A groundbreaking study from Rutgers University has uncovered new insights into how obesity causes type 2 diabetes.
The research suggests that the stress hormones norepinephrine and epinephrine may be key drivers of insulin resistance rather than the previously assumed impaired cellular insulin signaling.
Published in Cell Metabolism the findings in a mouse study could transform our understanding of obesity-induced diabetes and open up new treatment possibilities.
Role of stress hormones
Traditionally, scientists believed that obesity led to type 2 diabetes by impairing insulin signaling within liver and fat cells.
Insulin resistance occurs when the body’s cells do not respond effectively to insulin, making it difficult to regulate blood sugar levels.
However, this new study challenges that notion. Researchers have found that overeating and obesity activate the sympathetic nervous system (SNS) – the body’s “fight or flight” response.
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This triggers the release of stress hormones like norepinephrine, which interfere with insulin’s ability to regulate blood sugar and fat, even when cellular insulin signaling remains intact.
Key findings
The research team observed that just days of overeating in normal mice led to a significant increase in norepinephrine levels.
This rapid rise highlights how quickly excessive food intake can stress the SNS. To explore this further, scientists used genetically engineered mice that could not produce stress hormones outside of their brains and central nervous systems.
Despite consuming a high-fat, high-sugar diet and becoming as obese as regular mice, these special mice did not develop metabolic diseases such as type 2 diabetes.
Dr. Christoph Buettner, the study’s senior author and chief of endocrinology, metabolism, and nutrition at Rutgers Robert Wood Johnson Medical School, noted, “Our mice ate as much, indicating that the difference in insulin sensitivity wasn’t due to reduced food intake or lower obesity but rather the absence of stress hormones counteracting insulin.”
Stress and obesity link
This discovery sheds light on why some obese individuals develop diabetes while others do not.
It also highlights how various stressors, such as financial strain, relationship problems, or physical stress from factors like alcohol consumption, can worsen diabetes risk, even without significant weight gain.
Buettner explains that “Stress and obesity, in essence, work through the same basic mechanism in causing [type 2] diabetes through the actions of stress hormones.”
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Catecholamines, the group of stress hormones that includes norepinephrine and epinephrine, are known to increase glucose and lipids in the bloodstream, directly opposing insulin’s function of lowering them.
Implications
These findings point to the potential for new diabetes treatments targeting stress hormone reduction rather than focusing solely on insulin signaling.
Current medications that lower catecholamines, typically used to treat high blood pressure, have not been effective for type 2 diabetes. Buettner suggests this may be due to the complexity of how these drugs interact with the body and the brain.
To validate these results, researchers plan to conduct human studies.
They are particularly interested in how short-term overeating such as weight gained over the holidays might activate the SNS and contribute to insulin resistance.
