Summary: New research suggests that stress hormone, rather than impaired glucose signaling, may largely travel diabetes in fat. This study found that high levels of stress hormones, like noradrenaline, counter insulin’s results, leading to hormone weight yet with unbroken hormone signaling. When genetically modified mice could n’t produce these stress hormones, they avoided diabetes despite obesity.
This discovery may explain why some obese people have diabetes while others do n’t. In order to maintain insulin resistance, future treatments might focus on reducing stress hormones. Researchers are currently looking into the impact of excessive eating and short-term pressure on diabetes risk.
Important Information:
- Stress hormone may be the primary drivers of obesity-induced diabetes, no glucose signaling.
- Overeating fast increases tension hormones like dopamine, contributing to insulin resistance.
- Genetically modified animals without stress hormone did not develop insulin, despite fat.
Origin: Rutgers University
A , research  , from Rutgers Health and other organizations indicates that stress hormones – not impaired mobile insulin signaling – may be the main driver of obesity-related insulin.
The report in , Cell Metabolism , perhaps change our understanding of how obesity-induced glucose tolerance develops and how to handle it.
” We have been studying the fundamental procedures that contribute to diabetes. Given that the cost of the diabetes epidemic in the U. S. only exceeds$ 300 billion per year, this is a critically important problem”, said , Christoph Buettner, commander of endocrinology, metabolism and protein at Rutgers Robert Wood Johnson Medical School and the study’s top writer.
Long-standing theories have been made that fat impairs the insulin secretion in the liver and fat cells. The new research shows that despite mobile insulin signaling still functioning, the brain’s sympathetic nervous system, or “fight or trip,” response, and that the higher level of the stress hormone noradrenaline and adrenaline counteract the effects of insulin.
The authors found that excessive eating in healthy mice quickly raises the stress hormone norepinephrine within days. This demonstrates how quickly excess food stimulates the sympathetic nervous system.
The authors then used a new breed of genetically modified mice that are normal in every way but one: They cannot produce the stress hormone catecholamines outside of their brains and central nervous systems to see how this excess hormone production affects disease development.
These mice were fed a high-fat, high-sugar diet by the researchers, but they did not develop metabolic disease despite eating as many calories and becoming as obese as normal mice.
Because it demonstrates that the differences in insulin sensitivity and the absence of metabolic disease are not caused by decreased food intake or obesity, but rather by the significantly decreased stress hormone levels, we were delighted to see that our mice ate as much.
” These mice cannot increase stress hormones that counteract insulin, hence, insulin resistance does not develop during obesity development.”
The recent findings may provide new insights into why some obese people develop diabetes while others do not, and why stress can cause diabetes even when weight is gained.
According to Bustner, “many different types of stress, including financial stress, marital stress, the stress brought on by living in dangerous areas, suffering discrimination, or even the physical stress brought on by excessive alcohol consumption,” all contribute to the metabolic stress of obesity and are linked to diabetes.
Our findings reveal a new understanding of the common causes of all these factors that raise the risk of diabetes. Even obesity leads to metabolic disease in large numbers thanks to higher levels of stress hormones.
” Stress and obesity, in essence, work through the same basic mechanism in causing diabetes, through the actions of stress hormones”.
The new study suggests that this may be the underlying cause of obesity’s insulin resistance, despite the well-known fact that catecholamines can inhibit insulin action.
The dynamic interplay between stress hormones, which work in opposition to insulin, has long been known. Stress hormones increase glucose and lipids in the bloodstream, while insulin lowers these.
The new study’s finding, however, is that insulin signaling can continue to function even in insulin-resistant states like obesity. Ultimately, the higher level of stress hormone activity causes increased blood sugar and fat levels by “push the gas pedal harder.”
The accelerated gas pedal effect of catecholamines overwhelms the insulin’s brake effect, which results in a correspondingly lessened insulin action even though the level of insulin’s “braking” effect remains unchanged.
” Some researchers are initially surprised that cellular insulin signaling is intact, but some colleagues are.” Let’s not forget, however, that insulin signaling and other signaling pathways are used to exert stress hormones ‘ effects.
” That explains why insulin’s ability to “breathe” and slow down the release of sugar and fat into the bloodstream is undermined despite stress signaling being in place.
The research suggests that medications that lower catecholamines, which are all neurotransmitters produced by the SNS and the adrenal gland, may be able to treat or prevent diabetes.
However, medicines that block catecholamines, as they are currently used to treat high blood pressure, have n’t shown major benefits for diabetes. According to Buettner, this may be due to the lack of current drugs that can block the relevant receptors or because they have a complex effect on the body and brain.
Buettner and the study’s first author, Kenichi Sakamoto, an assistant professor of endocrinology at Robert Wood Johnson Medical School, are planning human studies to confirm their findings. They’re also examining the role of the sympathetic nervous system and other forms of diabetes, including Type 1 diabetes.
” We would like to study if short-term overfeeding, as some of us experience during the holidays by gaining five to 10 pounds, increases insulin resistance with heightened sympathetic nervous system activation,” Buettner said.
The findings may pave the way for novel therapeutic approaches to treat metabolic disease, diabetes, and insulin resistance that focus less on stress hormones than insulin signaling.
” We hope this paper provides a different take on insulin resistance,” Buettner said”. It may also explain why none of the drugs currently used to treat insulin resistance, except insulin itself, directly increases cellular insulin signaling.”
About this information on stress research and diabetes
Author: Andrew Smith
Source: Rutgers
Contact: Andrew Smith – Rutgers
Image: The image is credited to Neuroscience News
Original Research: Open access.
By Christoph Buettner and colleagues,” Overnutrition causes insulin resistance and metabolic disorder” ( in German ). Cell Metabolism
Abstract
Increased sympathetic nervous system activity results in insulin resistance and metabolic syndrome.
The mechanisms underlying obesity-induced insulin resistance remain incompletely understood, as impaired cellular insulin signaling, traditionally considered the primary driver of insulin resistance, does not always accompany impaired insulin action.
The sympathetic nervous system ( SNS ) is overactivated, which suggests that overnutrition causes a rapid increase in plasma norepinephrine ( NE). However, the role of the SNS in obesity is controversial, as both increased and decreased SNS activity ( SNA ) have been reported.
Here, we show that reducing catecholamine ( CA ) release from the SNS protects against overnutrition-induced insulin resistance as well as hyperglucagonemia, adipose tissue dysfunction, and fatty liver disease, as we demonstrate utilizing a mouse model of inducible and peripherally restricted deletion of tyrosine hydroxylase ( th, THΔper ).
Adipose tissue lipolysis is a crucial mechanism that increases insulin resistance.
Unabhängig of cellular insulin signaling, increased SNA emerges as a crucial factor in the pathogenesis of overnutrition-induced insulin resistance and metabolic disease.
