Posted: Dec 01, 2022
Aiming for equitable precision medicine in diabetes.
et al. Nature medicine 2022 11 (11) 2223
New initiatives aimed at reducing the burden of diabetes are laudable, but they will have to account for the disease’s complexity and heterogeneity to be truly effective and equitable at a global scale. A growing body of evidence supports the idea that variation exists not only in disease presentation and progression but also in individual responses to therapy, which suggests that a ‘one-size-fits-all’ approach to meeting the global coverage targets will be insufficient.
DNA Methylation Implicated in Human Obesity and Diabetes
ME Tucker, Medscape, November 2022
Previous attempts to identify causal associations between DNA methylation and both obesity and type 2 diabetes have been hindered by challenges in collecting and isolating cells from human tissue. Recent data suggest that manipulation of DNA methylation enzymes in adipocytes can induce or prevent obesity and type 2 diabetes through cellular effects on energy expenditure and insulin sensitivity.
Broad-capture proteomics and machine learning for early detection of type 2 diabetes risk
Nature Medicine, November 10, 2022
Impaired glucose tolerance (IGT) is a common condition that affects glucose control after sugar consumption. Isolated IGT is undetected by screening and diagnostic strategies, leaving affected individuals at high risk of developing diabetes. Here, a machine-learning framework identifies a three-protein signature for detecting isolated IGT from a single blood sample.
Proteomic signatures for identification of impaired glucose tolerance
JC Zanini et al, Nature Medicine, November 10, 2022
We applied machine learning to the proteomic profiles of a single fasted sample from 11,546 participants of the Fenland study to test discrimination of iIGT defined using the gold-standard OGTTs. We observed significantly improved discriminative performance by adding only three proteins (RTN4R, CBPM and GHR) to the best clinical model (AUROC = 0.80 (95% confidence interval: 0.79–0.86), P?=?0.004), which we validated in an external cohort. Increased plasma levels of these candidate proteins were associated with an increased risk for future T2D in an independent cohort and were also increased in individuals genetically susceptible to impaired glucose homeostasis and T2D.