By Jennifer Xu, Columnist
Published March 18, 2013
We’re caught in the midst of an obesity epidemic. One-third of American adults are considered overweight; another third is clinically obese. Michigan is frequently cited as one of the fattest states in the nation, with an adult obese population that teeters past the 30-percent mark. Obese people live shorter lifespans, and their quality of life is decreased by diseases such as diabetes, hypertension, stroke and cancer.
Exhortations to improve nutrition and increase physical activity have only made a dent in the underlying issue. As any dieter can tell you, it’s not so easy to shed the extra pounds once they’re packed tight on the belly. Try as we might to eat more greens and hit the treadmill, our bodies appear to have a tightly regulated set point: If we deviate from the norm, we just gain the weight back later.
What’s more, overly aggressive governmental efforts to curb the obesity problem have drawn ire from social activists. Advertisements depicting children loading shopping carts with processed foods were denounced as discriminatory and ineffective. “There is nothing that anyone is going to do or say that’s going to make fat people skinny tomorrow,” said Jezebel writer Lindy West.
But what if there was something we could do? What if the answer to the obesity epidemic lay in a Japanese asthma and canker sore drug from the 1980s?
Researchers at the University have found that the off-patent drug Amlexanox, originally developed as a topical paste for canker sores and a tablet for asthma by the Takeda Pharmaceutical Company in 1987, is effective in reducing fat deposits and type-2 diabetes in obese mice.
The study, headed by Alan Saltiel, the Mary Sue Coleman Director of the Life Sciences Institute, discovered that populations of genetically obese mice and mice on a high-fat diet lost significant amounts of weight after being treated with this Japanese asthma drug. The drug also caused obese mice to have improved glucose tolerance — a sign of decreased diabetic effects on their metabolism — and produced less fatty tissue in their livers.
Most significantly, the drug didn’t reduce the animals’ food intake. That’s right: the obese mice bulked down considerably — even while they continued to gorge themselves on food.
Why? The researchers think it has something to do with metabolism.
Though the Amlexanox-injected mice didn’t stop overeating, they were much more active than those not exposed. Normally, the fatter you are, the less you move, and if you restrict calories, you’re likely to move even less. That’s because our brains have a tricky way of regulating body weight: cut calories, and the body will respond by slowing down metabolism. It’s a key reason why it’s so difficult to lose weight even after diet restriction. But the Amlexanox-treated mice had metabolisms comparable to those mice of a much lower weight, dissipating the extra energy in their fat cells as heat.
Obviously, mice are not people, so researchers can’t draw strong conclusions about the drug’s effectiveness on obese patients. But the benefit of using Amlexanox is that we already know it’s safe — it’s been used in Japan to treat canker sores and asthma for the past 25 years. Researchers can begin clinical trials immediately, without the usual rigmarole involved in getting a drug approved for human studies.
The sequestration — a governmental cut that slashed National Institutes of Health’s $31-billion budget by $1.5 billion — couldn’t come at a more inopportune time. It’s frustrating to know that, though the pieces to combating the obesity epidemic are in front of us, the receptacle holding the money is perpetually shrinking.
Jennifer Xu can be reached at firstname.lastname@example.org.