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  #1   ^
Old Mon, Nov-20-17, 08:23
teaser's Avatar
teaser teaser is offline
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Default Gene prompts fat cells to take in more glucose, fueling obesity

Quote:
Obesity is often attributed to a simple equation: People are eating too much and exercising too little. But evidence is growing that at least some of the weight gain that plagues modern humans is predetermined.

New research from the Research Triangle suggests that variants in a gene called ankyrin-B -- carried by millions of Americans -- could cause people to put on pounds through no fault of their own.

The study, which was conducted in mice, shows that the gene variation causes fat cells to suck up glucose faster than normal, more than doubling their size. When an aging metabolism or high-fat diet is added to the equation, obesity becomes all but inevitable.

"We call it fault-free obesity," said Vann Bennett, M.D., Ph.D., senior author of the study and George Barth Geller Professor of Biochemistry at Duke University School of Medicine.

"We believe 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."

The results appear the week of November 13 in the Proceedings of the National Academy of Sciences.

Bennett discovered the protein ankyrin-B more than thirty years ago. It is present in every bodily tissue and acts like an anchor by tethering important proteins to the inside of the cell's membrane. Bennett and other researchers have linked defects in ankyrin-B to a number of human diseases, including autism, muscular dystrophy, aging, diabetes and irregular heartbeat.

Several years ago, Jane Healey, an MD/PhD student working in the Bennett laboratory, noticed that mice with cardiac arrhythmia caused by mutations in ankyrin-B were fatter than their wildtype litter mates. To figure out why, she created mouse models that carried a couple of common human variants of the gene.

Damaris Lorenzo, Ph.D., a postdoctoral fellow in the lab at the time, found that these mice quickly grew fat, locking away most of their calories in fat tissue rather than sending them to other tissues to burn as energy. These findings were published in 2015 in the Journal of Clinical Investigation.

"The problem is, we still didn't know how this gene worked," said Bennett. "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?"

To study that question, Lorenzo, now an assistant professor of cell biology and physiology at the University of North Carolina at Chapel Hill, had her research group completely knock out the ankyrin-B gene in the fat tissue of mice.

They repeated many of the same experiments that had been conducted in the previous mouse models, which carried mutant versions of ankyrin-B throughout their bodies. Like before, the knock-out mice gained weight, and their energy-storing white fat cells doubled in size -- despite eating and exercising the same amount as normal mice. What's more, the weight gain increased as the mice aged or were fed a high-fat diet.

"We quickly learned that the increased accumulation of lipids in fat cells "spilled over" to the liver and muscles," Lorenzo said. "The abnormal accumulation of fat in these tissues led to inflammation and disruption of response to insulin, a hallmark of type II diabetes. A similar cascade of events is what often takes place in humans, and that is why obesity can be so detrimental to our health," Lorenzo said.

After conducting a number of biochemistry experiments, Lorenzo showed that eliminating or mutating ankyrin-B changed the dynamics of Glut4, the protein that allows glucose to enter fat cells. As a result, the flood gates were effectively opened, allowing glucose to flow into the cells more quickly than normal.

Lorenzo wondered if the same mechanism held true for other known human mutations of ankyrin-B. Variants in ankyrin-B are carried by 1.3% of Caucasians and 8.4% of African Americans, accounting for millions of people in the United States alone. Lorenzo cultured fat cells carrying these variants and found that they too sucked up glucose at a higher rate. The disease seems to originate in fat tissue, though it likely has effects elsewhere in the body.

"We found that mice can become obese without eating more, and that there is an underlying cellular mechanism to explain that weight gain," Bennett said. "This gene could enable us to identify at-risk individuals who should watch what kind of calories they eat and exercise more in order to keep their body weight under control."

But first, Bennett says their findings in the laboratory must be confirmed in the general population. To do so, the researchers will need to identify individuals with ankyrin-B variants, and then assess family histories, height and weight, and characteristic physiological traits as well as glucose metabolism, to determine the impact of these variants on human health.


Quote:
What's more, the weight gain increased as the mice aged or were fed a high-fat diet.



