Thanks to copious amounts of cheezeburgers, there’s now too many obese people on Earth, mostly in developed countries. Since diet plans and working out in gyms doesn’t work for everyone, researchers at Johns Hopkins may have found a viable means of regulating food intake. A series of tests involving mice reveled that inhibiting a specific protein controls the mammals’ appetites, by doing this, the food intake is better controlled.
Here’s a highly technical summary of the experiment from Cell.com:
Hypothalamic neuropeptide Y (NPY) has been implicated in control of energy balance, but the physiological importance of NPY in the dorsomedial hypothalamus (DMH) remains unclear. Here we report that knockdown of NPY expression in the DMH by adeno-associated virus-mediated RNAi reduced fat depots in rats fed regular chow and ameliorated high-fat diet-induced hyperphagia and obesity. DMH NPY knockdown resulted in development of brown adipocytes in inguinal white adipose tissue through the sympathetic nervous system. This knockdown increased uncoupling protein 1 expression in both inguinal fat and interscapular brown adipose tissue (BAT). Consistent with the activation of BAT, DMH NPY knockdown increased energy expenditure and enhanced the thermogenic response to a cold environment. This knockdown also increased locomotor activity, improved glucose homeostasis, and enhanced insulin sensitivity. Together, these results demonstrate critical roles of DMH NPY in body weight regulation through affecting food intake, body adiposity, thermogenesis, energy expenditure, and physical activity.
What the above translates as in layman’s terms is the fattened mice who were injected with the virus had reactions that indicated the DMH NPY could have a positive effect on their diet.
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