This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
We’ve known for some time that leptin hormone deficiency leads to obesity. Your bodily fat releases leptin after you eat, which then travels in the blood stream to the brain to signal the end of hunger. It’s as if your fat cells were screaming “we’re too fat, stop eating!”. The neurons that respond to leptin in the blood are in the arcuate nucleus of the hypothalamus, a region of the brain that is well known for mediating homeostasis in the body, such as temperature, thirst, and even the need for hugs from mommy. So it’s no surprise that another energy regulating system resides in the hypothalamus: the system for hunger.
Viola Nördstrom and colleagues at the German Cancer Research Institute (and other institutes) in Germany, found a new pathway that causes these hypothalamic neurons to fail to signal satiety, even when the leptin levels are normal. Their report was published in PLoS Biology.
The researchers found that the molecular machine that produces a specific type of neuronal cellular membrane lipid, called glycosylceramide synthase, is critical for proper function of leptin receptors in arcuate nucleus neurons. The discovery opens a new potential therapeutic pathway to explore in the search for an obesity cure.
On supporting science journalism
If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.