This article discusses the results of an experiment involving a group of genetically engineered mice, which are on high fat diets. The findings were that these mice do not become obese – or overweight for that matter – but the researchers concluded that they are more susceptible to developing gallstones.
Gallstones are deposits of cholesterol or calcium salts that form in the bile (from the liver) or the gallbladder and are the result of high concentrations of these substances in the body. Normally, people who are obese or have diabetes tend to develop gallstones. The researchers involved in the experiment hypothesized that because these mice do not become obese, they are protected against gallstones. However, the results show that these mice were actually more susceptible to the problem.
The experiment went as follows:
Two groups of mice ate a high fat diet for two weeks. One group consisted of normal mice, the other were genetically engineered mice. The normal mice had a particular protein in their bodies called, “Liver Fatty Acid Binding Protein” (L-Fab protein). The genetically engineered mice lacked this protein. After two weeks the normal mice became obese and developed gallstones and the genetically engineered mice maintained their normal weight but still developed gallstones. The researchers concluded that not having the L - Fab protein would make an individual more susceptible to gallstones. Hang on, didn’t the normal mice develop gallstones as well?
What the scientists should have also tested were the two types of mice on a healthy diet. If the genetically engineered mice weren’t on a high fat diet, would they develop gallstones? It is very likely that neither groups of mice would develop gallstones or even become obese. Therefore, I don’t think that lacking the L-Fab protein is a factor causing gallstones. The real problem is the diet. Whether you are obese or not, if you consume excessive amounts of fat and “bad” cholesterol, then you will develop gallstones. It’s as simple as that.
The article did not mention what the L-Fab protein actually does to the body, so it’s difficult to make any judgment on how this protein has anything to do with gallstones or whether lacking this protein is the cause for not being obese. It could be interpreted that because it’s a fat binding protein, the high cholesterol and fat consumed are “bound” by these proteins to produce actual fat deposits in the body. Thus, having the L-fab protein could be a possible factor aiding in the cause for an individual’s obesity. This premise is supported by the fact that, on a high fat diet, the mice with this protein became obese but the mice lacking this protein maintained a normal weight.
The researchers insist that studying this protein in the mouse genome would offer clues to the genetic factors related to gallstones in humans. I think this offers a bigger clue into the genetics involved in obesity in humans. Do humans have the L-Fab protein? If we do have this protein (and if the premise that an individual was not obese due to lacking the L-Fab protein were true), wouldn’t it be beneficial if we removed this protein from our genome? If doing this were possible, the obesity rates would certainly go down. However the problem here lies in “personal discipline” (ethical problems are involved as well – but everybody’s aware of that already).
Knowing that you cannot become obese, could typically result in a person choosing not to eat healthy foods – after all, without the L –Fab protein, you can’t get fat after spending the day at McDonald’s. So if this were the case, then yes, individuals without the protein (who have poor diets) would still be susceptible to gallstones. We would be better off to leave our genome alone!
So if everyone just lived a healthy lifestyle it wouldn’t necessary to alter our DNA and we wouldn’t be obese or have gallstones either.
Reference:
Washington University School of Medicine (2009, May 13). Genetically Engineered Mice Don’t Get Obese, But Do Develop Gallstones. Science Daily. Retrieved May 20, 2009 from http://www.sciencedaily.com/releases/2009/05/090507094216.htm
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