Cairo: Hani Kamal El-Din
Researchers from Rutgers University have uncovered that stress hormones, rather than insulin signal disruption, might be at the core of diabetes development in individuals with obesity. The findings of the study were published in Cell Metabolism journal.
For a long time, it was believed that obesity led to diabetes through a disruption in insulin signaling in the liver and fat cells. However, American researchers have proposed that overeating causes the disease in an entirely different way. They hypothesized that excess weight increases the activity of the sympathetic nervous system, which triggers the “fight or flight” response. This counters the blood sugar-lowering effect of insulin, even if its signaling system is functioning correctly.
Experiments on mice confirmed that overeating rapidly raises the levels of the stress hormone norepinephrine, activating the sympathetic nervous system within just a few days. To delve deeper into the mechanism, the researchers used genetically modified rodents that could not produce catecholamines (stress hormones) outside of the central nervous system. These mice, when fed a high-calorie diet, gained weight just like regular mice, but they did not develop metabolic diseases such as diabetes.
The study authors highlighted that various types of stress—be it financial, social, or physical (e.g., alcohol abuse)—can increase the risk of diabetes and intensify the metabolic stress associated with obesity in humans.
“The activity of stress hormones can be compared to pressing the gas pedal, which increases sugar and fat levels in the blood,” explain the researchers. Meanwhile, insulin, which acts as a brake, remains at the same level and becomes unable to counteract the effect of catecholamines.
This discovery sheds light on the interaction between stress, obesity, and diabetes, offering new pathways for the development of therapies aimed at reducing hormonal activity and preventing metabolic disorders.
