Kamran Atabai
University of California-San Francisco, CA·Physiology
Insulin resistance happens when the body's tissues stop responding well to insulin, the hormone that tells cells to take up sugar from the blood. It is becoming more common as obesity rises worldwide.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
insulin resistance
insulin sensitivity
type 2 diabetes
- Grants
- 1 known grant, through Jun 2027
What they work on
- Determine the cellular mechanism by which insulin moves MFGE8, a secreted protein, through the endoplasmic reticulum and Golgi to the muscle cell surface, where it binds the αvβ5 integrin.
- Test whether MFGE8–αvβ5 signaling raises the activity of PTP1β, a phosphatase enzyme, which removes activating phosphates from the insulin receptor (IRβ) and IRS1 and reduces GLUT4 sugar-transporter delivery and glucose uptake in skeletal muscle.
- Test whether systemic blockade of the β5 integrin or MFGE8 relieves insulin resistance in a mouse model of diet-induced obesity.
- Measure how much skeletal muscle MFGE8/β5 signaling contributes to normal (basal) insulin sensitivity and to obesity-induced insulin resistance in mice.
More about the research
It is a major risk factor for cardiovascular disease, which is the leading cause of illness and death in people with diabetes. This project asks how integrins, proteins on the cell surface that grip the surrounding tissue scaffold and pass signals into the cell, help control insulin sensitivity in skeletal muscle.
Why it matters
Insulin resistance drives type 2 diabetes and the heart disease that causes most diabetes-related illness and death. By mapping a pathway in which insulin switches on an integrin signal that later shuts insulin signaling down, this work could identify new drug targets, such as MFGE8 or the β5 integrin. Blocking these targets might restore insulin sensitivity in people with obesity-related diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Bo Wang
University of Illinois Urbana-Champaign, IL·Physiology
Examine how SEC16B, a scaffold protein on the endoplasmic reticulum, regulates the formation of lipid droplets (fat-storage bodies) in liver cells, using cell-culture and in vivo experiments.
Sona Kang
University of California-Berkeley, CA·Physiology
Define how FAM3D, a protein genetically linked to type 2 diabetes, suppresses heat production and mitochondrial function in mouse and human brown fat cells.
Dongmin Liu
Virginia Polytechnic Institute and State University, VA·Pharmacology
Characterize the anti-diabetic and anti-obesity effects of daily oral elenolic acid in diet-induced obese and db/db diabetic mice, using metabolic profiling and euglycemic-hyperinsulinemic clamps to measure insulin sensitivity.
The school
University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.
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