Obesity Begins in the Brain

A recent study has provided new insights into the role of the brain as a crucial control center and the origin of obesity and type 2 diabetes. The hormone insulin plays a key role in the development of obesity. The brain’s sensitivity to insulin is linked to long-term weight gain and unhealthy body fat distribution. What are the specific functions of insulin in the brain and how does it affect people of normal weight?

The Brain Plays a Central Role in the Development of Obesity

The number of obese people has increased significantly in recent decades, causing considerable difficulties for those affected, healthcare systems and those treating them. The hormone insulin plays a key role in the development of obesity. Until recently, there was ample evidence that insulin causes neurodegenerative and metabolic disorders, particularly in the brain. A recent study by the University Hospital of Tübingen, the German Center for Diabetes Research (DZD) and the Helmholtz Center Munich offers fascinating new insights into the development of type 2 diabetes and obesity and the function of the brain as a critical control center.

Obesity has only been officially recognized as a disease in Germany since 2020, although it has long been known to cause a number of diseases, including diabetes, heart attacks and even cancer. The World Health Organization has already declared obesity to be an epidemic, affecting over one billion people worldwide and almost 16 million in Germany alone. A body mass index of 30 or more is considered obese, and poor diet and insufficient exercise are often cited as causes of this chronic disease. However, the mechanisms in the body that lead to obesity and cause the disease are more complex.

Obesity and the Role of Insulin in the Brain

Unhealthy body fat distribution and chronic weight gain are linked to the brain’s sensitivity to insulin. What specific functions does insulin perform in the brain and how does it affect people of normal weight? In their study, Prof. Dr. Stephanie Kullmann and her colleagues at the University Hospital for Diabetology, Endocrinology and Nephrology in Tübingen have found the answer to this question. “Our results show for the first time that even short-term consumption of highly processed, unhealthy foods (such as chocolate bars and potato chips) causes a significant change in the brain of healthy individuals, which may be the cause of obesity and type 2 diabetes,” says study leader Prof. Kullmann. In a healthy state, insulin has an appetite-suppressing effect in the brain.

However, in people with obesity in particular, insulin no longer regulates eating behavior properly, which leads to insulin resistance. Interestingly, according to Kullmann, the brain of the healthy study participants shows a similar decrease in insulin sensitivity after a short-term high calorie intake as in people with obesity. This effect can even be observed a week after returning to a balanced diet. She is also deputy head of the Department of Metabolic Neuroimaging at the DZD partner Institute for Diabetes Research and Metabolic Diseases (IDM) of Helmholtz Zentrum München at the University of Tübingen.

Prof. Dr. Andreas Birkenfeld, Medical Director of Internal Medicine IV, Director of the IDM and DZD Board Member and last author of the study, summarizes: “We assume that the brain’s insulin response adapts to short-term dietary changes before weight gain occurs, thus promoting the development of obesity and other secondary diseases.” In view of the current findings, he calls for more research into how the brain contributes to the development of obesity and other metabolic diseases.

Far-Reaching Consequences

29 male volunteers of average weight took part in the study and were divided into two groups. For five days, the first group had to supplement their normal diet with 1500 kcal from highly processed, high-calorie snacks. The additional calories were not consumed by the control group. After an initial assessment, both groups underwent two separate examinations. One examination was carried out immediately after the five-day period and another seven days after the first group had resumed their normal diet.

The researchers used magnetic resonance imaging (MRI) to examine the fat content of the liver and the insulin sensitivity of the brain. It was not only the fat content of the liver of the first group that increased significantly after five days of increased calorie intake. Surprisingly, the significantly lower insulin sensitivity in the brain compared to the control group also persisted one week after the return to a normal diet. This effect had previously only been observed in overweight people.

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