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A High Fat, High Sugar Diet Activates Weight-Gain Genes
March 3, 2010
It is not simply a matter of the extra calories in and of themselves. Excessive caloric intake turns on gene signals that actively promote the storage of calories as fat. If those gene signals are repetitively activated and conditioned to stay on, you are in real metabolic trouble. A new study in the FASEB journal is part of an emerging body of science showing how improper food consumption sets gene-related metabolic signaling1 that cripples healthy metabolism.
Researchers conducted tests in two groups of mice on the brain's opioid receptors involved with pleasure signaling and metabolism. One group had the kappa opioid receptor genetically deactivated ("knocked out") and the other group was normal. Both groups were given a high fat, high sucrose, energy dense diet for 16 weeks. While the control group of mice gained significant weight and fat mass on this diet, the mice with the deactivated receptor remained lean.
According to Traci Ann Czyzyk-Morgan, one of the researchers involved in the work, "the data presented here support the hypothesis that overactivation of kappa opioid receptors contribute to the development of obesity specifically during prolonged consumption of high-fat, calorically dense diets."
One of the great problems facing overweight Americans is that for every mechanism we have to activate fat burning and promote weight loss are a dozen mechanisms to promote weight gain. This was useful during evolution as food scarcity was a primary threat to survival. Ironically, we are now killing ourselves by eating too much.
This research helps make the point that individuals who struggle with weight loss efforts despite eating well and exercising are likely to have genes set wrong. These gene settings are not necessarily permanent, but if a person is to get over the problem and reset nerve-related gene settings they will also need to get more energy into their brain and restore synaptic plasticity in nerve function.
Researchers conducted tests in two groups of mice on the brain's opioid receptors involved with pleasure signaling and metabolism. One group had the kappa opioid receptor genetically deactivated ("knocked out") and the other group was normal. Both groups were given a high fat, high sucrose, energy dense diet for 16 weeks. While the control group of mice gained significant weight and fat mass on this diet, the mice with the deactivated receptor remained lean.
According to Traci Ann Czyzyk-Morgan, one of the researchers involved in the work, "the data presented here support the hypothesis that overactivation of kappa opioid receptors contribute to the development of obesity specifically during prolonged consumption of high-fat, calorically dense diets."
One of the great problems facing overweight Americans is that for every mechanism we have to activate fat burning and promote weight loss are a dozen mechanisms to promote weight gain. This was useful during evolution as food scarcity was a primary threat to survival. Ironically, we are now killing ourselves by eating too much.
This research helps make the point that individuals who struggle with weight loss efforts despite eating well and exercising are likely to have genes set wrong. These gene settings are not necessarily permanent, but if a person is to get over the problem and reset nerve-related gene settings they will also need to get more energy into their brain and restore synaptic plasticity in nerve function.
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