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Degeneration of the beta cell as diabetes progresses has been a broadly reviewed topic. [2] [4] [9] Another topic of interest for beta-cell physiologists is the mechanism of insulin pulsatility which has been well investigated. [41] [42] Many genome studies have been completed and are advancing the knowledge of beta-cell function exponentially.
Additionally, beta-cell function has to be interpreted in light of the prevailing insulin sensitivity. [21] [20] This is necessary since the beta cell mass is adjusted as required by dynamical compensation, [22] giving rise to a hyperbolic relationship between insulin sensitivity and beta cell function.
In this updated version it is possible to determine insulin sensitivity and β-cell function from paired fasting plasma glucose and radioimmunoassay insulin, specific insulin, or C-peptide concentrations. The authors recommend the computer software be used wherever possible. [4] [5]
Because the beta cells in the pancreatic islets are selectively destroyed by an autoimmune process in type 1 diabetes, clinicians and researchers are actively pursuing islet transplantation as a means of restoring physiological beta cell function, which would offer an alternative to a complete pancreas transplant or artificial pancreas.
Disposition metrics integrate beta cell function and insulin sensitivity in a way so that the results remain constant across dynamical compensation. Changed from Cobelli et al. 2007 and Hannon et al. 2018 [1] [2] The Disposition index (DI) is a measure for the loop gain of the insulin-glucose feedback control system.
People with type 2 diabetes who were given ketones before exercise had increased cardiac output, stroke volume, and peripheral muscle oxygenation, which are all indicators of improved heart function.
This forms threads that create tangles inside nerve cells, ultimately interfering with the way cells in the brain communicate. Most research has focused on early detection for beta-amyloid plaques ...
The second phase is a slow release of newly formed vesicles that are triggered regardless of the blood sugar level. Glucose enters the beta cells and goes through glycolysis to form ATP that eventually causes depolarization of the beta cell membrane (as explained in Insulin secretion section of this article). The depolarization process causes ...