Obesity, Diabetes & Stress: New Research Findings
- New research from Rutgers Health indicates that stress hormones, rather than impaired insulin signaling, could be the key factor in obesity-related diabetes.
- Christoph Buettner, chief of endocrinology, metabolism and nutrition at Rutgers Robert Wood Johnson Medical School, said understanding the mechanisms by which obesity induces diabetes is a critical question,...
- The study reveals that overeating and obesity elevate the body's sympathetic nervous system, triggering a "fight or flight" response.
New research flips the script on how we understand diabetes. It suggests stress hormones, not impaired insulin signaling, are the primary driver of obesity-related diabetes. This groundbreaking study, published in Cell Metabolism, provides critical insight into an illness costing the U.S. billions.The study indicates overeating rapidly increases stress hormones, impacting metabolism substantially. Even while obese, mice lacking stress hormones avoided metabolic disease. This revelation challenges traditional approaches to managing insulin resistance, suggesting new avenues for treatment. News Directory 3 is covering this vital research that could explain why not all obese people develop diabetes and why stress exacerbates the disease. Discover whatS next in this interesting field.
Stress Hormones May Drive Obesity-Related Diabetes, Study Finds
Updated June 22, 2025
New research from Rutgers Health indicates that stress hormones, rather than impaired insulin signaling, could be the key factor in obesity-related diabetes. The study,published in Cell Metabolism,challenges conventional wisdom regarding the development and treatment of obesity-induced insulin resistance.
Christoph Buettner, chief of endocrinology, metabolism and nutrition at Rutgers Robert Wood Johnson Medical School, said understanding the mechanisms by which obesity induces diabetes is a critical question, given the diabetes epidemic’s $300 billion annual cost in the U.S.
The study reveals that overeating and obesity elevate the body’s sympathetic nervous system, triggering a “fight or flight” response. This, in turn, increases levels of norepinephrine and epinephrine, stress hormones that counteract insulin’s effects, even when cellular insulin signaling is functioning correctly. Researchers observed that norepinephrine levels increased within days of overeating in mice, demonstrating the rapid impact of excess food on the sympathetic nervous system.
To investigate the role of these hormones,scientists studied genetically engineered mice unable to produce catecholamines,stress hormones,outside their brains.Despite consuming a high-fat,high-sugar diet and becoming obese,these mice did not develop metabolic disease.This suggests that reducing stress hormones could be a new therapeutic approach to tackle insulin resistance, diabetes and metabolic disease.
“We were delighted to see that our mice ate as much because it indicates that the differences in insulin sensitivity and their lack of metabolic disease are not due to reduced food intake or reduced obesity but due to the greatly reduced stress hormones,” researchers said.
These findings may explain why some obese people develop diabetes while others do not, and why stress can worsen diabetes even without notable weight gain. Buettner noted that various stressors, including financial, marital, and environmental factors, can increase diabetes risk, synergizing with the metabolic stress of obesity. The study suggests that stress and obesity may share a common mechanism in causing diabetes through the actions of stress hormones.
While catecholamines’ ability to impair insulin action is known, the study suggests it may be the essential mechanism behind insulin resistance in obesity.The interplay between stress hormones and insulin has long been recognized, with stress hormones increasing blood glucose and lipids, while insulin lowers them. The research highlights that insulin signaling can remain intact even in insulin-resistant states, but the heightened activity of stress hormones overwhelms insulin’s effects.
What’s next
Buettner and Kenichi Sakamoto, assistant professor of endocrinology, plan human studies to validate these findings and explore the role of the sympathetic nervous system in other forms of diabetes, including Type 1. They also aim to study if short-term overfeeding increases insulin resistance with heightened sympathetic nervous system activation.