Scientists identify a key player that helps prevent “insulin shock” and may lead to a therapeutic alternative to the hormone used by millions of persons with diabetes. Just over a century has passed since the discovery of insulin, a time period during which the therapeutic powers of the hormone h
Researchers identified a metabolic enzyme called fructose-1,6-bisphosphate phosphatase that acts as a natural defense against insulin shock. FBP1 controls gluconeogenesis, a process where the liver synthesizes glucose and maintains a steady supply in the bloodstream. The researchers discovered that FBP1 inhibits the protein kinase AKT, preventing insulin hyper-responsiveness and related complications.
“Although insulin is one of the most essential hormones, whose insufficiency can result in death, too much insulin can also be deadly,” said senior study author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at UCSD School of Medicine. Some antidiabetic drugs, such as metformin, inhibit gluconeogenesis but without apparent ill effect. Children born with a rare, genetic disorder in which they do not produce sufficient FBP1 can also remain healthy and live long lives.
To better understand the roles of FBP1, researchers created a mouse model with liver specific FBP1 deficiency, accurately mimicking the human condition. Like FBP1-deficient children, the mice appeared normal and healthy until fasted, which quickly resulted in the severe hypoglycemia and the liver abnormalities and hyperlipidemia described above.
Working with Yahui Zhu, a vising scientist from Chongqing University in China and second author of the study, Gu developed a peptide derived from FBP1 that disrupted the association of FBP1 with AKT and another protein that inactivates AKT. Reference: “Fructose-1,6-bisphosphatase is a nonenzymatic safety valve that curtails AKT activation to prevent insulin hyperresponsiveness” by
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