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Kartik Shankar, PhD, DABT


​Visiting Professor of Pediatrics
Section of Nutrition
University of Colorado School of Medicine

 

Assistant Director for Basic Research
Lifecourse Epidemiology of Adiposity & Diabetes (LEAD) Center
 
University of Colorado Denver – Anschutz Medical Campus
12700 East 19th Ave
Research Complex 2, Room 5121
Aurora, CO  80045
 
Email: Kartik.Shankar@CUAnschutz.edu  
Work Phone:  303-724-3796
 
Biosketch_Shankar-Aug2019.pdfBiosketch_Shankar-Aug2019.pdf
 

Education & Certifications

  • Diplomate, American Board of Toxicology (Board Certification)
  • Postdoctoral fellowship, University of Arkansas for Medical Sciences, Nutrition and Pregnancy
  • Ph.D., University of Monroe Louisiana, Toxicology
  • B. Pharm., University of Mumbai, Mumbai India, Pharmaceutical Sciences
 

Research Interests

The Shankar Maternal-Child Nutrition Lab conducts research leading to fundamental understanding of the role of maternal and early nutrition in development of obesity, metabolic disease and associated co-morbidities. The laboratory leverages a wide range of experimental approaches including animal models, clinical studies, cell and molecular techniques, and physiological approaches. We widely utilize high-dimensional “-omics” methods to comprehensively understand biological mechanisms of developmental programming.
 
We collaborate extensively with multidisciplinary groups to understand offspring physiology and placental biology. Our work has begun to elucidate the nature and mechanisms by which maternal obesity and diet impact the offspring, including new insights regarding epigenetic and microbiome changes that can occur in offspring in response to maternal obesity, diet and physical activity.
 

Ongoing Projects

Maternal Obesity & The Offspring
As the prevalence of obesity increases, so does the incidence of maternal overweight during pregnancy. A major area of investigation in our lab is to understand the developmental origins of childhood and adult obesity, specifically the long-term consequences of maternal obesity. Using genetic manipulations in mouse models of maternal obesity, an important goal is to examine the roles of specific obesity-associated changes (inflammation in utero; maternal and offspring gut microbiome; nutrient transport; and lipotoxicity in the placenta) as causative mechanisms leading to epigenetic changes. The overall objective of these studies is to gain a better mechanistic understanding of the physiological basis of fetal programming.
 
Sex differences in Development and Developmental Programming
Sex underlies ubiquitous differences observed in many aspects of physiology, development and disease susceptibility, with far-reaching public health consequences. In the context of developmental programming, sexually dimorphic differences have been frequently observed in offspring following maternal dietary and nutritional exposures in both human and animal studies. Despite the ubiquitous evidence, underlying mechanisms contributing to sex differences in offspring remain sparse. We are using genetic and systems biology tools to examine the extent and underlying pathways contributing to sex differences in the placenta and developing offspring.
 
Obesity & The Placenta
The proper development of the placenta is critical to the health of the baby. The placenta also may be central in determining the long-term health of the baby. We are currently studying the effects of maternal obesity on the development and function of the placenta in animal models and in samples from human subjects at the end of pregnancy. This provides a unique “window” into the intrauterine environment, and molecular changes in the placenta may report on similar changes that occur in the tissues of the offspring.
  
Epigenetic Mechanisms of Placental Development
The development of the hemochorial type of placenta (found in humans and rodents) critically depends on the formation of the syncytiotrophoblast (STB), which serves as the definitive materno-fetal barrier. Formation and constant renewal of the syncytium occurs via cell-syncytial fusion of the underlying mononuclear cytotrophoblasts (CTB). Hence, the process of syncytialization is critical to the integrity of the STB and in maintaining the essential functions of the placenta. Using a combination of genome-scale methods (RNA-seq, ChIP-seq) and systems biology tools, in conjunction with genetic loss-of-function approaches, we are characterizing novel epigenetic processes required for syncytial fusion.
 

Complete list of published work in My Bibliography:

(list of 111)
  
https://www.ncbi.nlm.nih.gov/sites/myncbi/kartik.shankar.1/bibliography/40642557/public/?sort=date&direction=descending
 

Research Support

Active:
  1. National Institute of Child Health and Development, 1R21HD086194-01 Role: PI, “Epigenetic Mechanisms Underlying Trophoblast Syncytialization”, Years 1-2. 2.4 cal months. Period of Support 08/2017 - 07/2019. (No cost extension).
  2. National Institutes of Health / University of Utah, R01 (PI: Pon Velayuthan AB) Role: Co-I, “Biological Signatures of blueberry derived microbial metabolites”, Years 1-5. 0.3 cal months. Period of Support 08/2018 - 07/2021.
  3. National Institutes of Health/ Kansas University Medical Center (PI: John Thyfault) Role: Co-I, “Aerobic Fitness, Mitochondrial Dysfunction, and Fatty Liver Disease”, Years 1-5, 1.8 cal months. Period of support 07/2019 – 06/2024.
 
Completed:
  1. United States Department of Agriculture. ARS Project CRIS # 6251-51000-005-02S-3A, “Interventions to Mitigate Maternal Obesity-Associated Programming”. Role: PI.  Period of Support 2014 - 2019. This project is aimed at addressing if specific dietary / lifestyle interventions will mitigate maternal obesity associated programming. Studies in this project are evaluating the efficacy of probiotics, PUFA and physical activity on the offspring.
  2. National Center for Advancing Translational Sciences. “COBRE Center for Childhood Obesity Prevention”. Role: Co-I (PI: Judy Weber). Years 1-5. 0.6 cal months. Period of Support 01/2017 – 07/2019.
  3. National Institute of Diabetes and Digestive and Kidney Diseases, R01 DK084225 “Maternal Overweight: Consequences for Insulin Signaling in Offspring”, Role: PI. Period of Support 07/2009-05/2014.  This project investigates the influence of maternal obesity on insulin signaling in rat offspring. Using labeled tracers, these studies are investigating if maternal obesity redirects nutrient flux to adipose tissue rather than skeletal muscle, thus favoring adipose accretion.
  4. United States Department of Agriculture. ARS Project CRIS # 6251-51000-005-02S-3A, “Prevention of Obesity in the Offspring of Obese Mothers”. Role: PI.  Period of Support 2009 - 2014. This project is aimed at addressing if maternal obesity leads to intergenerational-transmission of obesity to the F2 and F3 generations. Studies in this project are also examining the effect of gestational obesity in a rat model on placental and embryonic development.
  5. United States Department of Agriculture. ARS Project CRIS # 6251-51000-005-02S-3B. Role: Co-I, Effects of maternal body composition on offspring body phenotype: potential fetal programming (Glowing Study). 2009 – 2014.
  6. National Institute of Alcohol Abuse and Alcoholism, R01 AA018282 “The role of oxidative stress in alcohol-induced bone resorption” Role: Co-I (PI: Martin J. Ronis). Period of Support 07/2009 - 05/201National Institute of Health, National Center for Research Resources, University of Arkansas for Medical Sciences Translational Research Institute Pilot Award (#1UL1RR029884). Role: Co-I, “Effects of maternal adiposity on oocyte gene expression” 4/1/2011 – 8/1/2012. PI: A. Andres.