Biological weigh scales could be in our bones
Researchers call it ‘gravitostat’
It may sound like a kitchen gadget but researchers say they have discovered a “gravitostat,” a kind of biological bathroom scale meant to keep weight and fat mass constant.
When miniature weights were implanted inside the bellies of mice the rodents ate less and gained less fat.
The scientists postulate that cells in weight- bearing bones in our skeletons called osteocytes produce a protein that may signal the brain to stop eating — cells that may somehow be defective in people with obesity.
“Quite simply, we have found support for the existence of internal bathroom scales,” co-author John- Olov Jansson, of the University of Gothenburg, said in a release with the study.
“The weight of the body is registered in the lower extremities. If the body weight tends to increase, a signal is sent to the brain to decrease food intake and keep the body weight constant.”
The finding may explain why too much sitting can make us fat, even if we exercise regularly. One theory is that the internal scales "give an inaccurately low measure when you sit down,” said coauthor Claes Ohlsson. “As a result you eat more and gain weight.”
The study, published recently in the Proceedings of the National Academy of Sciences, was conducted in rodents, and while mice are useful models they aren’t t i ny humans. The only known “homeostatic” regulator of fat mass — leptin — was also discovered in mice 24 years ago, and it hasn’t proven the holy grail of antiobesity treatments despite the initial hype.
“As much as we’d love to advise people to strap on some extra weights and off you go — you’ll be less hungry and you’ ll lose weight — we have no idea whether or not this would carry over into humans,” cautioned Dr. Daniel Drucker, of the Lunenfeld-Tanenbaum Research Institute i n Toronto and whose lab provided some of the mice for the “gravitosat” work.
“But it does make a little bit of sense that we should have multiple ways that we sense how much we weigh and regulate that.”
Drucker said his Swedish colleagues set out to ask: Does how much we carry around affect how much we eat and, ultimately how much we weigh?
In a simple experiment, the researchers implanted capsules that weighed 15 per cent of the body weight into the abdomens of rats and mice. ( In humans, the equivalent would be implanting about a 10kg weight inside a 70- kg person.)
“Control” animals were implanted with an empty capsule of equal size, but weighing only three per cent of the body weight.
When t he extra l oads were added, body weight in both the rats and mice decreased. After two weeks, the total body weight ( biological body weight, plus the capsule weight) was similar in both groups of mice. The artificially loaded mice lost about as much weight as had been added. They ate less, and also saw a reduction in the amount of white adipose tissue — the “bad” fat that hoards calories.
When t he miniature weights were removed, the mice gained more body weight and fat mass, “demonstrating that the body weight sensor is functional in both directions,” the team wrote.
The mechanism isn’t at all clear. However, the findings held whether they tested normal mice, obese mice fed high- fat diets or mice lacking leptin, the hormone thought to suppress appetite.
“If we said to a bunch of scientists who study body weight and appetite today, ‘ did you know that your bone cells send a signal to your brain to control your appetite,’ the answer before this paper was published would be ‘no,’’ Drucker said.
But what explains the j ump to obesity? When people put on weight, why wouldn’t their bodies communicate that i ncreased load to their brains, and lower their food intake?
Drucker’s guess is that the signalling system from the bones misfires in obesi ty “and that’s why simply carrying around more weight when you’re obese doesn’t automatically shut off your appetite.”