Runners and walkers work out with dumbbells to strengthen their bones, but could strapping on a little bit of extra weight influence how much we eat?
A new study found that when obese mice were loaded down with artificial weights implanted inside their bellies, the rodents ate less and gained less fat.
The scientists postulate that specialized cells in weight-bearing bones called osteocytes act as an internal body weight sensor — a “gravitostat” that sends signals to the brain to eat less.
It might explain the “anti-obesity” effects of simply standing, they said. Sitting makes the brain think the body isn’t as heavy as it actually is. We eat more and gain more weight.
“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 study, published recently in the Proceedings of the National Academy of Sciences, was conducted in rodents, which, while useful models, aren’t miniature humans. The only known “homeostatic” regulator of fat mass — the hormone leptin, which controls appetite — was also discovered in mice 24 years ago. But it didn’t lead to the hoped for cure for obesity. Obese humans have proven stubbornly resistant to leptin.
“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 in 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 colleagues in Sweden asked a simple question: Does your actual body mass affect how much you eat and ultimately, how much you weigh?
For their experiments, 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 percent of the body weight.
When the extra loads 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 the miniature weights were removed, the mice gained more body weight and fat mass, suggesting the internal body weight sensor works in both directions, the team wrote.
The mechanism isn’t 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. When the team used genetic techniques to deplete the mice of osteocytes, the effect went away.
Quite simply, we have found support for the existence of internal bathroom scales
“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 jump to obesity? When people put on weight, why wouldn’t their bodies communicate that increased load to their brains, and lower their food intake?
Drucker’s guess is that the signalling system from the bones is defective in obesity “and that’s why simply carrying around more weight when you’re obese doesn’t automatically shut off your appetite.”
At least, that’s the hypothesis. “We first need to figure out what the signal is, and then we need to see if it’s functional or defective in obese people,” Drucker said.
If the research holds up in humans and if scientists discover what kind of “magical factor” the bone cells might be producing, theoretically it could lead to new treatments for obesity, Drucker said.
The international work fits with emerging evidence that the skeleton acts like an organ unto itself, regulating energy and glucose metabolism, blogged Dr. Arya Sharma, professor of medicine at the University of Alberta. It also offers a reasonable explanation, he said, “for the weight gain and change in fat mass seen with prolonged sedentariness (which literally takes the weight off the bone).”