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The "Skinny Gene": Mass Media v. Scientific Writing

Overview: Obesity and Its Causes

Obesity is defined to be a BMI of 30 (for example, a 5'9" male weighing more than 203 pounds) or greater and is a major health concern in the United States. In 2006, 33.3% of adult men and 35.5% of women were clinically obese. Additionally, in 2006 16.3% of adolescents between the ages of 2-19 were clinically obese (CDC). Compare thise with statistics from 1985 where in all states collecting data, less than 14% of the population was obese (National). Obesity comes with many health concerns, including hypertension, osteoarthritis, high cholesterol, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, sleep apnea, endometrial cancer, breast cancer, and colon cancer (CDC). The Centers for Disease Control maintain that contributors to body weight incude genes, metabolism, behavior, environment, culture, and socioeconomic status, but the two biggest areas of focus to change body weight are behavior and environment. In order to reach and maintain a healthy weight, one must be mindful of the caloric balance - calories consumed in food and beverages must be offset by bodily functions and physical activity. Actions people can take to create an environment conducive to a healthy lifestyle include reducing time watching television, making sure healthy food options are provided at every meal (especially in schools), creating more opportunities for physical activity at work and in one's everyday routines, and watching meal portions. According to the Human Obesity Gene Map, there are over 350 genes linked to human weight control (Bouchard). In my review, I am going to look at a recently characterized gene, adp, to see how it is presented in scientific research and in mass media.

Scientific Writing and Adp

In an article in September 2007's Cell Metabolism, Jae Su and colleagues published their research on Adipose, or Adp, in an article titled "Adipose Is a Conserved Dosage-Sensitive Antiobesity Gene". The authors cite many other previously discovered genes that may have some role in adipocyte formation. First, there are several transcriptional activators, like C/EBPs, PPARg, and SREBP. PPARg is a nuclear hormone repressor (NHR) that represses transcription by interacting with corepressor molecules in the absence of ligand. These corepressor molecules recruit chromatin modifying enzymes that can be genes that affect metabolism too, such as HDAC3, which deacetylates histones to make chromatin accessible to transcriptional activators. ADP functions in the nucleus by binding histones and HDAC3, which suggest that ADP is a transcriptional corepressor of adipocyte formation.

Image1 Image2

These images show the localization of ADP to the nucleus, indicated by the white arrow. The original pictures, in color, indicate that an ADP-GFP fusion is found primarily in the nucleus. (Suh 204. Permission Requested)

Suh and colleagues found that orthologs of the adp gene are found in C. elegans, Drosophila melanogaster, and Mus musculus, despite the fact that in invertebrates, fat is not stored in adipose cells as it is in mammals, but rather in multifunctional cells. Suh's work built off of Dr. Winifred Doane's hypothesis 50 years ago that environments marked by famine might select for efficient fat storage in D. melanogaster populations. The allele that codes for efficient fat storage is the mutant adp gene, which has a 23 base pair deletion. The wild type adp gene is found in thin flies, and has been conserved in the human population. Introducing wild type adp RNAi increases fat accumulation in C. elegans. Introducing the wild type ADP in fat cells returned adult mutant adp flies to a normal weight. Adp+/- flies had a fat biology intermediate of mutants and wild types, and survived a starvation assay intermediate of mutants and wild types, indicating that Adp has dosage-sensitive effects on fly fat storage. Similar experiments were repeated on wild type mice, mutant mice, and heterozygous mice with similar results: the heterozygous mice had an intermediate phenotype and wild type mice cells exposed to ADP RNAi increased fat storage within the cell. Interestingly, mice on a high-fat diet or with genetic obesity (coded by other genes, not Aadp) had significantly lower levels of Adp expression, while mice who fasted expressed much higher levels of ADP, suggesting that to some extent, the environment can control ADP expression. Noticeably, the majority of Adp homozygous mutant mice that the authors attempted to generate died in utero. The authors could not conclude the cause of lethality.


In these images, the fly species labelled control are the adp mutants, and Adp fat tg species are under transgenic ADP expression, and are normal sized. (Suh 197. Permission Requested)

Obviously, the authors make a strong relationship between the adp gene and obesity using RNAi technology, starvation assays, and fluorescence assays; but are quick to point out the various other factors that contribute to weight, including diet and multitudes of other genes.

Mass Media and the Miraculous Skinny Gene

In an article posted on October 1st, 2007, MSNBC heralded the solution to America's obesity problem: the 'skinny gene'. It describes a gene found in a small subset of the situation: literally, small people who eat a lot, do not exercise, yet remain thin for some indescribable reason. MSNBC correspondant Linda Carroll begins with a description of a woman who seems to have the skinny gene and a daughter who is also naturally thin. The woman assumed that her daughter's thinness was due to hereditary. The article then segues into the world of science, saying that she may have been correct in thinking that her thinness was passed on to her daughter, and the gene of note controls fat formation. Carroll's article interviews Jonathan Graff, the senior author of the paper, who said that his lab built their research after Winifred Doane's forgotten discovery 50 years earlier of a gene she termed "adipose". Carroll gives a basic description of how the gene works, a famine study on fruit flies that the lab performed, a gene deletion study in worms, and a test tube experiment. MSNBC also interviews other scientists for their input about the importance of Suh's find. The article concludes by pointing out that mice engineered with efficient copies of the skinny gene have 1/3 the body fat of normal mice, which is approximately the difference between a normal woman and a supermodel.

