Current Funding Awardees

Nicholas Chavkin Ph.D.
Assistant Professor
Department of Pediatrics

Age-related loss of Y Chromosome on Metabolic Dysfunction
As men age, a portion of blood cells undergo mosaic loss of the Y chromosome (mLOY), which is the most common post-zygotic mutation in people. Men with mLOY have higher rates of mortality and age-related disease progression, but the effects of mLOY on metabolic dysfunction have not been investigated. In this project, we will test the hypothesis that mLOY affects metabolic dysfunction from diet-induced obesity by establishing and evaluating models of mLOY in human primary blood cells and transgenic mice. Understanding the role of mLOY in metabolic dysfunction could determine new hematopoietic-related mechanisms regulating metabolism and provide new insights into the relationship between aging and obesity.

Stephen McCartney, M.D., Ph.D.
Assistant Professor
Department of Obstetrics & Gynecology
Division of Maternal Fetal Medicine

Determining the Role of Glucose Utilization in Immune Cell Function at the Maternal Fetal Interface
Pregnancy complications including fetal growth restriction, preeclampsia, and preterm birth are linked to both placental inflammation and metabolic dysfunction, yet treatment options remain limited due to gaps in understanding the complex interactions between immune and metabolic processes at the maternal-fetal interface. This proposal investigates how glucose metabolism influences immune cell function at the maternal-fetal interface across normal pregnancy. Using single-cell flow cytometry, transcriptomics, and metabolomics assays, we will assess energy pathway utilization and metabolic phenotypes of immune cells during each trimester of pregnancy. Findings from this study will clarify how immune and metabolic networks coordinate during normal pregnancy and may provide insight into novel pathways to develop targeted therapeutics for pregnancy complications.

Jocelyn Cervantes
Ph.D. Candidate
Department of Medicine
Division of Metabolism, Endocrinology and Nutrition

Does Diabetic Dyslipidemia Stimulate the Expansion of Lipid-associated Macrophages in Diabetic Kidney Disease (DKD), and Does this Augment of Diminish DKD Progression?
Emerging evidence suggests that diabetic dyslipidemia, characterized by elevated triglyceride-rich lipoproteins (TRLs), contributes to DKD progression. Although lipid-laden macrophages (macrophages with engulfed lipids) are often found and expanded in DKD, their role is unclear. Recent single-cell RNA-sequencing identifies a lipid-associated macrophage population in the kidney marked by high TREM2 expression, which is suggested to play a protective rather than detrimental role in people with obesity and DKD. The goal of this Stroum Fellowship is to investigate if lipid-associated macrophages are expanded in the kidney in response to diabetic dyslipidemia and if suppression of these via deletion of TREM2 results in augmented tissue injury and DKD progression.