Brains, Brains, Brains, Brains, Brains,.....
Posted on 08/02/2011 11:27:46 PM PDT by neverdem
A report in the August issue of the Cell Press journal Cell Metabolism might help to explain why it's so frustratingly difficult to stick to a diet. When we don't eat, hunger-inducing neurons in the brain start eating bits of themselves. That act of self-cannibalism turns up a hunger signal to prompt eating.
"A pathway that is really important for every cell to turn over components in a kind of housekeeping process is also required to regulate appetite," said Rajat Singh of Albert Einstein College of Medicine.
The cellular process uncovered in neurons of the brain's hypothalamus is known as autophagy (literally self-eating.) Singh says the new findings in mice suggest that treatments aimed at blocking autophagy may prove useful as hunger-fighting weapons in the war against obesity.
The new evidence shows that lipids within the so-called agouti-related peptide (AgRP) neurons are mobilized following autophagy, generating free fatty acids. Those fatty acids in turn boost levels of AgRP, itself a hunger signal.
When autophagy is blocked in AgRP neurons, AgRP levels fail to rise in response to starvation, the researchers show. Meanwhile, levels of another hormone, called -melanocyte stimulating hormone, remain elevated. That change in body chemistry led mice to become lighter and leaner as they ate less after fasting, and burned more energy.
Autophagy is known to have an important role in other parts of the body as a way of providing energy in times of starvation. However, unlike other organs, earlier studies had shown the brain to be relatively resistant to starvation-induced autophagy.
"The present study demonstrates the unique nature of hypothalamic neurons in their ability to upregulate autophagy in response to starvation that is consistent with the roles of these neurons in feeding and energy homeostasis," the researchers wrote.
Singh said he suspects that fatty acids released...
(Excerpt) Read more at sciencedaily.com ...
Autophagy in Hypothalamic AgRP Neurons Regulates Food Intake and Energy Balance
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“When we don’t eat, hunger-inducing neurons in the brain start eating bits of themselves.”
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Wonder what Michelle Obama’s problem is?
Did you know that if you eat nothing but your own body, you will lose weight.
Brains, Brains, Brains, Brains, Brains,.....
Did you know that if you eat nothing but your own body, you will lose weight.
Look, I made dumbness. Heh...
It explains a lot about the Hollywood crowd.
Remember what the Dormouse said.
Words for the ages!
FReepmail me if you want on or off the diabetes ping list.
Interesting.
That starvation diets don´t work over the long haul is hardly news, but it´s always interesting to hear new hypotheses regarding the mechanisms behind apetite control.
Now, the other side of the coin is that normal apetite and metabolism is not supposed to lead to obesity, NAFLD, diabetes, etc. Hence, it is likely that the “gluttony and sloth” hypothesis of metabolic derangement is wrong.
This EJCN article outlines what I believe is the best (partial) alternative hypothesis of why we have seen such a tremendous increase in obesity, diabetes and NAFLD over the past decades (free abstract only):
http://www.nature.com/ejcn/journal/vaop/ncurrent/abs/ejcn2011132a.html
TLDR version:
“An alternative model emphasises the capacity of fructose and fructose-derived sweeteners (sucrose, high-fructose corn syrup) to perturb cellular metabolism via modification of the adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio, activation of AMP kinase and compensatory mechanisms, which favour adipose tissue accretion and increased appetite while depressing physical activity.
This conceptual model implicates chronic hyperinsulinaemia in the presence of a paradoxical state of ‘cellular starvation’ as a key driver of the metabolic modifications inducing chronic weight gain.”
HFCS has come under a lot of scrutiny and blame as it came into vogue as an economically driven substitute for ordinary cane and beet sugar (i.e. sucrose) about the same time as people started getting fat at an increasing rate. Sucrose, dating way back in modern history, still somehow didn’t provoke much of an obesity problem of itself.
Every meal should include the 6 basic food groups, caffeine, nicotine, sugar, salt, fat, and preservatives.
You forgot alcohol
Have you ever noticed that liberals are always starting a new diet of some kind?
We need to encourage liberals to eat more not less.
It wouldn't cure their mental disease since the damage has been done, but it might help their brains to function at 10% of the capacity of a normal brain.
The hypothesis is that it is fructose that is a problem, regardless of the source (HFCS, sucrose, etc.).
HFCS is most likely not more “evil” than sucrose in metabolic terms, although it might have slightly increased fructose concentrations in soda, etc.
However, it is cheaper and more ubiquitous than sucrose (partially because of federal corn subsidies and sugar tariffs).
Refined sugar used to be a rare and expensive commodity, until the early 20:th century. On average, people consumed perhaps 16-24 grams per day of fructose before WW II.
In the late 70-ies, according to the USDA (NFCS), americans consumed 37 grams per day of fructose.
In 1994, fructose consumption had increased to 54,7 grams per day (NHANES III).
In certain important subgroups, consumption has exploded. US adolescents on average consume about 73 grams / day of fructose.
As the fructose hypothesis is based on the problem being a threshold effect, I.e. the liver getting overwhelmed in a manner similar to what happens in chronic alcoholics (not a coincidence, ethanol is fermented sugar), the effect of fructose on NAFLD and obsesity is most likely strongly non-linear. A little is completely harmless, a lot is dangerous.
I personally believe there might be more going on than just the fructose, in terms of disrupting people´s appetite control systems, but I am pretty convinced that fructose consumption is an important piece of the puzzle.
Sucrose brings on the fructose more gradually as it undergoes enzymatic breakdown in digestion, rather than right up front all at once as in HFCS.
Fructose in fruits is usually tempered by the fiber present.
I used to gobble sugar like a glutton when a kid, and I remained embarrassingly skinny. The bay window caught up with me only when well into my adulthood.
“Sucrose brings on the fructose more gradually as it undergoes enzymatic breakdown in digestion, rather than right up front all at once as in HFCS.”
Sounds interesting, but I haven´t seen any research on that. Got a link?
“I used to gobble sugar like a glutton when a kid, and I remained embarrassingly skinny. The bay window caught up with me only when well into my adulthood.”
That´s the way it usually works, though many kids get fat (or fatty livers) these days too. It takes a while for most people to crash one´s metabolism and induce systemic insulin resistance. (I.e. fructose -> fatty liver / liver insulin resistance -> loss of liver blood glucose regulation -> hyperinsulinemia -> systemic insulin resistance)
I personally think trans fats have played an important role as well. If researchers want to introduce metabolic derangement, diabetes and obesity in rats, few things beat a fructose + trans fat cocktail in sheer efficiency...
I understood this to be basic high school biology. Saliva enzymes begin the process of digesting dietary sucrose, but hardly manage to split all of the sucrose before it gets to the stomach. The digestive tract can’t absorb sucrose as such — only simple sugars. HFCS has no polysaccharides in it — it’s all simple sugars.
As for the rats — the only sure thing that can be said about this is that trans fats and HFCS are a lousy diet for rats and should be considered animal cruelty. How many cures for cancer in rats have flopped in humans?
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