Scientists from Indiana University (IU), University of Michigan, and Case Western Reserve University have determined that the insulin sequence has become anchored at the edge of impaired production – an unconvincing intrinsic weakness with rare mutations in the insulin gene that causes childhood diabetes
Ian | New York | November 8, 2020, 7:10 pm
Previous studies have suggested that impaired biosynthesis may be the result of a variety of mutations that impede the folding ability of bronsolin (stylized image: iStock)
The development of insulin in vertebrates – including humans – ran into a hurdle, which limited their ability to adapt to obesity, and thus left most people vulnerable to developing type 2 diabetes, according to important research
Scientists from Indiana University (IU), the University of Michigan and Case Western Reserve University have determined that the insulin sequence is becoming entrenched at the edge of impaired production – a fundamental weakness revealed by rare mutations in the insulin gene that causes childhood diabetes.
Insulin is produced by a series of very specific processes that take place in specialized cells called beta cells
A key step is folding a biosynthetic precursor, called proinsulin, to achieve the three-dimensional functional structure of the hormone.
Previous studies have suggested that impaired biosynthesis may be the result of a variety of mutations that impede the folding ability of the broncolin.
« Biological processes usually evolve to be robust, and in most cases this protects us from birth defects and diseases » said Michael Weiss, Distinguished Professor at IU College of Medicine, « Diabetes appears to be an exception »
The group discovered that even the slightest difference in the insulin sequence process not only impedes insulin folding (and ultimately insulin secretion), but also induces cellular stress that leads to beta cell dysfunction and ultimately permanent damage.
The study, published in the Proceedings of the National Academy of Sciences, highlights the importance of folding efficiency as a critical but hidden factor in the evolution of insulin over the past 540 million years.
Humans have evolved to be susceptible to various mutations in the insulin gene and that this vulnerability underlies a rare, monogenic form of diabetes and provides an evolutionary background to the current obesity-related diabetes epidemic.
“The authors highlight the fact that the insulin gene was prone throughout evolution to mutations that impair insulin function or stress beta cells,” said Barbara Kahn of Harvard Medical School.
“As we approach the centenary of insulin discovery, these elegant observations may lead to a better understanding of the pathogenesis of type 2 diabetes”
The group will fully identify the sequence markers that make insulin protein foldable in beta cells.
Insulin, Type 2 Diabetes, Diabetes, Bronsolin, Beta Cells, Obesity
World News – Australia – Most humans are at risk of developing diabetes as insulin develops
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