New research has shown that modifications found in a gene called ankyrin-B embedded in millions of Americans, could add pounds to people’s bodies without their will.
Naturally, obesity is often blamed on a petty human behavior. People consume excessive portions of food but are too lazy to work out. However, there are factual proofs that are emerging which makes us know that at least not all weight gains are deliberate on the part of the affected people who are victimized by it.
The experiment was tried on mice, and the consequence showed that the gene variation generates fat cells and make them lick glucose quicker than usual, more than twice their normal size. The meaning of this outcome is that the addition of highly concentrated fat in diet or a declining metabolism causes obesity which cannot be avoided.
Vann Bennett, MD, Ph.D., senior author of the study and George Barth Geller Professor of Biochemistry at Duke University School of Medicine, explained in an interview that the nickname given to such occurrence is ‘fault-free obesity.’ He further expressed a belief that this gene might have been a good source of help to the ancient dwellers to stock up energy during famine. In modern times, he says, which has an abundant food supply, ankyrin-B variants could be accelerating obesity spread.
Bennett stumbled on the protein ankyrin-B over three decades ago. The gene lives in every physical tissue and serves as a host by restraining vital proteins from within the cell’s membrane. The researcher and his colleagues have identified flaws in ankyrin-B to a large number of human diseases such as muscular, dystrophy, autism, diabetes, aging and unstable heartbeat.
Many years ago, Jane Healey, an MD/Ph.D. student working in the Bennett laboratory, observed mice with cardiac arrhythmia brought about by mutations in ankyrin-B and realized that they had more fleshy mass than their wildtype litter contemporaries. To seek for a reason, she designed mouse imitations that have a couple of normal human variants of the gene.
A Ph.D. and postdoctoral fellow in the lab at the time, Damaris Lorenzo, Ph.D., saw that these mice were fattened quickly, with the majority of their calories concealed in fat tissue instead of transporting them to other tissues to be shed as energy. These reports were contained in a publication in 2015 as published in a clinical journal.
Bennett confessed that they are yet to discover the real workings of the gene. He further said that there is a common norm in the field that the source of most obesity can be tracked down to appetite and the appetite modification hinges on what lives in the brain. However, Bennett added, there is a possibility that it doesn’t live in our heads.
But this prediction can be examined. Lorenzo who is currently an assistant professor of cell biology and physiology in the UNC School of Medicine gathered her research team, and they eliminated the ankyrin-B gene in the fat tissue of mice with no traces.
They replicated most of the same trials that had been done with the mouse models in the past, which conveyed the mutant versions of ankyrin-B all over their bodies. As experienced in the past experiments, the mice whose ankyrin-B gene was eliminated, acquired weight, and their energy-saving white fat cells became twice in size in spite of eating and training the same amount as the ordinary mice. The weight gain skyrocketed as the mice grew older or ate a high-fat diet.
Bennett noted that mice can acquire excessive weight even with small amount of food and that a primary cellular mechanism can explain that weight storage. This gene, Bennett continued, could give us room to recognize people who are at risk and that they should be conscious of the kind of calories they eat. They should engage more in physical exercise to maintain their body weight.
But he quickly added that their findings in the research center must be ascertained among the general populace. To achieve this, they will need to recognize persons with ankyrin-B variants, and then study hereditary history in terms of height, weight, and characteristic physiological traits in addition to glucose metabolism, to discern the effect of these variants on the health aspects of human life.