100 years after the discovery of insulin, scientists have finally found an insulin suppressor

Today, a hundred years later, there is still no drug treatment to stop or reverse the progression of diabetes, and popular sugar-lowering drugs such as smeglutide can only slow the progression of diabetes.
Previous studies have found that insulin-enhanced therapy may improve blood sugar control and relieve diabetes, but it can also lead to weight gain or more serious side effects, such as an increased risk of a sharp drop in blood sugar, which can lead to confusion.
On the 100th anniversary of the discovery of insulin, on January 27th Nature published a landmark study in the field of diabetes, and researchers from Helmholtz Zentrum Muenchen of the Technical University of Munich, Germany, and the German Diabetes Research Centre found a new, drug-ready insulin suppressor , known as incepter, that blocked the function of insulin signaling in pancreas β cells.
study focuses on the development of regenerative methods for treating diabetes to complement and replace classic immunological and metabolic therapies.
's insulin inhibitor is a promising molecular target in β cell protection and regeneration therapy, and regenerative therapy does not have unintended side effects similar to those caused by insulin-enhanced therapy.
insulin resistance of β islet" cells can trigger diabetes, and insulin-sensitive therapy that makes β cells sensitive may protect diabetics from β cell loss and failure.
," said Professor Heiko Lickert, author of the paper.
researchers observed in mouse experiments that insulin-suppressing inhibitors (incepters) inhibit the activity of INSR-IGF1R (INSR: insulin subjects; IGF1R: insulin-like growth factor 1s).
it is worth noting that this subject is expressed in diabetes and may cause insulin resistance by blocking insulin signaling.
Photo The insulin inhibitor receptor (black) desensits insulin receptors (color) on pancreatic β cells, and the team of researchers in blue is insulin (source: Helmholtz Zentrum München) to explore the function of insulin-suppressing receptors by inhibiting insulin inhibitors genetically or pharmacologically.
results showed an increase in inactivity and β cell proliferation of INSR-IGF1R after insulin inhibition-specific knock-off of β cells in adult mice and ionosome islets.
, insulin inhibitors interact with INSR-IGF1R to promote mesh protein-mediated internal swallowing, resulting in INSR and IGF1R desensitation.
researchers were able to maintain the insringR-IGF1R in β cells by using monoantimmune blocking of this physical interaction in the extracellular field of the target.
" results are exactly what we want, with an increase in insulin signals β and functional cells.
this makes insulin suppressor a very promising target.
," said Ansarullah, the paper's first author.
" Frederick Banting pointed out in his Nobel Prize-winning speech 100 years ago that insulin is not a cure for diabetes, but a cure for its symptoms.
future, our goal is to develop drugs that can regenerate cells from the β insulin inhibitor findings.
people with type 1 and type 2 diabetes may benefit from this and eventually move towards diabetes relief.
," says Professor Lickert.
: 1 s Ansarullah, Jain, C., Far, F. F. et al. Inceptor counteracts insulin signalling in β-cells to control glycaemia. Nature (2021) 2 s Diabetes: Neue Entdeckung könnte die Behandlung künftig verändern (Source: Helmholtz Zentrum München) 3 s Louis Rosenfeld. Insulin: Discovery and Controversy. Clinical Chemistry (2002)