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  #1   ^
Old Thu, Aug-03-17, 06:20
teaser's Avatar
teaser teaser is offline
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Default Brain 'switch' tells body to burn fat after a meal

https://www.sciencedaily.com/releas...70801193339.htm

Quote:
Scientists at Monash University's Biomedicine Discovery Institute have found a mechanism by which the brain coordinates feeding with energy expenditure, solving a puzzle that has previously eluded researchers and offering a potential novel target for the treatment of obesity.

Obesity -- a major risk factor for many diseases including cardiovascular disease, Type 2 diabetes, liver disease and several cancers -- is at epidemic levels in Australia.

Researchers from the Metabolic Disease and Obesity Program have shown in laboratory models that feeding controls the 'browning' of fat, that is, the conversion of white fat, which stores energy, into brown fat, which expends it. Fat in the human body is stored in specialised cells called adipocytes, which can change from white to brown states and back again.

Their study, published in Cell Metabolism today, shows that after a meal the brain responds to circulating insulin, which is increased after a rise in blood glucose. The brain then sends signals to promote the browning of fat to expend energy. By contrast, after a fast, the brain instructs these browned adipocytes to once more convert into white adipocytes, storing energy. These processes help prevent both excess weight gain and excess weight loss in response to feeding and fasting, meaning body weight remains relatively stable over time.

The researchers showed that the brain's ability to sense insulin and coordinate feeding with energy expenditure via browning is controlled by a switch-like mechanism turned on after fasting to inhibit the response to insulin, repressing browning and conserving energy, and turned off after feeding to facilitate the insulin response to promote browning and to expend energy.

"What happens in the context of obesity is that the switch stays on all the time -- it doesn't turn on off during feeding," lead researcher Professor Tony Tiganis said.

"As a consequence, browning is turned off all the time and energy expenditure is decreased all the time, so when you eat, you don't see a commensurate increase in energy expenditure -- and that promotes weight gain," Professor Tiganis said.

Previous investigations by the researchers that showed how the brain coordinates white adipose tissue browning attracted considerable attention after it was published in early 2015.

"For a long time, the missing piece to the puzzle was always why this occurs in the body," first author Dr Garron Dodd said.

"We've shown not only why this occurs but also the fundamental mechanism involved. It's very exciting," Dr Dodd said.

The researchers are further exploring the possibility of inhibiting the switch for therapeutic purposes to promote the shedding of excess fat.

"Obesity is a major and leading factor in overall disease burden worldwide and is poised, for the first time in modern history, to lead to falls in overall life expectancy," Professor Tiganis said.

"What our studies have shown is that there is a fundamental mechanism at play that normally ensures that energy expenditure is matched with energy intake. When this is defective, you put on more weight. Potentially we may be able to rewire this mechanism to promote energy expenditure and weight loss in obese individuals. But any potential therapy is a long way off," he said.



Interesting because it sort of ties together studies where insulin administered directly to the brain reduced bodyweight with the observation that the elevated insulin levels in obesity and insulin resistance don't exactly seem to be slimming. For a while it was very fashionable when criticizing a low carb diet to bring up the supposed appetited-suppression, anti-obesogenic role of insulin, I don't know if that's fallen out of fashion or if I've just stopped visiting those websites.

Quote:
"What happens in the context of obesity is that the switch stays on all the time -- it doesn't turn on off during feeding," lead researcher Professor Tony Tiganis said.


One thing about meal timing, eating windows or intermittent fasting--besides abstaining from food, often when you do eat, you'll eat more. It's possible there's a stronger "fed" signal. The prolonged absence of food lowers insulin, maybe increasing sensitivity to this mechanism, with a good solid feeding taking advantage of the increased sensitivity.
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  #2   ^
Old Thu, Aug-03-17, 06:41
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khrussva khrussva is offline
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This does seem to make some sense given my experiences. I get cold and tolerate the heat much better when I'm fasting. If I'm eating regularly, I'm not cold at a normal room temperature. I've also noticed that if I overeat I will roast at night and sleep only with a sheet. If I'm fasting I bundle up at night with a blanket and comforter. I've also been fairly weight stable for the past year. Perhaps this is just brown fat & white fat doing its job.

IMO it appears that they have missed the boat (again) implying that obesity is the problem through association. What came first? The chicken or the egg. If you follow the logic in their own analysis of the issue that body wants to remain weight stable. Then something breaks that turns off the brown fat signaling. After that the weight starts piling on. So again, it seems to me that obesity is just a symptom of the problem. The focus should be on what causes the system to break down and stop functioning properly. For me, I think I've figured that out. Too many carbohydrates in my diet.

