A significant discovery has emerged in the scientific quest to understand the relationship between obesity and diabetes. Obese individuals are found to be 10 times more likely to develop diabetes compared to their underweight counterparts, prompting extensive research to uncover the fundamental connection.
Traditionally, it was believed that the core issue in obese diabetes was abnormal insulin activity, with the body unable to halt the perilous release of fatty acids. However, a recent study led by a team involving Rutgers University New Brunswick in the United States has challenged this view. The new research indicates that the problem lies not in a “brake failure” but rather in the “accelerator” – a sudden increase in neurotransmitters within the liver and other tissues. The focus has shifted to the sympathetic nervous system, which triggers the body’s “fight or flight” response. It has been determined that a high-fat diet prompts a surge of neurotransmitters throughout the body, leading to the rapid breakdown of liver fat tissue, a process typically regulated by insulin release.
The study zeroed in on insulin resistance, a well-known factor in the progression of diabetes when insulin fails to effectively lower blood sugar. The research team delved into the nature of insulin resistance by examining the role of the sympathetic nervous system, which distributes neurotransmitters like norepinephrine to tissues. Mice with genetically edited neurotransmitters were fed a diet rich in fats such as lard, coconut oil, and soybean oil. Over a two-month observation period, both the edited and unedited mice consumed similar amounts of food, gained comparable weights, and exhibited similar insulin signaling. However, the gene-edited mice did not experience an increase in adipose tissue breakdown or insulin resistance and did not develop fatty liver disease or tissue inflammation, while the unedited mice showed signs of insulin resistance, inflammation, and liver disease. This clearly points to neurotransmitters as the culprits behind insulin resistance and related issues.
Despite these revelations, scientists note that drugs blocking the activity of sympathetic nervous system-associated neurotransmitters have not yet demonstrated benefits in obese individuals. However, there is hope that if these drugs can be targeted to specific tissues while avoiding the brain, they may hold more promise in the future treatment of obesity-related diabetes.
