Normally, when you eat, beta cells in the pancreas respond to the rise in glucose levels by secreting more insulin. Insulin attaches to other cells in the body and opens the cells, allowing glucose to enter the cells and provide energy. But researchers wanted to know what role fructose played in the release of insulin.
Using cells from humans and mice, the researchers found that fructose activated sweet-taste receptors on beta cells, causing them to secrete insulin. When glucose and fructose were encountered together, as would often happen with commonly consumed foods today, even more insulin was released.
When the researchers inactivated -- or turned off -- the sweet-taste receptors in the beta cells, they no longer secreted insulin when exposed to fructose. The researchers say these findings suggest that these sweet-taste receptors in the pancreas may play a role in metabolic diseases, such as obesity and type 2 diabetes. They're currently developing studies in humans to confirm what they've found in human and mouse cells in the lab.
Commenting on the study, Dr. Spyros Mezitis, an endocrinologist and clinical investigator at Lenox Hill Hospital in New York City, said that it showed that "when you eat fructose and glucose together, you get even more of an insulin release. That means sugar gets out faster, and the body is pushed harder."
And, he added, "if you have a high sugar consumption, you may tire out your pancreas, and that exhaustion might cause the pancreas to not release enough insulin anymore. If you already have type 2 diabetes, this could push the body more and hasten the progression of the disease."
But "right now this is speculation. We need human studies to understand this connection over time," Mezitis said. Still, this may be "one more piece of evidence that we should be curtailing fructose in our diets," he suggested.
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