By: Jean Johnson for Reflux1Obesity isn’t always a fast track to diabetes - and researchers think they may be figuring out why.
It all started in 1994 when researchers discovered a hormone that regulates appetite levels in mice and named it leptin. Since then, spurred by epidemic levels of obesity and overweight that in the United States doubled during the 1990s, researchers have initiated study after study aimed at plumbing the depths of leptin’s mysteries.
The results of the current study from the University of Michigan and the Joslin Diabetes Center suggest that leptin could become a household word for obese patients hoping to stave off adult onset or Type 2 diabetes.
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Basically the news is that leptin is not the type of hormone to just plod idly down a single well-worn trail toward the brain. Indeed, leptin’s a regular multi-tasker according to Martin G. Myers, Jr., MD, Ph.D. and Sarah H. Bates, Ph.D, the senior and lead authors on the paper, respectively. Not only does leptin let the brain know when nutrient levels are adequate, it also communicates on the subject with the liver.
Studies since 1994 have already shown that interference in lepton’s communication with the brain leads to obesity. So what the researchers did on this latest go-round was study obese mice in which they had disabled this pathway.
What they found was that only some of the fat mice got diabetes. When the medical science folks went looking for the reason, they discovered leptin’s second byway - its winding trail to the liver. Only in obese mice with diabetes was this pathway disabled.
“The blood sugar of the s/s mice [with specific brain pathways disrupted only] was high, but it was much more in control than mice that had no leptin receptors at all, and was not because of difference in their insulin production,” Myers said. “And when the s/s mice were put on calorie-restricted diets, their blood sugar normalized. These findings suggest that since the leptin-STAT3 [pathway that leads to the brain] signal was disrupted; some other signal must have been keeping glucose in check.”
“The classic thinking was that two things underlie Type 2 diabetes - how fat you are and how much insulin you can make. It is now clear that leptin and the brain also play an important role in this obesity-diabetes link. Going forward,” said Myers, “we need to define more about this new third player.”
The idea that there’s a third player doesn’t surprise Mary Castillo of Portland, Oregon. “I knew something had to be going on, because like the rest of the family, I’ve had a weight problem all my life, and I’m 85,” Castillo said. “None of us have ever had even the slightest suggestion of diabetes, despite our love of those good old Iowa Sunday suppers back when we were kids in the Midwest.”
Conversely, Lois Sampson of Portland who has less than 30 percent body fat and thus is not technically considered obese, developed diabetes in her 50s. “I guess I’m a little heavy,” she said. “But I’m certainly not as big as many of my friends who don’t have diabetes.”
Whatever the relationship between excess poundage and diabetes, the experts are concerned enough about not only the connection but also sky-rocketing rates, that some have coined a new term: diabesity. If researchers have their way, though, they’ll soon understand even more about leptin, and thus at the very least be able to explain to Americans who can’t stay away from the groceries just how it is that our bodies react to our behavior.
