Obesity Inflammation Trigger Identified by Scientists
- Researchers at Weill Cornell Medicine have identified teh protein FAM20C as a key trigger for inflammation in fat cells, perhaps leading to Type 2 diabetes in individuals with...
- James Lo, Rohr Family Clinical Scholar and an associate professor of medicine at Weill Cornell Medicine, found that FAM20C acts as a "switch" activating inflammation and insulin resistance.
- Obesity is a major risk factor for Type 2 diabetes, fatty liver disease, and heart disease.
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FAM20C Protein Linked to Inflammation and Insulin Resistance in Obesity
Table of Contents
Published November 12, 2025, at 16:56:32 EST
What Happened?
Researchers at Weill Cornell Medicine have identified teh protein FAM20C as a key trigger for inflammation in fat cells, perhaps leading to Type 2 diabetes in individuals with obesity. Published on October 28, 2023, in the Journal of Clinical Investigation, the study demonstrates that inhibiting or removing the FAM20C gene in obese mice improved their metabolic health, reduced inflammation, and increased insulin sensitivity – even without weight loss.
The research team,led by Dr. James Lo, Rohr Family Clinical Scholar and an associate professor of medicine at Weill Cornell Medicine, found that FAM20C acts as a “switch” activating inflammation and insulin resistance. First author Ankit Gilani, a research associate in medicine, explained the protein was identified while searching for genes activated in inflamed fat cells of obese mice. FAM20C is a kinase, a protein that adds phosphate groups to other proteins, altering their function.
Why Does This Matter?
Obesity is a major risk factor for Type 2 diabetes, fatty liver disease, and heart disease. Chronic inflammation in fat tissue is a central component of the metabolic dysfunction associated with obesity. This study identifies a specific molecular mechanism driving this inflammation, offering a potential new therapeutic target. Current treatments often focus on weight loss or managing symptoms; targeting FAM20C could address the underlying inflammatory process, potentially improving metabolic health even in the absence of important weight reduction.
The study’s findings suggest that inhibiting or eliminating FAM20C in fat cells can promote a healthier metabolic state. This could involve developing drugs that specifically block the activity of FAM20C or using genetic therapies to reduce its expression in fat tissue.
How Was the Study Conducted?
the Weill Cornell Medicine team used a combination of genetic and biochemical techniques to investigate the role of FAM20C in fat cell inflammation. They began by identifying FAM20C as a gene upregulated in the fat cells of obese mice.Subsequently, they used genetic tools to either remove the Fam20c gene entirely or block its expression in these mice. The researchers then compared the metabolic health of these modified mice to that of control mice.
Key measurements included:
- Insulin Sensitivity: Assessing how effectively cells respond to insulin.