Most Humans are Vulnerable to Type 2 Diabetes: Study

New study found that insulin has met an evolutionary cul-de-sac, restricting its ability to adapt to obesity, thereby rendering most people vulnerable to Type 2 diabetes. The findings of the study is published in the journal Proceedings of National Academy of Sciences.

A recent study has determined that the sequence of insulin has become entrenched at the edge of impaired production, an intrinsic vulnerability revealed by rare mutations in the insulin gene, causing diabetes in childhood. The study utilizes biophysical concepts and methods to relate protein chemistry to the emerging field of evolutionary medicine.

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‘Even the smallest variation of the insulin-sequencing process not only weakens insulin folding but also causes cellular stress that leads to beta-cell dysfunction and, eventually, permanent damage. ’

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Insulin is produced by highly distinct processes that occur in specialized cells, called beta cells. An essential step is to fold a biosynthetic precursor, called proinsulin, to obtain the hormone's functional three-dimensional structure. Past research from this and other groups have suggested that impaired biosynthesis could result from diverse mutations that hinder the foldability of proinsulin.

This group sought to discover if the evolution of insulin in vertebrates, including humans, has encountered a roadblock. Has a complicated series of steps imposed constraints that have frozen the insulin sequence at a precipice of non-foldability? And if so, has this left humankind exposed to Type 2 diabetes as a pandemic disease of civilization?

Weiss and team looked at a subtle mutation in human insulin with other animals' insulins, such as porcupines and cows. The mutant human insulin functions within the range of natural variety among animal insulins, and yet this mutation has been eliminated by evolution. The solution to this seeming paradox is that the prohibited mutation selectively blocks the folding of proinsulin and stresses beta cells.

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The group discovered that even the smallest variation of the insulin-sequencing process not only weakens insulin folding (and eventual insulin secretion) but also causes cellular stress that leads to beta-cell dysfunction and, eventually, permanent damage.

National experts admit that this discovery provides a key insight to better understand Type 2 diabetes development in adults and kids.

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