Shiwali Goyal (United States of America)

University of Oklahoma Health Sciences Center Pediatrics
I am currently working as an Associate Research Scholar in Dr. Sanghera’s Lab at University of Oklahoma Health Sciences Center. The current goal of my research is to dissect the underlying genetic mechanisms that may contribute to etiology of Type 2 Diabetes using metabolome GWAS in different ethnic groups. After completing my Ph.D. I joined Dr. Sanghera’s lab with an aim to expand my skill set. I am very much enthusiastic in giving my contribution to the research going on in her lab.I started my work by analyzing the genome-wide association study (GWAS) data on dyslipidemia cases of Punjabi Sikhs and Metabolome in Ischemic Stroke Study (MISS) populations and identified vast majority of rare variants in Apo CIII associated with high plasma triglyceride levels. I have a strong background in Human Genetics and my existing knowledge of different bioinformatics software and techniques will help me to excel in this field further.

Author Of 1 Presentation

O028 - Association of APOCIII common variants with risk of coronary artery disease: A Mendelian randomization study (ID 823)

Session Type
Lipoproteins and Metabolism
Session Time
16:00 - 17:30
Date
Mon, 31.05.2021
Room
Hall C
Lecture Time
16:33 - 16:41

Abstract

Background and Aims

Background: Hypertriglyceridemia has emerged as an important coronary artery disease (CAD) risk factor. Rare loss of function (LOF) variants in apolipoprotein CIII have been reported to reduce triglycerides (TG) and decrease the risk of CAD in American Indians and Europeans. However, there is a paucity of data on whether these variants are cardioprotective in other European and non-European populations. Also, whether genetically increased TG due to ApoCIII is causally associated with increased CAD risk is still unclear and inconsistent.

Objective: The goal of this study was to evaluate the causal association of genetically raised TG for increasing the risk for CAD and type 2 diabetes (T2D) using a Mendelian randomization approach.

Methods

Methods: Using genome-wide genotypes and sequencing data of ten independent multiethnic cohorts comprising up to 397,460 individuals, we have evaluated the role of genetic variation in APOCIII for affecting circulating TG and the risk for developing CAD and T2D.

Results

Results: Two common variants (rs5128 and rs734104) in the APOCIII were robustly associated with elevated TG across all cohorts showing an allelic risk-score p-value of 1.74x10-674 in joint meta-analysis. A per risk allele-associated increase of TG of 12mmol/L ± SE 0.02mmol/L was predicted to enhance CAD risk by 5% 95%CI (3% to 6%; p=2.01x10-05). On the contrary, the same TG raising variants reveal marginal protection from T2D (OR 0.99 95%CI 0.98-1.00; p=0.02).

Conclusions

Conclusions: Our Mendelian randomization study suggests that the genetically regulated HTG via APOCIII may be causally associated with the increased risk for CAD.

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Presenter of 1 Presentation

O028 - Association of APOCIII common variants with risk of coronary artery disease: A Mendelian randomization study (ID 823)

Session Type
Lipoproteins and Metabolism
Session Time
16:00 - 17:30
Date
Mon, 31.05.2021
Room
Hall C
Lecture Time
16:33 - 16:41

Abstract

Background and Aims

Background: Hypertriglyceridemia has emerged as an important coronary artery disease (CAD) risk factor. Rare loss of function (LOF) variants in apolipoprotein CIII have been reported to reduce triglycerides (TG) and decrease the risk of CAD in American Indians and Europeans. However, there is a paucity of data on whether these variants are cardioprotective in other European and non-European populations. Also, whether genetically increased TG due to ApoCIII is causally associated with increased CAD risk is still unclear and inconsistent.

Objective: The goal of this study was to evaluate the causal association of genetically raised TG for increasing the risk for CAD and type 2 diabetes (T2D) using a Mendelian randomization approach.

Methods

Methods: Using genome-wide genotypes and sequencing data of ten independent multiethnic cohorts comprising up to 397,460 individuals, we have evaluated the role of genetic variation in APOCIII for affecting circulating TG and the risk for developing CAD and T2D.

Results

Results: Two common variants (rs5128 and rs734104) in the APOCIII were robustly associated with elevated TG across all cohorts showing an allelic risk-score p-value of 1.74x10-674 in joint meta-analysis. A per risk allele-associated increase of TG of 12mmol/L ± SE 0.02mmol/L was predicted to enhance CAD risk by 5% 95%CI (3% to 6%; p=2.01x10-05). On the contrary, the same TG raising variants reveal marginal protection from T2D (OR 0.99 95%CI 0.98-1.00; p=0.02).

Conclusions

Conclusions: Our Mendelian randomization study suggests that the genetically regulated HTG via APOCIII may be causally associated with the increased risk for CAD.

Hide