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We are usually used to attribute obesity to a simple reason: eating too much and exercising too little. But there is growing evidence that at least some of the weight gains that are harmful to modern humans are written in genes. A new study by the Research Triangle in the United States suggests that the variant gene ankyrin-B, carried by millions of Americans, may be the reason why these people are prone to getting fat.
The study, published in the November 13 issue of the Proceedings of the National Academy of Sciences, showed that genetic variation causes fat cells to absorb glucose faster than normal, more than doubling in size. Obesity is almost inevitable when the metabolism is aging or when eating a high-fat diet.
Vann Bennett, a senior author and professor of biochemistry at Duke University School of Medicine, said: "We call it obsessive obesity. We believe this gene may help our ancestors store energy during famine. In today's era, food is abundant. , the variation of the ankyrin-B gene will promote the prevalence of obesity."
Ankyrin-B mutant mice are fatter
Bennett discovered the ankyrin-B protein more than 30 years ago. This is the existence of every tissue in the body, acting as an anchor-like protein. It anchors important proteins within the cell membrane. Bennett and other researchers have linked the lack of ankyrin-B to a number of human diseases, including autism, muscular dystrophy, aging, diabetes, and irregular heartbeats.
A few years ago, a Ph.D. student, Jane Healey, who worked at Bennett's lab, found that mice with arrhythmia caused by mutations in the ankyrin-B gene were fatter than wild-type mice. To find out why, she created a mouse model that carries some common human genetic variants.
The ankyrin-B mutant mouse on the right is fatter than the wild-type mouse on the left.
Dr. Damaris Lorenzo, a postdoctoral researcher at the lab, found that the mice quickly gained weight, locking most of their energy into adipose tissue rather than sending them to other tissues for consumption. These findings were published in the Journal of Clinical Investigation in 2015. But at the time I didn't know how this gene worked.
ankyrin-B is the gate of glucose inflow
To investigate this issue, Lorenzo's team, now an assistant professor at the University of North Carolina at Chapel Hill, completely knocked out the akyrin-B gene in mouse adipose tissue.
In this mouse, they repeated many of the same experiments that had been done before. Although the knockout mice had the same diet and exercise as normal mice, their body weight increased and the white fat cell volume doubled. More importantly, weight gain is more pronounced as the aging of the mice and the increase in the high-fat diet increase.
Lorenzo said: "We quickly observed that the increase in lipid accumulation in fat cells spilled over into the liver and muscles. This led to inflammation and disruption of insulin response, a feature of type 2 diabetes. A similar series of events would also It happens to humans, which is why obesity can have such a negative impact on our health."
According to the results of biochemical experiments: knocking out the ankyrin-B gene or mutation of the gene changes the kinetics of GLUT4, a protein that allows glucose to enter fat cells. As a result, the flood gate is opened, which allows glucose to flow into the cell faster than normal.
Mouse results need to be verified in the population
Lorenzo wondered if the same mechanism applies to the human genetic variant ankyrin-B. Ankyrin-B carries 1.3% in American whites and 8.4% in African Americans, and millions in the United States. Lorenzo cultured adipocytes carrying these variants and found that they also absorbed glucose at a higher rate. The disease seems to originate in adipose tissue, although it may work in other parts of the body.
Bennett said: "We found that mice become obese without eating more, and there is a potential cellular mechanism to explain weight gain. This gene allows us to identify individuals at risk who should observe them frequently. How much heat is added and exercise to control their weight."
But first, Bennett said their findings in the lab must be confirmed in the general population. To do this, researchers need to identify individuals with ankyrin-B mutations and explore family history, height and weight, and physiological traits of glucose metabolism to determine the effects of these variations on human health.
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