PIPages
Labs

Yumei Feng Earley

University of Rochester, NY·Neuroscience

Type 2 diabetes accounts for about 90–95% of diagnosed diabetes in the United States, yet the brain's role in controlling blood sugar is still poorly understood. This project asks whether a hormone system in the brain, best known for regulating blood pressure, also helps set blood glucose levels.

Fields

Neuroscience

Physiology

Pharmacology

Topics

type 2 diabetes

glucose homeostasis

blood glucose

Grants
1 known grant, through Apr 2027

What they work on

  1. Test whether (pro)renin receptor (PRR) signaling in tyrosine hydroxylase-positive neurons of the hypothalamus (THPVN neurons) impairs glucose balance, using neuron-specific targeting and wireless blood glucose monitoring in mice.
  2. Determine whether activating or silencing THPVN neurons changes blood glucose, using DREADDs, engineered receptors that switch neurons on or off with a designer drug.
  3. Define the molecular and synaptic mechanisms by which PRR alters THPVN neuron activity, using electrophysiology recordings in brain slices.
  4. Test whether this PRR-driven autonomic pathway contributes to impaired glucose metabolism during high-fat diet consumption, including effects on liver glucose metabolism.

More about the research

If it does, it could help explain how type 2 diabetes develops.

Why it matters

Type 2 diabetes is the most common form of diabetes. By showing how a brain circuit and the (pro)renin receptor may push blood sugar up, especially on a high-fat diet, this work could reveal a new therapeutic target for type 2 diabetes. It could also clarify how the brain and liver together contribute to glucose control in people with this disease.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Neural mechanisms regulating glucose homeostasis

NIH · Jul 2024 – Apr 2027

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Test whether activity in the pathway from stress-hormone CRH neurons in the hypothalamus to the brainstem's nucleus of the solitary tract is increased in chronically epileptic mice at risk of SUDEP.

Teresa A Milner

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Test whether altered GluA1 signaling in PVN neurons contributes to angiotensin II-induced hypertension in post-AOF mice. GluA1 is part of AMPA glutamate receptors, which relay fast excitatory signals between neurons.

The school

University of Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.

More about University of Rochester

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