U.S. Department of Health and Human Services

 Contact Info

Tel: 240-274-9150
Email: vipulp@mail.nih.gov

 Select Experience

  • Assistant ProfessorPhysics Department, Princeton University1993-2001
  • MemberThe Institute for Advanced Study1991-1993
  • Research PhysicistInstitute for Theoretical Physics, University of California1988-1991
  • Ph.D.Princeton University1988
  • M.A.Princeton University1984
  • B.S.California Institute of Technology1983

 Related Links

  • Computational Biology
  • Physics/Biophysics
  • Systems Biology
Research Summary/In Plain Language

Research in Plain Language

Insulin resistance is a major risk factor for several common diseases.  These include diabetes, heart disease, high blood pressure, and some forms of cancer.  Scientists do not yet understand how cells become insulin resistant.  Our research group studies three processes related to insulin resistance.

We study problems in insulin’s ability to control the breakdown of fat.  This leads to increased levels of free fatty acids (FFA) in the blood.  With elevated FFA levels, insulin does not work as well as it should in tissues or cells.  A way to measure insulin’s effects on fat break down and blood FFA levels would help monitor various conditions of insulin resistance.  We are developing an index to show how FFA levels respond to insulin.  Many disease complications relate to oxidative stress.  These include problems associated with diabetes, Parkinson's, Alzheimer's, and hardening of the arteries.  In oxidative stress, the body cannot remove toxins and repair damage caused by reactive oxygen species (ROS).  But ROS are not always bad.  ROS signaling is important in how cells work.  Cellular structures that produce energy, mitochondria, have ROS but do not show oxidative stress.  Using math, we develop models to describe how this happens.  The goal is to understand the damage of oxidative stress in insulin resistance and obesity.

Our research also aims to understand how fat tissue growth relates to insulin resistance and diabetes.  Fat tissue grows in two ways—when the number of cells increase and when the size of cells increase.  How do genetics and diet affect the number and size of fat cells in obesity?  We focus on the role played by particular agents that increase insulin sensitivity.  Using math, we model changes in fat cell size over time under several conditions.  This work will provide a global view of fat cell size and fat tissue growth in conditions featuring insulin resistance.