Karuna Rasineni
University of Nebraska Medical Center, NE·Physiology
Heavy drinking often causes fat to build up in liver cells, a condition called steatosis or fatty liver. It is the earliest stage of alcohol-associated liver disease and is usually reversible, but it is thought to lead to scarring, cirrhosis and liver cancer.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
alcohol-associated liver disease
alcohol-associated fatty liver disease
hepatic steatosis
- Grants
- 1 known grant, through May 2027
What they work on
- Determine how alcohol-induced ghrelin alters gut-liver communication through GLP-1, a gut hormone that regulates energy use, and whether ghrelin blocks GLP-1's effects on liver cell metabolism during alcohol-associated fatty liver.
- Test whether ghrelin drives fatty liver through the fat tissue-liver axis by increasing fat breakdown and lowering release of adiponectin, a protective hormone from fat cells, using alcohol-fed rats including ghrelin receptor knockouts.
- Examine how alcohol-induced ghrelin lowers LEAP-2, a natural blocker of the ghrelin receptor, and whether this loss strengthens ghrelin signaling and fat buildup in the liver.
More about the research
Fatty liver does not arise from the liver alone: the gut, pancreas and fat tissue all send hormone signals that affect it. This project asks how one gut hormone, ghrelin, coordinates these organs to drive alcohol-related fatty liver.
Why it matters
Fatty liver is the earliest and most reversible stage of alcohol-associated liver disease, which can progress to cirrhosis and liver cancer. Understanding how the hormone ghrelin links the gut, fat tissue and liver could reveal targets for therapies that may prevent or slow alcohol-associated liver disease in people who drink heavily.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Elif Oral
University of Michigan, MI·Medicine & Clinical Research
Test in a randomized clinical trial whether tirzepatide, a drug that activates GLP1 and GIP gut-hormone receptors, improves body weight and fat mass in patients with familial partial lipodystrophy (FPLD).
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.
The school
University of Nebraska Medical Center: 20 labs on PI Pages, $657M a year on research, 82 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.