Researchers from Lund University, in collaboration with Newcastle University, have uncovered a potential breakthrough in understanding type 2 diabetes.
Their study highlights the role of a protein, IGFBP7, which appears to impair insulin secretion in people with the disease.
The findings open the door to the possibility of targeting this protein for new treatments that could improve insulin release and overall metabolic health.
Understanding Type 2 Diabetes
Type 2 diabetes is characterized by the body’s inability to produce enough insulin or use it effectively. Insulin, a hormone released by beta cells in the pancreas, helps regulate blood sugar levels.
When insulin secretion is reduced, blood sugar levels rise, increasing the risk of complications such as heart disease, nerve damage, and kidney problems. Despite years of research, the precise mechanisms behind impaired insulin release remain unclear.
The Role of IGFBP7 in Beta Cells
The research team focused on beta cells located in the pancreas’s islets of Langerhans. These cells are critical for insulin production. They discovered that the protein IGFBP7, already studied for its links to heart and kidney disease, also plays a key role in regulating insulin secretion.
When examining beta cells from people with type 2 diabetes, the researchers found elevated levels of IGFBP7. To explore how this protein affects insulin secretion, they treated beta cells from people without diabetes with IGFBP7.
The results were striking: insulin secretion was reduced in these cells, and their overall function appeared to be impaired. Specifically, the treated cells showed lower levels of another protein essential for maintaining healthy cell function.
“This suggests that elevated levels of IGFBP7 impair the function of beta cells and their ability to secrete insulin,” explains Lena Eliasson, a professor of experimental diabetes research at Lund University. “This may be an important part of the explanation for reduced insulin secretion in type 2 diabetes.”
Knocking Out IGFBP7 Improves Insulin Secretion
The researchers then investigated whether reducing IGFBP7 levels could enhance insulin secretion. Using beta cells from people with type 2 diabetes, they “knocked out” the gene responsible for producing IGFBP7. The results were promising: insulin secretion increased in these cells.
This suggests that targeting IGFBP7 could potentially improve insulin release in people with type 2 diabetes. “One treatment option could be to reduce the expression of this protein in people with type 2 diabetes to improve insulin secretion,” says Eliasson.
Broader Implications
IGFBP7’s influence may not be limited to the pancreas. The protein is also involved in the functioning of other organs, including the heart, liver, and kidneys, which are often affected by type 2 diabetes. This makes it an especially intriguing target for developing treatments that could address the broader impacts of the disease.
“It would be interesting if IGFBP7 could be used as a drug target to improve the function of several organs,” notes Efraim Westholm, the study’s first author.
The Path Forward
While the findings are promising, the researchers stress the need for further studies. More work is required to understand how IGFBP7 is expressed in a broader population and to determine its precise role in type 2 diabetes.
With additional research, these insights could pave the way for new treatments designed to reduce IGFBP7 levels, thereby improving insulin secretion and offering better outcomes for people with type 2 diabetes.
This discovery marks an important step toward unraveling the complex mechanisms of type 2 diabetes and developing innovative strategies to manage the disease. By targeting IGFBP7, researchers hope to provide new hope for millions of people living with this challenging condition.
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The research findings can be found in iScience.
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