Tuomas O. Kilpeläinen

This study identifies peripheral immune and metabolic tissues as key contributors to Alzheimer's disease genetic risk, independent of brain-specific factors.

This study links obesity and type 2 diabetes to Alzheimer's disease through genetic and transcriptomic analyses, identifying shared pathways and potential drug targets.

This study identifies 282 genetic loci associated with insulin resistance through multi-trait GWAS, highlighting adipose-specific and systemic regulators and potential therapeutic targets.

This study identifies chondroitin sulfate as a potential therapeutic target for type 2 diabetes through genetic and preclinical evidence showing its effects on glycemic control and insulin action.

The paper identifies REPS1 as a regulator of muscle glucose uptake through phosphoproteomic analysis of insulin and exercise responses in human skeletal muscle.

The paper refines a gene-physical activity interaction affecting HDL-cholesterol by analyzing lipoprotein subfractions and exploring sex differences across multiple cohorts.

This study uses whole genome sequencing to identify 18 novel genetic loci associated with plasma fibrinogen levels, including variants more common in African populations and linked to liver-related traits and disease.

This study identifies 17 genetic loci associated with sleep duration and lipid levels, offering potential druggable targets for dyslipidemia in individuals with sleep disturbances.

This study uses Mendelian randomization to estimate the causal effect of smoking on abdominal obesity, finding positive causal effects on waist-hip ratio and visceral fat.

This study uses Mendelian randomization to show bidirectional causality between sedentary time and BMI, with implications for weight management and health interventions.

The paper identifies novel genetic loci associated with blood pressure that interact with sleep duration across multiple ancestries.

The paper identifies 49 novel blood lipid loci associated with gene-sleep interactions in 126,926 individuals across 5 ancestry groups, with gene-short-sleep interactions explaining 4.25% of triglyceride variance.