Diabetes is a disease that affects millions of people around the world. Blood-sugar raising hormones such as glucagon counterbalance the blood- sugar lowering hormone insulin. Disrupting this delicate equilibrium can lead to diabetes.
The findings published in Cell Metabolism by Harvard researchers suggest that a chronic high-calorie diet can lead to high blood sugar simply by boosting the gut hormone activin-beta, which in turn stimulates activity of the fly version of glucagon—without affecting insulin.
Up until now researcher thought that activin-beta was produced only in the brain and peripheral nerves, but the new study reveals that endocrine cells in the midgut—at least, the midguts of flies—can make activin-beta. Further experiments fingered activin-beta as the culprit. The high-calorie diet was pushing activin-beta into overdrive, which boosted AKH, which told the fat body to release more sugar than was healthy.
Adipokinetic hormone (AKH): it is the fly equivalent of mammalian glucagon.
Fat body: the fly equivalent of the human liver and fat tissue.
Adipokinetic hormone (AKH) activity spiked in the fat body obeyed the AKH hormonal signal and released glucose into the bloodstream. The flies developed high blood sugar, insulin resistance and obesity, all similar to what happens in Type 2 diabetes.
“This activin-AKH axis is totally independent of insulin,” said Song. “It’s a different mechanism from what was known before.” “This gut-to-fat-body communication is essential for the development of high blood sugar. We didn’t know that before.”
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