Leptin Takes Its Lumps

Ever wonder why our stomachs aren’t bottomless pits? Or why we wind up feeling “full” when our appetites have been sated?

It’s largely due to a protein in our bodies that all of us have called leptin. Leptin is a protein hormone that has a variety of functions, including, but not limited to, helping the body maintain weight by signaling to the brain when it’s full, regulating the body’s metabolic rate, helping the body burn fatty tissue and regulating energy intake and expenditure.

Not surprisingly, the relative strength of leptin varies from person to person, partially explaining why some of us have larger appetites than others, and why some don’t put on a pound despite a ravenous appetite, while others’ weight control requires strict eating and regular exercise.

What explains this discrepancy of leptin levels? There’s no one answer to that question, but a recent study could very well be a partial explanation for this phenomenon.

Researchers from the University of Florida’s College of Medicine believe that leptin resistance – i.e. where people’s ability to feel satiated after a meal is diminished, thus eating more as a result – may be a function of fructose and how much fructose people eat in a given day.

As I’ve written in the past, all fructose is not built the same. Natural fructose – the natural sweetener found in fruits – is completely healthy and not at issue in this study. The fructose this study is concerned with is the kind that’s manufactured – the fructose with a “high” before it and a “corn syrup” after it. Just take a look at the list of ingredients in any packaged snack, dessert or sweetened cereal, I guarantee you’ll find “high fructose corn syrup” high on the list.

Anyway, the researchers took two groups of rats and fed them the exact same diet, the one difference being the manner in which the food was sweetened: one group’s food was high in fructose; the other group’s food contained no fructose. The researchers were operating under the hypothesis that increased fructose consumption leads to leptin resistance.

What was surprising about the study was that despite six months of eating a high fructose corn syrup-based diet, the rats’ weight did not change over the entire period. What did change was their blood content: the fructose rats’ blood had more triglycerides than the non fructose group. Triglycerides are the chemical composition of fat the body stores in the blood and cells for energy. When they aren’t used for energy purposes, triglycerides build up, leading to high cholesterol levels, increased weight gain and high blood pressure.

Seeing the difference in blood composition, the researchers then injected both groups with leptin. If their hypothesis proved true, then the fructose-eating rats’ consumption rate would not diminish. And just as they predicted, the fructose-eating rats’ appetite was not changed by the injection of leptin (the non-fructose eating rats, however, did consume less).

Again, both groups of rats did not gain weight over the six month period, but that all changed when the researchers gave both groups of rats high fat, high calorie diets. The fructose-eating group ate much more food than the non-fructose eating group and put on much more weight, presumably because of their leptin resistance.

While this study was done on rats, the researchers believe this can be applied to humans as a potential explanation for bulging belt buckles. The researchers also believe that the high triglyceride levels in the blood – a direct result of high fructose consumption –served as the catalyst for the diminished production of leptin. Without the production of said leptin, the body’s internal “fullness indicator” becomes inoperable.

The researchers plan on doing a follow-up to this study, testing to see if removing high fructose corn syrup from the diet can reverse the effects of fructose on leptin resistance.