It's okay to call it a high-fat diet, everybody knows that unless specified otherwise, high-fat in research means high fat with a significant amount of carbohydrate. Without kicking them in the shins over that, it's more obvious than usual this time around that if what's making these animals fat is increased uptake of glucose by fat cells--and this makes for increased storage of dietary fat--then minimizing carbohydrate is something to look at.

https://www.sciencedaily.com/releas...71113153824.htm
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  #2   ^
Old Mon, Nov-20-17, 08:25
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teaser teaser is offline
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I used their headline, 'Gene prompts fat cells to take in more glucose, fueling obesity' might be better.
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  #3   ^
Old Mon, Nov-20-17, 10:11
Zei Zei is offline
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Quote:
Originally Posted by teaser
It's okay to call it a high-fat diet, everybody knows that unless specified otherwise, high-fat in research means high fat with a significant amount of carbohydrate. Without kicking them in the shins over that, it's more obvious than usual this time around that if what's making these animals fat is increased uptake of glucose by fat cells--and this makes for increased storage of dietary fat--then minimizing carbohydrate is something to look at.

Definitely. I hope if they do pursue this that research is also done in humans and not just restricted to laboratory mice, since the results could be quite different considering mice and humans thrive on very different diets; ratios of carbohydrate to fat, etc. Humans tend to do well with carbohydrate restriction and higher levels of fat than mice might be built to tolerate.
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  #4   ^
Old Mon, Nov-20-17, 10:43
teaser's Avatar
teaser teaser is offline
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Plan: ketosis/IF
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I agree mice are different, but I don't think studies really capture the difference. Wild mice not being subject to at least periods of high fat diet doesn't seem that likely to me. Give a mouse a high fat diet, and give it an enriched environment, which can mean as little as a running wheel, which the animals use voluntarily, can do a lot to reverse their supposed inability to tolerate a high fat diet. I think you have to assume that their natural environment is probably a bit more stimulating than just adding a running wheel to a cage. Throw in environment-induced meal-timing, natural light cycles, etc.

A drug that targets fat cell uptake of glucose would probably work, but also be diabetogenic unless combined with a safe diet.
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  #5   ^
Old Mon, Nov-20-17, 10:54
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doreen T doreen T is offline
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Quote:
Originally Posted by teaser
... 'Gene prompts fat cells to take in more glucose, fueling obesity' might be better.

Abracadabra POOF!

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  #6   ^
Old Mon, Nov-20-17, 11:28
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GRB5111 GRB5111 is offline
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Excellent information that requires further research and understanding how to deal with this genetic situation to achieve/ maintain health. Now we're all wondering whether we carry the ankyrin-B variant.
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  #7   ^
Old Mon, Nov-20-17, 14:59
khrussva's Avatar
khrussva khrussva is offline
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Plan: My own - < 30 net carbs
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I was fat before the food pyramid. Before fat made you fat. Before soda pop was a daily beverage. Before fast food and convenience stores came to town. Before high fructose corn syrup. I was fat raised on breast milk. I wore Sears "Husky" sized jeans from my earliest memory. I was the fat kid in class back when there was just one or two of us. I was predisposed to put on weight at a time when kids spent the entire summer outside playing. So I don't think I need to wonder if I have that ankyrin-B variant. It's as good of a reason as any to explain why I've had an issue with putting on excess fat my entire life. We ate eggs, meat, whole milk, fruit, veggies, bread and potatoes. We had our fair share of sweets, too. I ate normal food like everybody else. I could not eat a diet high in carbohydrates and be lean as those other kids (including my brothers).

I have an interesting memory from kindergarten... I overheard the teacher talking with some of the moms concerning what kind of snacks to bring for our Christmas celebration at school. Someone suggested frosted cupcakes and another adult nixed that idea saying that "the kids always get so hyper" with that kind of thing. I don't remember if I said it or just thought it, but what popped into my head was that "I don't get hyper when I eat cupcakes." And the truth is, I didn't. Some kids went burzerk when they ate sweets. I never did. I liked sweets. I wanted them. But I was never one of those kids who needed recess to burn off excess energy in order to settle down and learn. Maybe it was my fat cells sucking up all that glucose - leaving my muscles wanting. I was different than the other kids. There has to be a reasonable explanation. I think that I was pre-programed to put on weight from carbohydrates. I have no off switch when I eat carbs. Eating carbs makes me want to eat more... carbs. If no more carbs are available, then I'd just eat more of what ever was around. When I don't eat carbs I feel like I behave more like a normal person when it comes to food.

Quote:
"We call it fault-free obesity," said Vann Bennett, M.D., Ph.D., senior author of the study and George Barth Geller Professor of Biochemistry at Duke University School of Medicine.

I know that carb restriction solves much of my problem. I might be blameless if I didn't know better. But I know now. If I get obese again it is on me.

Last edited by khrussva : Mon, Nov-20-17 at 15:20.
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