(Tracey Watson) Anyone who’s ever gone on a diet knows that how delicious a piece of chocolate cake looks is directly proportionate to how long it’s been since you allowed yourself to have a slice. If not for that universal truth we’d all be slim and healthy, right? It almost feels like the second we decide to go on a diet we suddenly crave all the foods we’ve decided to restrict.
Related The Ultimate Guide to Intermittent Fasting
by Tracey Watson, October 8th, 2018
Interestingly, a recent study by Professor Kazuyoshi Ukena of Hiroshima University in Japan has confirmed that there is a protein that your body releases to regulate energy levels – a protein which makes you feel hungry as soon as you restrict your calorie intake – no matter how much willpower you have!
It really isn’t just about self-control …
Scientists have understood for some time that the hormone leptin reduces appetite, while another hormone – ghrelin – makes us want to eat more. These hormones then activate neurons in the area of the brain which controls body energy: the hypothalamus. Professor Ukena’s study indicates that this process is even more complicated than previously understood, however. His research has confirmed that a neuron-exciting protein called NPGL increases appetite during periods of fasting, and then decreases it when the body feels full. Basically, our bodies have been designed in an amazing way to regulate appetite so as to maintain our weight at a constant level. (Related: Appetite-suppressing bread with fiber, protein, dried fruit can reduce calorie intake between meals.)
Professor Ukena first became curious about how metabolism is regulated after observing that chickens grow larger irrespective of how much they are fed. After investigating and determining that these birds possess NPGL to regulate energy metabolism, the research team did further research and found that this molecule is present in all vertebrates, including humans.
To further investigate the role of NPGL in mammals, Professor Ukena’s team fed three groups of mice three different diets to see how what they ate affected their NPGL levels. The first group was given a low-calorie diet for one day, the second group was put on a high-fat diet for only five weeks, while the final group was fed a high-fat diet for a longer period of 13 weeks.
A press release by Hiroshima University explained the results:
The mice fed on a low calorie diet were found to experience an extreme increase in NPGL expression, while the 5-week high-fat-diet group saw a large decrease in NPGL expression.
Further analysis found that mice possess NPGL, and its associated neuron network, in the exact same locations of the brain as those regions already known to control appetite suppression and energy use.
Professor Ukena proposes that NPGL plays a vital role in these mechanisms – increasing appetite when energy levels fall and reducing appetite when an energy overload is detected – together, helping to keep us at a healthy and functioning weight, and more importantly alive!
The research team concluded that NPGL promotes appetite, working against hormones like leptin which suppress appetite. To confirm this hypothesis the team injected mice directly with NPGL and found that their appetites immediately increased dramatically. (Related: Appetite stimulating hormone decreases following gastric bypass surgery.)
Another interesting finding was the fact that the mice whose NPGL levels dropped dramatically after being on the five-week high fat diet, returned to normal after being fed the high fat diet for a longer period.
Professor Ukena hopes to undertake further studies into the interaction of previously known appetite mechanisms with NPGL. Clearly, we have much to learn about appetite, metabolism and body weight. And self-control really can only take us so far, so stop beating yourself up about that piece of cake you ate at lunchtime!
Discover tips to help you win the weight loss struggle at Slender.news.
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Source:
https://www.naturalnews.com/2018-10-08-new-research-looks-at-how-our-body-controls-appetite.html
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