rs11664369 - RNU6-567P - LINC03111
Magnitude 2.2 · 3 studies on file
Reported associations
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Comprehensive genetic study of the insulin resistance marker TG:HDL-C in the UK Biobank. - Nature genetics (2024) · Oliveri A, Rebernick RJ, Kuppa A, Pant A, Chen Y, Du X, Cushing KC, Bell HN, Raut C, Prabhu P, Chen VL, Halligan BD, Speliotes EK · PubMed 38200128
Insulin resistance (IR) is a well-established risk factor for metabolic disease. The ratio of triglycerides to high-density lipoprotein cholesterol (TG:HDL-C) is a surrogate marker of IR. We conducted a genome-wide association study of the TG:HDL-C ratio in 402,398 Europeans within the UK Biobank. We identified 369 independent SNPs, of which 114 had a false discovery rate-adjusted P value < 0.05 in other genome-wide studies of IR making them high-confidence IR-associated loci. Seventy-two of these 114 loci have not been previously associated with IR. These 114 loci cluster into five groups upon phenome-wide analysis and are enriched for candidate genes important in insulin signaling, adipocyte physiology and protein metabolism. We created a polygenic-risk score from the high-confidence
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Gene polymorphisms associated with heterogeneity and senescence characteristics of sarcopenia in chronic obstructive pulmonary disease - Unknown journal (n.d.) · Unknown authors · PubMed 36856146
ABSTRACT: Abstract Background Sarcopenia, or loss of skeletal muscle mass and decreased contractile strength, contributes to morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). The severity of sarcopenia in COPD is variable, and there are limited data to explain phenotype heterogeneity. Others have shown that COPD patients with sarcopenia have several hallmarks of cellular senescence, a potential mechanism of primary (age‐related) sarcopenia. We tested if genetic contributors explain the variability in sarcopenic phenotype and accelerated senescence in COPD. Methods To identify gene variants [single nucleotide polymorphisms (SNPs)] associated with sarcopenia in COPD, we performed a genome‐wide association study (GWAS) of fat free mass index (FFMI) in
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Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: A multivariable Mendelian randomisation analysis - Unknown journal (n.d.) · Unknown authors · PubMed 32203549
ABSTRACT: Background Circulating lipoprotein lipids cause coronary heart disease (CHD). However, the precise way in which one or more lipoprotein lipid-related entities account for this relationship remains unclear. Using genetic instruments for lipoprotein lipid traits implemented through multivariable Mendelian randomisation (MR), we sought to compare their causal roles in the aetiology of CHD. Methods and findings We conducted a genome-wide association study (GWAS) of circulating non-fasted lipoprotein lipid traits in the UK Biobank (UKBB) for low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B to identify lipid-associated single nucleotide polymorphisms (SNPs). Using data from CARDIoGRAMplusC4D for CHD (consisting of 60,801 cases and 123,504 controls), we per
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Lifestyle context
Concrete actions anchored to the cited research. We do not prescribe, we describe.
Diet
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omega-3 fatty acids for HDL High
C allele reduces HDL; omega-3s raise HDL cholesterol levels
1-2g EPA+DHA daily or 2-3 fatty fish servings weekly
Exercise
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aerobic exercise for HDL support High
C allele reduces HDL; aerobic activity increases HDL cholesterol
150 minutes moderate-intensity aerobic exercise weekly
Screening
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HDL cholesterol level High
C allele reduces HDL cholesterol; early detection enables intervention
check HDL annually, target greater than 40 mg/dL (men) or 50 mg/dL (women)