Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease
Technische Universität München News
Scientists
from the Technical University of Munich (TUM) and Helmholtz Zentrum
München have developed a ‘smart’ drug that safely clears the liver of
fat and prevents blood vessels from clogging up. Similar to a trojan
horse, the drug enters the liver with a trick: It uses a pancreatic
hormone glucagon as a vehicle to transport a thyroid hormone to the
liver while keeping it away from other organs. Once delivered, it
improves both the cholesterol and the lipid metabolism while avoiding
typical side effects of thyroid hormones.
The newly developed glucagon/T3 molecule delivered the T3 selectively to the liver and thereby safely improved within a few days cholesterol metabolism in diet–induced obese mice. The molecule further decreased body weight, corrected non–alcoholic fatty liver disease, and improved glucose metabolism without deleterious effects of T3 in the heart and bone. Notably, the molecule failed to improve metabolism in mice lacking either the glucagon receptor or which lack the thyroid hormone receptor in only the liver, demonstrating the liver–specific signal specificity of this new molecule.
“The next task is to see whether this drug candidate will reach the same level of targeted tissue–selectivity in clinical studies”, says diMarchi. “If the molecule shows equal efficacy and safety in humans, then this particular ‘smart’ drug design may indeed offer perspectives for metabolic precision medicine”, summarizes Tschöp.
The paper "Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease" was published in the journal Cell.
The newly developed glucagon/T3 molecule delivered the T3 selectively to the liver and thereby safely improved within a few days cholesterol metabolism in diet–induced obese mice. The molecule further decreased body weight, corrected non–alcoholic fatty liver disease, and improved glucose metabolism without deleterious effects of T3 in the heart and bone. Notably, the molecule failed to improve metabolism in mice lacking either the glucagon receptor or which lack the thyroid hormone receptor in only the liver, demonstrating the liver–specific signal specificity of this new molecule.
“The next task is to see whether this drug candidate will reach the same level of targeted tissue–selectivity in clinical studies”, says diMarchi. “If the molecule shows equal efficacy and safety in humans, then this particular ‘smart’ drug design may indeed offer perspectives for metabolic precision medicine”, summarizes Tschöp.
The paper "Chemical Hybridization of Glucagon and Thyroid Hormone Optimizes Therapeutic Impact for Metabolic Disease" was published in the journal Cell.
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