As overeating leads to type 2 diabetes: the role of neurotransmitters
As overeating leads to type 2 diabetes: the role of neurotransmitters
People with obesity have a ten -time risk of developing diabetes compared to slim people. Researchers who wanted to get to the bottom of this phenomenon have found an answer in the same system that controls the body's combat or escape reaction. The results 1 , which were determined on mice, long-cherished assumptions in question of how excessive food can lead to diseases.
The study suggests that consumption of a high-fat diet triggers an increase in neurotransmitters throughout the body, which leads to a quick breakdown of adipose fabric in the liver-a process that normally by distributing Insulin . The release of high quantities of fatty acids is associated with a number of health problems, from diabetes to liver failure, 2 .
In the past, researchers thought that the main problem with obesity-related Diabetes lies in incorrect insulin activity, which means that the body does not stop the dangerous release of fatty acids. However, according to the latest study, it can be seen that instead of a non -functioning "brake system" there is a separate lever - neurotransmitter in the liver and other tissues - who are violently pressing on the accelerator, explains Martina Schweiger, biochemist at the University of Graz, Austria. "This is actually a paradigm shift."
The study was published in Cell Metabolism on October 21st.
insulin resistance
worldwide are more than 890 million people of Objection affected that a is a great risk for the development of diabetes and other metabolic disorders. Researchers have known for a long time that the disease progresses , if insulin is no longer able to reduce blood sugar levels. Christoph Buettner and Kenichi Sakamoto, both physiologists at the Rutgers University in New Brunswick, New Jersey, and her colleagues wanted to better understand the nature of this insulin resistance.
Buettner had long examined the role of insulin in the brain when regulating the metabolism 3 . Therefore, his team concentrated on the sympathetic nervous system, which transports neurotransmitter such as noradrenaline in tissue throughout the body. The researchers used a mouse model in which they deleted a gene that expressed a key enzyme for the production of these neurotransmitters. The gene was only deleted in the limbs and some organs of the mouse, but not in the brain to ensure that it remained survival.
The modified mice received a high -fat diet with lard, coconut oil and soybean oil. Over a period of more than two months, both the modified and the unmodified mice ate as much food, increased comparable amounts of weight and showed a similar insulin signaling activity that the cascade of events describes after insulin binds to its target receptor on a cell.
The modified mice, however, did not show any increased degradation of adipose tissue and no insulin resistance and ultimately showed no increased signs of fatty liver and tissue infections. In contrast, the unmodified mice developed insulin resistance, which can lead to diabetes. They also showed increased signs of inflammation and liver diseases.
signals in the brain
The results indicate that neurotransmitters are responsible for creating insulin resistance and associated problems, says Buettner. He and his colleagues are now researching the role of these neurotransmitters in other conditions, such as insulin resistance caused by menopause.
"This study is quite well -founded", says Schweiger, but "there are still a few puzzle pieces". The question of how the high -fat nutrition triggers the increase in neurotransmitter remains to be clarified.
It adds that additional work is necessary to better understand the implications of the results for people. So far, medication that blocks the activity of the neurotransmitters in the sympathetic nervous system has shown no advantages in overweight people. It could be possible that targeted administration of these drugs in specific tissue, whereby the brain is avoided, could be more promising, says Buettner.
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Sakamato, K. et al. Cell Metab. https://doi.org/10.1016/J.cmet.2024.09.012 (2024).
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Saponaro, C., Gaggini, M., Carli, F. & Gastaldelli., A. Nutrents 13, 9453–9474 (2015).
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Sherer, T. et al. Journal of Biological Chemistry 287, 33061–33069 (2012).