Want to know if metformin-lowering sugars will work? Make a simple blood test to predict it first.

Metformin is a first-line drug that lowers blood sugar levels in people with type 2 diabetes.
, however, one third of patients did not respond to metformin treatment and 5% experienced serious side effects.
according to international guidelines, if metformin does not have the expected effect of lowering blood sugar levels, or if a patient experiences serious side effects, he or she can continue to try other medications.
, however, these patients have spent a long time before receiving the right treatment, which puts blood sugar levels at risk of complications.
therefore, for those with type 2 diabetes who do not respond to metformin, it is important to use another drug from the outset, and to identify these patients after diagnosis.
, a team led by researchers at the National Centre for Cardiovascular Research in Madrid, Spain, published a new study in Science Translational Medicine, which identified blood-based biomarkers that can pre-empt patients' responses to metformin treatment with simple blood tests.
DOI: 10.1126/scitranslmed.aaz1803 Specifically, by analyzing the whole genome DNA methylation of untreated type 2 diabetics at diagnosis, the researchers explored whether blood-based extrinsic genetic markers can distinguish between metformin response and tolerance.
In the discovery and replication queues, DNA methylation was different at 11 bits of the blood glucose responder/non-reactor, and DNA methylation was different at 4 bits in patients with metformin tolerance/insoluble tolerance.
the higher the degree of methylation of these bits, the higher the risk of non-reaction or inability to be resistant to metformin, with a ratio of 1.43 to 3.09 for each increase in methylation of 1-SD.
In addition to the methylation differential points associated with future metformin response or insatiability in meta-analysis of the discovery and replication queues, the methylation risk score (MRS) was different for blood glucose responders and non-reactors at 11 identified locations, with a sub-curve area (AUC) of 0.80 to 0.98.
AUC produced by MRS at four bits associated with future metformin indescability was 0.85 to 0.93.
Combined MRS can distinguish between untreated type 2 diabetes participants' blood sugar-reactive and non-reactive combined MRS can distinguish between untreated type 2 diabetes participants' tolerance and inability to metformin-based methylated markers, some of which reflect the obihydrological genetic patterns of adipose tissue (the key tissue in the pathogenesis of diabetes).
, the genes of these markers have biological functions in liver cells that alter metformin-related esotypes.
silencing associated with metformin response (SEPT11 and CST1) or inability (FOXA2 and PPM1) in hepatic cells affects the expression of metformin transport proteins, AMPK activity, and key regulations of glycogenics Overall, this study showed that by measuring blood-based metagenetic markers in patients with type 2 diabetes who had not been treated with medication, it was necessary to distinguish between blood glucose responders/non-reactors and participants' tolerance/inability to metformin at diagnosis.
to some extent, drug-based mesogenetics has been used in cancer treatment to predict a person's response to treatment, but has never been done before in diabetes treatment.
this study is the first drug-based on-the-surface genetics study in diabetes to help ensure that patients receive the right care immediately after diagnosis, an important step towards the goal of providing personalized care for people with diabetes.
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