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Is there a ´healthy´ obesity gene?

View:93 Time:2012-Jun-01 13:03

The study, which will appear in a July issue of the Journal of Biological Chemistry, used genetically modified mice to investigate the genetic aspects of why some obese people do not develop certain medical problems typically associated with obesity, especially Type 2 diabetes.

 

Wu noted that Xin Guo, a Ph.D. candidate in the colleges department of nutrition and food sciences, contributed significantly to the study.

 

"Previous research had indicated that a regulatory enzyme which is encoded by the gene PFKFB3 protects against diet-induced fat tissue inflammation and systemic insulin resistance," said Wu, who also has a Texas AgriLife Research appointment. "Increasing evidence shows that fat deposition, or amount, is not directly associated with the inflammation or insulin resistance in the development of obesity-related metabolic diseases."

 

Wu said the inducible 6-phosphorofructo-2-kinase (iPFK2) enzyme links metabolic and inflammatory responses and may underlie what he refers to as "healthy" obesity.

 

"While many obese people develop Type 2 diabetes, heart conditions and other chronic health problems associated with being significantly overweight, other obese people do not," he said. "And while obesity in general is not healthy, some obese people do not develop the diseases more commonly associated with a less-than-healthy diet. Furthermore, a number of thinner people may have the sort of health problems more typically associated with obesity."

 

Wu said he and the other researchers theorized that these diseases are associated with the cellular inflammatory response brought on by obesity.

 

"We also thought this gene could conceivably be targeted for use in the treatment of diabetes, especially Type 2, commonly associated with obesity," he said. "We wanted to find out what might happen to a subject if that particular gene was activated."

 

Wu and his fellow researchers used laboratory mice to explore the effect of a targeted adipocyte overexpression of the gene/enzyme combination on diet-induced inflammatory responses and insulin sensitivity.

 

"We were trying to find out what it is in adipose, or fat, tissue that may trigger a negative response that leads to disease — and how to modulate that response," he said. "In our study, we learned overexpression of the iPFK2 enzyme increases fat deposition, suppresses inflammatory responses and improves insulin sensitivity in both adipose and live tissues."

 

The study, which will appear in a July issue of the Journal of Biological Chemistry, used genetically modified mice to investigate the genetic aspects of why some obese people do not develop certain medical problems typically associated with obesity, especially Type 2 diabetes.

 

Wu noted that Xin Guo, a Ph.D. candidate in the colleges department of nutrition and food sciences, contributed significantly to the study.

 

"Previous research had indicated that a regulatory enzyme which is encoded by the gene PFKFB3 protects against diet-induced fat tissue inflammation and systemic insulin resistance," said Wu, who also has a Texas AgriLife Research appointment. "Increasing evidence shows that fat deposition, or amount, is not directly associated with the inflammation or insulin resistance in the development of obesity-related metabolic diseases."

 

Wu said the inducible 6-phosphorofructo-2-kinase (iPFK2) enzyme links metabolic and inflammatory responses and may underlie what he refers to as "healthy" obesity.

 

"While many obese people develop Type 2 diabetes, heart conditions and other chronic health problems associated with being significantly overweight, other obese people do not," he said. "And while obesity in general is not healthy, some obese people do not develop the diseases more commonly associated with a less-than-healthy diet. Furthermore, a number of thinner people may have the sort of health problems more typically associated with obesity."

 

Wu said he and the other researchers theorized that these diseases are associated with the cellular inflammatory response brought on by obesity.

 

"We also thought this gene could conceivably be targeted for use in the treatment of diabetes, especially Type 2, commonly associated with obesity," he said. "We wanted to find out what might happen to a subject if that particular gene was activated."

 

Wu and his fellow researchers used laboratory mice to explore the effect of a targeted adipocyte overexpression of the gene/enzyme combination on diet-induced inflammatory responses and insulin sensitivity.

 

"We were trying to find out what it is in adipose, or fat, tissue that may trigger a negative response that leads to disease — and how to modulate that response," he said. "In our study, we learned overexpression of the iPFK2 enzyme increases fat deposition, suppresses inflammatory responses and improves insulin sensitivity in both adipose and live tissues."

 

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