Philipp Scherer
University of Texas Southwestern Medical Center, TX·Physiology
Fat tissue does far more than store energy. It soaks up fatty acids after a meal and releases them when the body needs fuel.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
adipose tissue
adipocytes
fat cells
- Grants
- 3 known grants, through Apr 2030
What they work on
- Adjust insulin signaling only in mouse fat cells, by lowering insulin receptor levels on demand, switching on an artificial insulin receptor, or manipulating the signaling brake PTEN. Measure the effects on whole-body metabolism.
- Use β-KIR6.2V59M and β-mitoKiller mice, whose pancreatic β-cells release less insulin, to test how reduced insulin from the pancreas changes insulin signaling in fat cells.
- Test whether fat cell insulin responsiveness is needed for the weight loss and metabolic benefits of drugs that activate GLP-1, GIP and glucagon receptors, using mice with insulin-resistant fat cells.
- Determine how insulin and β-adrenergic (adrenaline-type) signaling control leptin production and release from fat cells. Examine whether leptin promotes inflammation and scarring in the liver, kidney and lung.
- Find the lowest circulating leptin level that triggers energy-conserving responses, using leptin-deficient ob/ob mice in which leptin levels can be set with dosed treatment.
- Test how mitochondrial stresses in white fat cells feed into the Integrated Stress Response, a cellular alarm system, with and without its mitochondrial sensor DELE1. The stresses include loss of mitochondrial DNA and iron overload from mitoNEET or mitoferritin.
- Determine how mitochondrial stress and endoplasmic reticulum stress interact in fat cells. Test whether they drive the release of mitochondrial fragments in exosomes and reduce adiponectin secretion.
More about the research
This protects other organs from fat overload. It also sends hormones throughout the body. When fat cells (adipocytes) stop working well, the liver, pancreas and other organs suffer, which contributes to obesity, diabetes and heart disease. These grants ask what makes a fat cell healthy. They study three topics: how fat cells respond to insulin, how the fat hormone leptin is controlled and acts on other organs, and how stress inside a fat cell's mitochondria (its energy-producing compartments) disrupts its function. Most of the work uses specially engineered mice in which a single pathway can be switched up or down in a specific cell type at a chosen time.
Why it matters
Obesity, type 2 diabetes and cardiovascular disease are rising, and healthy fat tissue is central to preventing them. This work could show whether new weight-loss drugs targeting GLP-1, GIP and glucagon receptors work partly through fat cells. It could help set safe, effective targets for future leptin-lowering treatments that may reduce weight and inflammation and scarring in organs. It could also point to mitochondrial stress pathways in fat cells as new targets for anti-diabetic and anti-cardiovascular therapies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jonathan Campbell
Duke University, NC·Physiology
Test whether pericytes, cells lining blood vessels, are the main GIP receptor (GIPR)-expressing cells in fat tissue, using mouse models that mark and lineage-trace GIPR-positive cells over time.
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.
Bethany Cummings
University of California-Davis, CA·Physiology
Compare liver and islet responses to injected glucagon in obese mice and after dietary or bariatric-surgery weight loss, to test whether α-cell signaling shifts from the liver to insulin secretion.
The school
University of Texas Southwestern Medical Center: 40 labs on PI Pages, $869M a year on research, 86 research doctorates a year.
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