Welcome to Suzuki Lab!
Our research goal is to identify mechanisms of how the offspring memorize their environmental exposure status in utero throughout life and how the genetic variations contribute to the effects.
We focus on the effects of an in utero micronutrient deficiency on cell subtype proportions and cell memory and diseases later in life, such as asthma, metabolic, and immune diseases.
Our hypothesis is that adverse prenatal exposures can change the repertoire of cell subtypes that compose the mature organ, conferring much of the risk of developing disease phenotypes.
Our long-term goal is to understand the mechanisms by which genetic and prenatal environmental factors contribute to congenital disabilities and disease risks later in life to develop preventative interventions ultimately in the line of Developmental Origins of Health and Disease (DOHaD) and health disparity.
Prenatal vitamin A deficiency
Vitamin A is an essential micronutrient that plays critical roles in many biological functions of the body. This micronutrient, along with its downstream retinoid signaling (VA-sig), is pivotal in the organogenesis and homeostasis of multiple organs, including the lungs. Vitamin A deficiency is found worldwide, including in the US, in various race and ethnicity groups. While it is well reported that maternal vitamin A deficiency increases the risk of adverse health outcomes for both mother and child later in life, the long-term memory mechanisms in the body remain unexplained.
Our project aims to identify the molecular mechanisms through which prenatal vitamin A deficiency influences disease risks in adulthood, as well as how genetic variation impacts the effects of prenatal vitamin A deficiency on cell subtype proportions, cell memory, and diseases. This project has been funded by NLBHI/NIH through an R01 funding mechanism.
Prenatal vitamin D deficiency
Vitamin D (VitD) deficiency or insufficiency is commonly observed in women of reproductive age and in children in the US. Prenatal vitamin D deficiency (VDD) increases susceptibility to many immune-related diseases (such as asthma, multiple sclerosis, and type I diabetes) later in life. It is widely accepted that VitD and the vitamin D receptor (VDR) signaling pathways play critical roles in the immune system and that VDD influences the properties of immune cells. However, the mechanism of how prenatal VitD deficiency leaves a lasting effect in the offspring and how it alters adult hematopoiesis are not yet known.
Our project focuses on identifying the molecular mechanisms of how the prenatal vitamin D deficiency alters immune cell proportion of the offspring in adulthood.
Prenatal Hidden Hunger
Hidden hunger stems from the intake of inadequate quality diets, resulting in micronutrient (vitamin) deficiencies that impact health conditions. In the U.S., food and nutrition insecurity often co-exist with obesity as these individuals tend to consume high-fat foods that are low in protein and micronutrients. The CDC reported that obesity in the U.S. is increasing; the age-adjusted prevalence of obesity in adults was 42.4% (2017-2018), and ~29% of U.S. women were obese before pregnancy (2019). Maternal obesity significantly increases the risks of obesity and liver diseases in adult offspring. We aim to understand how prenatal hidden hunger exposure affects childhood obesity.
Collaborators
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