A recent study led by Rutgers Robert Wood Johnson Medical School has uncovered a key factor in how overnutrition, or overeating, contributes to insulin resistance, a condition that often leads to type 2 diabetes.
Researchers found that in cases of high-fat diets, the sympathetic nervous system (SNS) becomes overactive, which can result in insulin resistance and other metabolic disorders.
This discovery may lead to new approaches for understanding and treating insulin resistance in people struggling with obesity.
Normally, insulin helps control blood sugar by signaling cells to absorb glucose from the bloodstream. When people develop insulin resistance, their bodies don’t respond well to insulin, causing blood sugar levels to stay high. This issue can eventually lead to type 2 diabetes.
Until now, insulin resistance was mainly linked to problems in the way cells respond to insulin signals. However, this new study suggests there’s more to the story—specifically, the role of the sympathetic nervous system in causing these issues.
The sympathetic nervous system is part of the body’s automatic, or involuntary, response system, often associated with the “fight-or-flight” reaction. It helps regulate various functions, including heart rate, blood flow, and how the body handles energy and fat storage.
Interestingly, past studies have shown mixed results on SNS activity in obese individuals, with some findings indicating it’s overactive, while others show it’s less active.
To investigate this further, the researchers used a special type of mouse that allowed them to study only the peripheral parts of the sympathetic nervous system (the parts outside the brain).
They could “turn off” a specific enzyme in these mice that’s essential for producing norepinephrine (NE), a stress hormone that the SNS releases. This allowed them to see what happened when only the body’s peripheral SNS activity was reduced.
When the researchers fed mice a high-fat diet for just a few days, they noticed several changes. The mice started gaining body fat, and their ability to control blood sugar worsened, leading to higher levels of glucose in the blood.
This happened even though insulin was still able to signal cells properly, which was surprising because it meant that insulin resistance was happening even without typical problems in insulin signaling.
In addition, the high-fat diet caused an increase in SNS activity, shown by higher levels of NE in the blood. This overactive SNS led to issues in fat cells, causing them to release more fats into the bloodstream.
In contrast, the mice with reduced SNS activity (the modified mice) did not develop insulin resistance even when fed the same high-fat diet. Their blood sugar levels remained stable, and they responded well to insulin, suggesting that reducing SNS activity can protect against insulin resistance.
Even after eating a high-fat diet, these modified mice had much lower NE levels and avoided many of the metabolic problems that the regular mice faced.
The researchers also observed longer-term effects of high-fat diets on regular mice. After several weeks, these mice developed “catecholamine resistance,” meaning their bodies stopped responding to the increased NE and other stress hormones.
This resulted in severe problems with blood sugar control, higher levels of hormones that counter insulin’s effects, and more significant inflammation and damage to fat tissues.
Meanwhile, the modified mice with reduced SNS activity were protected from these long-term effects. They showed fewer signs of inflammation and fat tissue damage, smaller fat cells, and healthier overall fat storage.
This discovery highlights how an overactive SNS, not just problems with insulin signaling, can play a major role in causing insulin resistance.
This research offers a fresh way to understand the link between obesity and insulin resistance.
By focusing on the SNS and its role in metabolic health, scientists may eventually develop new treatments aimed at reducing SNS activity to prevent or reduce insulin resistance. This could be especially helpful in preventing type 2 diabetes in people with obesity.
The findings, published in Cell Metabolism, open up new possibilities for research on treating metabolic diseases and managing the effects of obesity.
With further studies, researchers hope to learn more about how controlling SNS activity might help manage or even prevent insulin resistance and its complications.
If you care about diabetes, please read studies that MIND diet may reduce risk of vision loss disease, and Vitamin D could benefit people with diabetic neuropathic pain.
For more information about diabetes, please see recent studies that Vitamin E could help reduce blood sugar and insulin resistance in diabetes, and results showing eating eggs in a healthy diet may reduce risks of diabetes, high blood pressure.
The research findings can be found in Cell Metabolism.
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