The first critical question we must ask about this article is if the reporter did a sufficient job translating the scientific jargon to layman's terms (Kua 319). The article correctly states that the 'skinny gene' is actually a gene that controls adipose tissue formation, originally discovered in fruit flies by Winifred Doane more than 50 years ago. Doane noticed that fruit flies with two good copies of the gene are extremely thin, flies with two bad copies of the gene are fat, and those with one good and one bad copy are of a medium weight - which translates the dosage-sensitive nature of adp into layman's terms. The article touches on the use of RNAi technology when it notes that the scientists who discovered it this time around deleted the gene from worms to make them fat, but does not actually use the phrase "RNA interference", which is important scientific technology that would help put the article in context. The article also talks about knockout mice without actually using the word "knockout", which is once again an important scientific methodology that deserves mention. Carroll seems to put little faith in her lay audience and oversimplifies a lot of the scientific terminology, which in turn unfortunately leaves out any serious discussion of the methods used.

The article covers most of the tests Suh's lab did that eventually built enough of a foundation to classify the adp gene - RNAi interference in worms, dosage-sensitivity in flies, knockout mice, and heterozygous mice, but it glosses over others. Noticeably missing are the studies that show that ADP funtions in the nucleus by binding histones - important information for understanding how ADP actually works. Carroll does not talk about transcription factors or previous obesity-related genes that are also transcription factors. This brings us to the second critical question we must ask about scientific reporting: does the reporter put the findings in the context of other discoveries in the field (Kua 320)? Carroll does mention Winifred Doane's work 50 years ago on the same gene, but that is the extent of her coverage of past research. Some other 'obesity experts' are interviewed for the article - Dr. Louis Aronne, a clinical professor of medicine at the Comprehensive Weight Control Program and Eric Ravussin, a professor at the Pennington Biomedical Research Center. Aronne suggests that an obesity treatment could be made that mimics what the adp genes does. Ravussin says that a next step scientifically could include looking at this gene in populations predisposed for obesity, and cautions that the side effects of any possible medicine would have to be carefully researched. The two given interviews and single citation of a past finding leave much to desire. Perhaps more explanation about the potential medication would be helpful, or any mention of the numerous other genes that have already been linked to obesity would put Suh's findings in better perspective. A lay reader, after seeing this article, would think that obesity follows Mendelian inheritance, albeit with a separate heterzygous phenotype. Simply put, this article fails to put Suh's findings in the context of the greater scientific community.

A final question one should ask when reading a report on a scientific finding is if the article would allow the reader to think critically about the research being presented (Kua 320). This can be done by the author presenting a good explanation of the science and the long-term consequences of the research. Carroll, as mentioned previously, does mention most of the tests the scientists performed to reach their conclusions that adipose is a dosage-sensitive controller of obesity, but that fact that Carroll left out its biological functionality as a transcription factor in the nucleus and does not go into much detail about the methods she does mention can hardly be called a thorough explanation of the science. The end of MSNBC's article is very cautionary about the future of obesity research, the last line warning the reader that we are far away from a pill to cure obesity. The end of the article does offer two "next-step" options for obesity researchers: looking at the prevalence of the gene in obese populations, and trying to come up with a treatment that mimics the effects of the gene. While the ending of the piece is hopeful, it does include a dose of reality, which strengthens the entire article. Carroll's closing paragraphs do give readers a long-term picture of the consequence of Suh's research: it might be a while until the cure for obesity is as simple as a pill, and in the meantime we should not sit around and wait for science to hand it to us.

Works Cited

Bouchard, Claude. 2005. Human Obesity Gene Map Database. . Accessed 2008 Sept 9.

Carroll, Linda. 2007 Oct 1. Scientists discover 'skinny' gene. MSNBC. . Accessed 2008 Sept 9.

[CDC] Centers for Disease Control and Prevention. 2008. Overweight and Obesity. . Accessed 2008 Sept 9.

Kua, E, Reder M, and Grossel MJ. 2004. Science in the news: A study of reporting genomics. Public Understanding of Science 13(309-322). . Accessed 2008 Setp. 13.

National Office of Public Health Genomics. 2007 Nov 27. Obesity and Genetics: A Public Health Perspective. . Accessed 2008 Sept 9.

Suh, JM, Zeve D, McKay R, Seo J, Salo Z, Li R, Wang M, and Graff JM. 2007. Adipose is a Conserved Dosage-Sensitive Antiobesity Gene. Cell Metabolism 6(195-207). . Accessed 2008 Sept 5.

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