Blood sugar and cholesterol: why they climb you even if you diet according to science

Genomic
Both cholesterol and blood glucose in blood are known cardiovascular risk factors, among many others.Maintaining its levels in an adequate range, without excesses or deficits, is one of the main prevention objectives at the primary care level.However, it is not always fable task
On many occasions, genetic factors are not modifiable by diet or lifestyle, such as the well -known family hypercholesterolemia, where total cholesterol levels and LDL cholesterol are triggered without an apparent cause.So far, only genes responsible for 80% of cases were known, but a new work of Spanish origin has discovered a new mutation: the SREBF2 gene.

The disease, known as 'autosomic dominant hypercholesterolemia' or ADH, is a disease of genetic origin.It is known that the LDLR gene is the cause in most patients, around 80% of cases, although there are other genes known as APOB and PCSK9, responsible for approximately 1%.

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In this new study, in charge of the researchers of the Inclusive Health Research Institute, of the Clinical Hospital of Valencia, the objective was to identify new genes potentially responsible for ADH, which would help detect many other patients, thus being able to advance the applicationof adequate medical treatments and healthy living habits according to the disease, thus reducing long -term cardiovascular risk.
Already in previous studies the possibility that Srebf2 mutations were a cause of hypercholesterolemia or that even can influence the already high levels of cholesterol in patients with Mutations of the LDLR gene had been suggested.With this research it has been shown that Srebf2 mutation, by itself, is able to cause family hypercholesterolemia.

In addition, the detected mutation also results in higher levels of glucose and insulin, which suggests that it also has a role in the modulation of glucose metabolism.Some of the relatives of the patient who participated in the study were already diabetic, but others were at levels of prediabetes (high sugar levels, without reaching the range of diabetes as a diagnosis) and none of these people had any more genetic alteration that couldExplain its sugar elevation beyond the Srebf2 gene.

In conclusion, the authors suggest that this mutation is able to increase both cholesterol levels and glucose in humans, but more studies will be necessary to demonstrate a causal relationship between this mutation and family hypercholesterolemia.

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