HORTON HARVEY/CC BY 2.0 When a high-calorie diet is introduced, weight gain is particularly noticeable.
Obesity is a health issue that has been affecting growing numbers of Americans in recent years. While people generally believe that obesity is caused by eating and various lifestyle habits, researchers are working to pinpoint a gene that might be directly responsible for obesity.
The concept of genetically disposed obesity, otherwise known as fault-free obesity, has occupied the interests of a group of researches in the Research Triangle located in North Carolina.
Through studying mice, the group of researchers discovered that variations in a gene called ankyrin-B might be the reason obesity exists in many Americans.
Ankyrin-B is a gene that millions of Americans have, and certain variations of this gene cause fat cells to absorb glucose at an uncommonly rapid rate. This results in a significant size increase amongst fat cells, which is a phenomenon that is known to frequently induce obesity when combined with other stress factors such as a high-fat diet or a slowed-down metabolism.
Dr. G. Vann Bennett is currently a George Barth Geller Professor of Biochemistry at Duke University School of Medicine, and he is one of the senior authors of the ankyrin-B study.
Bennett discovered ankyrin-B more than three decades ago, and after extensive investigations he believes that this gene might have helped our ancestors store energy in times of famine.
“In current times, where food is plentiful, ankyrin-B variants could be fueling the obesity epidemic,” Bennett said in a press release.
In fact, it has been deduced that ankyrin-B functions like an anchor that attaches proteins to the internal cell membrane. It is present in essentially every tissue in the human body, and observed defects in ankyrin-B have often been correlated to a handful of diseases such as autism, diabetes and irregular heartbeat.
The functional implications of ankyrin-B were first discovered several years ago by two researchers in Bennett’s lab.
Jane Healey, an MD/PhD student at that time, noticed that mice with ankyrin-B mutations were fatter on average than their wildtype counterparts. To verify the observation, a postdoctoral fellow named Damaris Lorenzo carried out an experiment by isolating mice with various mutations in the targeted gene.
Healey and Lorenzo soon discovered that the mice quickly gained weight because their nutritional intake was converted into calories stored in fat tissues rather than burnt as energy in other tissues.
Although this discovery furthered the researchers’ insight into ankyrin-B’s functions, it still did not explain how the gene carried out these functions.
“There is this common belief in the field that much of obesity can be traced back to appetite and the appetite control centers that reside in the brain. But what if it isn’t all in our head?” Bennett said, according to Duke Today.
In an attempt to answer this question, Lorenzo and her group began to knockout the ankyrin-B gene in mice.
As expected these mice had fat cells that almost doubled in size and subsequently gained more weight than the other mice despite exercising a similar amount. Furthermore, the weight gain was especially noticeable as the mice aged or were introduced to a high-calorie diet.
From repeated experiments, Lorenzo’s team learned that mice can become obese without an increase in food consumption due to the underlying cellular mechanism of ankyrin-B. This could have significant clinical relevance because it could potentially help physicians identify high-risk individuals that are prone to obesity.
Before this goal can be reached, however, Bennett said that they must first find a way to confirm that the lab findings are consistent with trends within the general population.
The researchers’ study has been published in the most recent edition of the Proceedings of the National Academy of Sciences.
In the future, Bennett plans to study ankyrin-B variants in the population through assessing an individual’s family history, BMI index and rate of glucose metabolism.