How obesity leads to diabetes
Faulty insulin activity might not be driving diabetes in people with obesity, a new study hints. Instead, consuming a high-fat diet triggers a surge of neurotransmitters across the body, leading to the rapid breakdown of fatty tissue in the liver. Neurotransmitters are your body’s chemical messengers. They carry messages from one nerve cell across a space to the next nerve, muscle or gland cells. These messages help you move your limbs, feel sensations, keep your heart beating, and take in and respond to all information your body receives from other internal parts of your body and your environment.
People with obesity are ten times more likely to develop diabetes compared to lean people. Researchers trying to understand why have found an answer in the same system that drives the body’s fight-or-flight response. The findings, in mice, challenge long-held assumptions about how eating too much can make you sick.
A recent study suggests that consuming a high-fat diet triggers a surge of neurotransmitters across the body, leading to the rapid breakdown of fatty tissue in the liver, a process usually kept checked by the release of insulin. The liberation of high levels of fatty acids is linked to a host of health conditions, from diabetes to liver failure.
Researchers previously thought that the main problem in obesity-driven diabetes was faulty insulin activity, which means that the body cannot stop the dangerous release of fatty acids. But, instead of the brakes not functioning, the study finds that there is a separate lever, neurotransmitters in the liver and other tissues, pressing hard on the accelerator. This is indeed a paradigm shift. More than 890 million people worldwide have obesity, which is a major risk factor for developing diabetes and other metabolic disorders. Researchers have long known that the disease progresses when insulin stops reducing glucose levels in the blood.
Researchers from Rutgers University had been studying the role of insulin in the brain in regulating metabolism for a long time, so they turned their attention to the sympathetic nervous system, which delivers neurotransmitters such as norepinephrine to tissue all over the body. The researchers used a mouse model that they had previously developed, in which they deleted a gene that expresses a key enzyme required to produce these neurotransmitters. The gene was deleted in only the mouse’s limb and some organs, not its brain, to ensure it could survive.
The researchers gave the modified mice a diet rich in fats such as lard, coconut oil and soybean oil. During more than two months of observation, both modified and unmodified mice ate just as much food, gained similar amounts of weight and maintained similar insulin signalling activity, which is the cascade of events that takes place after insulin binds to its target receptor on a cell.
But the modified mice didn’t have increased signs of fatty liver and tissue inflammation. The unmodified mice, on the other hand, developed insulin resistance, which can lead to diabetes. They also showed increased signs of inflammation and liver disease.
These findings suggest that neurotransmitters are responsible for driving insulin resistance, and associated problems. They are now exploring the role of these neurotransmitters in other conditions, such as insulin resistance caused by menopause.
This study is pretty solid, but there are still some missing puzzle pieces. For example, the question now is how the high-fat diet triggers the surge in neurotransmitters.