Researchers reveal insulin resistance may be driven by insulin degradation during transit in the bloodstream, challenging the belief that cell defects are the primary cause.
By Hugo Francisco de SouzaReviewed by Susha Cheriyedath, M.Sc.Dec 22 2024 New study identifies insulin ‘chain-splitting’ during bloodstream transit as a game-changer in understanding and treating diabetes and insulin resistance.
They substantiate their chain-splitting hypothesis with fresh evidence from both in vitro and in vivo and demonstrate that the degradation of A- and B- HI chains results in lowered insulin availability at target cells, thereby directly contributing to observed insulin resistance. Notably, the study highlights that chain-splitting rates align with the redox potentials typically found in human plasma, supporting the physiological relevance of the findings.
Furthermore, insulin resistance forces the pancreas to compensate through increased insulin production and secretion. The persistent inability of cells to respond to this increased secretion triggers a positive feedback loop, eventually contributing to pancreatic diseases or failure.
In the present study, researchers hypothesize a novel mechanism of insulin resistance termed ‘chain-splitting.’ The hypothesis posits that the degradation of endogenous insulin during its journey from the pancreas to target cells, not defects in the cells themselves, results in insulin-resistant phenotypes. This hypothesis underscores the role of redox potentials in the plasma environment in driving the chain-splitting process.
All experimental data was acquired via liquid chromatography-mass spectroscopy systems . Nonlinear least squares carried out in GraphPad Prism 9.0.1 were used for statistical analyses of obtained data.
Blood Chromatography Diabetes Diet Exercise Glucose In Vitro In Vivo Insulin Resistance Liquid Chromatography Pancreas Receptor Research Sulfur Syndrome
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