamic neuropeptide orexin activates VMH neurons and thereby increases both insulin sensitivity and glucose utilization in skeletal muscle, with the orexin-VMH system being activated by taste stimulation and feeding [36]. These observations suggest that the orexin-VMH system preferentially increases glucose uptake in skeletal muscle during feeding. However, the physiological role of VMH neurons remains elusive, with further investigation being necessary to explore their contribution to the regulation of whole-body energy metabolism.
