Posted by: 4pack | October 5, 2008

The “Bigger” Picture On “Obesity”: Overeating Triggers Brain Response To Eat More

WE OFFER REASONS AT FOUR PACKS…NOT CHOICES…GIVING YOUR BODY AND BRAIN CHOICES IS NOW BEING SHOWN TO BE THE ASTROPHYSICAL EQUIVALENT OF A BLACK HOLE…WHEN YOU OVEREAT THE BRAIN MAY BE HIT WITH “METABOLIC INFLAMMATION”…CAUSING MORE CRAVINGS TO EAT MORE…A TRULY VICIOUS CYCLE…THIS IS NOT AN EXCUSE FOR OGGIES…JUST MORE PROOF THAT YOU HAVE TO COMPLETE THE SEEMINGLY DIFFICULT TASK OF MAINTAINING DAILY CALORIC INTAKE TO UNDER 2,000 CALORIES WHILE EATING THE RIGHT FOODS….READ EXCERPTS BELOW:

 

 

“Overeating triggers a metabolic response in the hypothalamus region of the brain which prompts people to eat even more, contributing to increased levels of caloric consumption, new research shows.

The new study, published in the journal Cell, examines the pathways that contribute to obesity. The researchers at the University of Wisconsin-Madison and the University of California, San Diego, investigated “metabolic inflammation,” a chronic, low-level condition often seen in obesity related diseases.

The research focused on the “master switch” of inflammation, called IKKbeta/NF kappa B that is usually turned off. When they fed mice a high-fat diet, it became active. When it was switched on in the hypothalamus of mice on a high-fat diet, the body ignored signals from leptin, a hormone that normally helps regulate appetite, and insulin, which helps convert food into energy.

Then the scientists used genetic engineering to flip that master switch off in the hypothalamus of other mice. In mice genetically altered to block the pathway, even with a high fat diet available, they were able to maintain a healthy weight. They were “significantly protected” from becoming obese, the researchers wrote.

Stimulating the protein complex, called IKKbeta/NK-kappaB, made the mice eat more, while suppressing it made them eat less.

“Persistent stimuli from excessive amount of calories can trigger this response before the overt onset of obesity, and this response when induced can promote overeating, contributing to increased levels of caloric overconsumption,” said Dr. Dongsheng Cai, senior author of the study. He said this process can be like a vicious cycle.

The “pathway” is normally associated with the immune system, and inflammation, one of the body’s defence systems. While in the past scientists believed the protein connected to inflammatory reactions used to help the body fight infection, it now appears to promote obesity. Suppressing that pathway might be a new strategy in the battle with obesity and related diseases. Dr Dongsheng Cai said that that the pathway could possibly be used in anti-obesity drugs. However, researchers warned that the pathway identified as a crucial player in this process could interfere with the body’s immune system because inflammation is one of the body’s weapons for fighting infection.

The findings add another element on the list of factors that predispose children and adults to obesity. A recent study showed that a brain chemical, known as BDNF (brain derived neurotrophic factor), plays a crucial role in regulating the quantity of food that people eat and their chances of becoming obese. The brain chemical is believed to work in a combination with other substances, including the hormone leptin, that regulate appetite and body weight. It appears that leptine indirectly triggers the release of BDNF in the hypothalamus, the part of the brain which helps to control body temperature and plays a role in controlling eating. “

 http://www.efluxmedia.com/news_Obesity_And_The_Brain_Switch_In_Brain_Triggers_the_Vicious_Cycle_of_Overeating_25687.html
 

 

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  1. […] The ?Bigger? Picture On ?Obesity?: Overeating Triggers Brain … By 4pack The new study, published in the journal Cell, examines the pathways that contribute to obesity. The researchers at the University of Wisconsin-Madison and the University of California, San Diego, investigated ?metabolic inflammation,? a … Four Packs For Oggies – https://4pack.wordpress.com […]


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