Posted on 11/04/2024 9:36:47 PM PST by ConservativeMind
Rutgers and collaborating institutions have found that overnutrition leads to insulin resistance and metabolic disorders through increased activity of the sympathetic nervous system (SNS). The study shows that reducing SNS activity can prevent insulin resistance induced by a high-fat diet, suggesting a new understanding of how obesity causes insulin resistance.
Obesity causes type 2 diabetes and metabolic diseases primarily by inducing insulin resistance. Impaired cellular insulin signaling is the most understood mechanism, but it does not always accompany impaired insulin action, indicating other factors must be involved.
Overnutrition has been known to rapidly increase plasma norepinephrine (NE) levels, indicating overactivation of the SNS. Methods that directly measure SNS activity, such as nerve recordings and NE turnover, often report increased SNS activity in obesity.
In contrast, studies focusing on adrenergic signaling pathways sometimes report reduced catecholamine responses, interpreted as decreased SNS activity.
This discrepancy may be explained by the development of catecholamine resistance due to chronic sympathetic overactivation, leading to diminished physiological responses despite elevated NE levels.
The researchers investigated the conflicting reports on SNS activity in obesity.
Wild-type mice fed an HFD for 12 weeks exhibited catecholamine resistance. Nerve recordings confirmed that SNS activity was elevated after 16 weeks of HFD feeding in wild-type mice. After 10 to 12 weeks of HFD feeding, these mice displayed glucose intolerance and elevated levels of NE, epinephrine, and glucagon, indicating increased activation of mechanisms that oppose insulin action.
HFD-induced adipose tissue dysfunction in wild-type mice was characterized by reduced expression of lipogenic enzymes in white fatty tissue, larger adipocyte sizes, and increased markers of inflammation, fibrosis, and senescence.
The researchers suggest their study is a paradigm shift in understanding obesity-induced insulin resistance. SNS overactivation rather than impaired cellular insulin signaling was the primary driver in the mice obtaining or avoiding insulin resistance.
(Excerpt) Read more at medicalxpress.com ...
They did a short and long term test with normal and special mice that can’t create norepinephrine in peripheral tissues, but can elsewhere, but this let them prove the points I left in the excerpt.
Basically, eating too much makes more norepinephrine. Norepinephrine beyond low normal levels raises blood pressure and does other things for the “fight or flight” response. It also is somewhat tied to the “sympathetic nervous system.”
Reducing norepinephrine or potentially doing things that can activate the “parasympathetic nervous system” helps counter this.
In sum, eating too much causes problems with insulin in part by increasing the response of the sympathetic nervous system. You don’t want that.
One can lower the sympathetic nervous system response by means of relaxation, deep breathing, going outside and enjoying nature, moderate exercise for short frequent periods, anything basically relaxing.
Syntonics is a form of this some eye doctors use to help correct alignment issues. That tapping of the shoulders we saw Prince Harry do is another. The Vagus nerve is part of what you want to stimulate for the parasympathic nervous system activation, in my understanding.
Makes no sense - why is T2D a wide spread problem today but not in the ‘50s and early ‘60s?
If “overnutrition “ starts the problem, what causes people to eat to much in the first place?
In appropriate insulin sensitivity in adipose tissue, NOT insulin resistance causes weight gain. Am I missing something. Or is this paper really that bad?
Overnutrition? LMAO!
Dr. Eric Berg, please school these fools.
There is more to insulin resistance than just obesity because there are a ton of people that are quite obese and sedentary and do not restrict sugars...and yet no diabetes.
Overnutrition?????
Maybe overeating, but too much nutrition?
Based on what I see the fattest people loading up their carts with, too much nutrition is not the issue.
.
They are using that as a euphemism, to avoid losing most of America.
I do intermittent fasting. Hence, I eat a meal big enough to tide me. I am also borderline pre-diabetic (fasting glucose varies from 90-110). Is this suggesting that one should graze during one's 'eating period' ("foraging" in paleo-speak) instead of the bigger meal?
Sound advice.
I’ve not heard of this. Am going to look into it. Thanks.
On Sunday, my brother visited from Hawaii. We went to an all-you-can-eat Japanese place. Cost was $22 per head. They had a huge buffet.
I ate too much good food and bad food.
The next morning, I woke up feeling miserable. It’s not quite as bad as a hangover. But it took a lot of work to drain the bad feeling from my body.
L8r!
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