AI Article Synopsis
- - Metabolic syndrome (MetS) is a combination of conditions, such as obesity and insulin resistance, that significantly raises the risk for heart disease and type 2 diabetes, and it is influenced by genetic factors.
- - A study used targeted next-generation sequencing on 48 individuals with MetS and 48 healthy controls to uncover genetic variants connected to the various clinical features of MetS.
- - Results showed that over half of the individuals with MetS had significant genetic variants linked to traits like obesity, high blood sugar, and hypertension, potentially expanding the understanding of genetic risks associated with MetS.
Article Abstract
Background: Metabolic syndrome (MetS) is a cluster of conditions associated with glucose intolerance, hypertension, abdominal obesity, dyslipidemia, and insulin resistance that increase the risk of cardiovascular diseases (CVD) and type 2 diabetes (T2D). Since MetS is known as a complex symptom with a high incidence of genetic factors, it is important to identify genetic variants for each clinical characteristic of MetS.
Methods: We performed targeted next-generation sequencing (NGS) to identify genetic variants related to obesity, blood glucose, triacylglycerol (TG), and high-density lipoprotein (HDL)-cholesterol level, and hypertension in 48 subjects with MetS and in 48 healthy subjects.
Results: NGS analysis revealed that 26 of 48 subjects (54.2%) with MetS had putative non-synonymous variants related to the clinical features of MetS. Of the subjects with MetS, 8 (16.7%) had variants in 4 genes (COL6A2, FTO, SPARC, and MTHFR) related to central obesity, 17 (35.4%) had variants in 6 genes (APOB, SLC2A2, LPA, ABCG5, ABCG8, and GCKR) related to hyperglycemia, 3 (6.3%) had variants in 4 genes (APOA1, APOC2, APOA4, and LMF1) related to hypertriglyceridemia, 8 (16.7%) had variants in 4 genes (ABCA1, CETP, SCARB1, and LDLR) related to low HDL-cholesterolemia, and 5 (10.4%) had variants in ADD1 related to hypertension.
Conclusions: Our findings may contribute to broadening the genetic spectrum of risk variants related to the development of MetS.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9396768 | PMC |
| http://dx.doi.org/10.1186/s13098-022-00893-y | DOI Listing |
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