Department of Reproductive Medicine
Obstetrics and Gynecology
Faculty_Thackray

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Department of Reproductive Medicine

Varykina G. Thackray, PhD

Division of Reproductive Endocrinology and Infertility

Center for Reproductive Science and Medicine

 

Associate Professor of Reproductive Medicine

 

  • PhD - University of Colorado Health Sciences Center, 2002
  • Postdoctoral Fellow - University of California, San Diego, 2002 - 2008

 

Link to Dr. Thackray's lab

Contact Information:

 

 

Email: vthackray@ucsd.edu

 

Administrative Assistant:

  • Ruth Montouri - 858.534.1140

 

Research Interests

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive-aged women, with a prevalence of 6-15%.  In addition to a reproductive phenotype that results in an increased risk of infertility, miscarriage and pregnancy complications, a majority of women with PCOS have metabolic abnormalities that result in an increased risk of type 2 diabetes, gestational diabetes and cardiovascular disease. The main objective of our research is to understand the etiology and pathophysiology of PCOS using relevant mouse and tissue culture models.

 

Current Research:

 

Genetic Influences on FSH Production

Research in my lab focuses on a G/T single nucleotide polymorphism (SNP) at ‑211 relative to the transcription start site of the human FSHB promoter (rs10835638) which is associated with reduced serum FSH levels in men and PCOS in women. This research is currently funded by an NIH/NICHD P50 grant (HD012303). We recently reported that the LHX3 homeodomain transcription factor binds to an 11 bp element in the human FSHB promoter which includes the -211 nucleotide. We also demonstrated that LHX3 bound with greater affinity to the wild-type human FSHB promoter compared to the ‑211 G/T mutation, and that FSHB transcription was decreased in gonadotrope cells with the ‑211 G/T mutation compared to the wild-type FSHB promoter. We are currently studying how LHX3 binding to the human promoter regulates FSH production especially with regards to the -211 G/T SNP. Comprehending the mechanisms of LHX3 regulation of FSHB may be useful for the development of novel diagnostic tools for infertility or infertility treatments in order to tailor fertility treatments appropriately to each patient to maximize the success rate and minimize side effects of fertility drugs.

 

Influence of the Gut Microbiome on the PCOS Metabolic Phenotype

Another focus of our research is to investigate the role of the intestinal microbial community (gut microbiome) in the etiology and development of the PCOS metabolic phenotype. While the gut microbiome is perturbed in individuals with obesity or type 2 diabetes, it is unclear whether the gut microbiome is dysregulated in women with PCOS and whether an altered microbiome influences the metabolic phenotype observed in PCOS. We recently demonstrated that there is a significant change in the gut microbiome of a letrozole-induced PCOS mouse model compared to placebo-treated mice, including changes in bacteria previously reported to be altered in mouse models of obesity. We are currently investigating mechanisms involved in the alteration of the gut microbiome in the PCOS mouse model using metagenomic sequencing and metabolic analyses. Understanding the role of the gut microbiome in PCOS may provide important insight into the pathology of the metabolic phenotype that occurs in PCOS women and the development of novel treatment options for women with PCOS, including pre- or probiotic therapies.

 

 

Honors/Awards

  • Women in Endocrinology Young Investigator Award, 2009
  • Endocrine Society Early Investigators Award, 2012

 

Recent Publications

 

For a full list of publications in PubMed click HERE