A study conducted by Rutgers Health and other institutions in the United States of America revealed that stress hormones may be behind the occurrence of obesity-related diabetes. The research paper, published in the journal Cell Metabolism on October 21, may change our understanding of how insulin resistance caused by obesity develops and how it is treated.
Insulin resistance
Insulin is a hormone secreted by the pancreas that facilitates the entry of glucose (blood sugar) into cells throughout the body, where it is converted into energy. After eating, the level of glucose in the bloodstream rises, and in response, the pancreas releases insulin into the bloodstream to help the glucose reach the cells it needs. This process returns the amount of sugar in the bloodstream to normal.
Insulin resistance occurs when the body does not respond well to insulin and glucose is less able to enter cells. In this case, the pancreas continues to pump out more insulin but glucose still has difficulty reaching the cells, causing blood sugar levels to rise.
Scientists have long believed that obesity causes diabetes by causing malfunctioning of insulin signaling within liver and fat cells. New research shows that overeating and obesity increase the activity of the body’s sympathetic nervous system – responsible for the “fight or flight” response – and that increased levels of the stress hormones norepinephrine and epinephrine antagonize the effects of insulin, although cellular insulin signaling remains It works.
Excess food increases stress hormones
The authors observed that overeating in normal mice increased the stress hormone norepinephrine within days, indicating how quickly excess food stimulates the sympathetic nervous system.
To find out what effect this excess hormone production has in stimulating the development of the disease, the researchers used a new type of genetically modified mice that are normal in every way except that they cannot produce stress hormones outside of their brains and central nervous systems.
The researchers fed these mice food containing a lot of fats and sugars that cause obesity, but although they ate the same number of calories and became obese as normal mice, they did not develop metabolic diseases such as diabetes.
The new findings may help explain why some overweight individuals develop diabetes while others do not, and the possibility that stress may worsen diabetes even when slightly overweight.
Dr. Christoph Buettner, Chairman of the Department of Endocrinology, Metabolism, and Nutrition at Robert Wood Johnson Medical School at Rutgers University and co-researcher of this study – according to the Eureka Alert website – says: “Our discovery that obesity leads primarily to the development of metabolic diseases through an increase in stress hormones provides “New insight into the common basis of all these factors that increase the risk of diabetes. Stress and obesity, essentially, work through the same basic mechanism in causing diabetes, through the action of stress hormones.”

Stress hormones work against insulin
Stress hormones can impair insulin action, and the new study suggests that this impairment may be the primary mechanism underlying insulin resistance in obesity.
Stress hormones increase glucose and fats in the bloodstream, while insulin reduces them. An unexpected finding of the new study is that insulin signaling can remain intact even in conditions of insulin resistance such as obesity.
But the problem lies in the increased activity of stress hormones that increase blood sugar levels, and although the level of insulin action remains the same, the accelerated effect of stress hormones overwhelms the effect of insulin in reducing blood sugar.