Last edited by khrussva : Thu, Aug-03-17 at 07:03.
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  #3   ^
Old Thu, Aug-03-17, 08:40
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GRB5111 GRB5111 is offline
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Quote:
Originally Posted by khrussva
IMO it appears that they have missed the boat (again) implying that obesity is the problem through association. What came first? The chicken or the egg. If you follow the logic in their own analysis of the issue that body wants to remain weight stable. Then something breaks that turns off the brown fat signaling. After that the weight starts piling on. So again, it seems to me that obesity is just a symptom of the problem. The focus should be on what causes the system to break down and stop functioning properly. For me, I think I've figured that out. Too many carbohydrates in my diet.

My concerns as well. It's nice to understand the underlying mechanism in order to "turn off" the switch. What's also nice is to understand how to manipulate the switch through diet composition. Wouldn't that seem the be the healthier approach?
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  #4   ^
Old Sun, Aug-06-17, 17:47
M Levac M Levac is offline
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Quote:
Their study, published in Cell Metabolism today, shows that after a meal the brain responds to circulating insulin, which is increased after a rise in blood glucose. The brain then sends signals to promote the browning of fat to expend energy. By contrast, after a fast, the brain instructs these browned adipocytes to once more convert into white adipocytes, storing energy.

No.
Quote:
"What happens in the context of obesity is that the switch stays on all the time -- it doesn't turn on off during feeding," lead researcher Professor Tony Tiganis said.

No.

If eating (therefore insulin) causes browning (therefore greater Eout) then how is obesity created in the first place, when obesity is said to be created by more eating (therefore more insulin, therefore more browing, therefore more greater Eout)? See what I mean by "No."?

I'd like to cite diabetes type 1, where there's no insulin, there's hyperphagia, and there's emaciation. Hyperphagia therefore expected insulin, but no insulin because diabetes type 1 therefore no browing, yet no fat accumulation. Pfft, go to hospital, diagnose, treat, inject insulin, voila - fat accumulation. Be not-smart, inject insulin in same spot for years, voila - localized excess fat accumulation in a process called insulin-induced lipohypertrophy. Eat more carbs, inject more insulin (because eat more carbs - insulin dose depends on carbs, you see), voila - more fat accumulation all over the place. Incidentally, when that happens, the insulin-induced lipohypertrophy becomes invisible due to the amount of fat everywhere. This suggests that insulin-induced lipohypertrophy is also a system-wide phenomenon rather than just localized to the injection site(s). Anyways, the whole thing contradicts the idea that insulin somehow causes adipocytes to go brown after a meal.

Finally, biology doesn't waste for no reason. If there's excess energy, it will be used, not merely disposed.
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  #5   ^
Old Mon, Aug-28-17, 10:03
kathleen24 kathleen24 is offline
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Quote:
Originally Posted by teaser

One thing about meal timing, eating windows or intermittent fasting--besides abstaining from food, often when you do eat, you'll eat more. It's possible there's a stronger "fed" signal. The prolonged absence of food lowers insulin, maybe increasing sensitivity to this mechanism, with a good solid feeding taking advantage of the increased sensitivity.


If we posit that the observations may have some validity, and set aside the attempt to explain, which is what the `no's addressed, then we could also consider that perhaps it's the degree of hunger that is the trigger here.

Easy experiment-of-one: IF'ers could track the hunger cues they feel before they eat, on a scale of `hmm, did I just hear a tummy-rumble' to `full-out-toddler-tantrum-must-eat-now', then note the amount that they eat, and then whether they feel hot or cold afterwards, perhaps with notes about how much physical activity follows the feed, and track weight as well. A few weeks of this might show whether the theory has any practical application for that individual's life, and they could make a choice then about any modifications they wish to make.

Any statistical relevance? Clearly, no. But our first responsibility is to ourselves, yes? If it makes a difference to the individual, it matters to that person.
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  #6   ^
Old Mon, Aug-28-17, 11:09
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teaser teaser is offline
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Quote:
Originally Posted by M Levac
No.

No.

If eating (therefore insulin) causes browning (therefore greater Eout) then how is obesity created in the first place, when obesity is said to be created by more eating (therefore more insulin, therefore more browing, therefore more greater Eout)? See what I mean by "No."?

I'd like to cite diabetes type 1, where there's no insulin, there's hyperphagia, and there's emaciation. Hyperphagia therefore expected insulin, but no insulin because diabetes type 1 therefore no browing, yet no fat accumulation. Pfft, go to hospital, diagnose, treat, inject insulin, voila - fat accumulation. Be not-smart, inject insulin in same spot for years, voila - localized excess fat accumulation in a process called insulin-induced lipohypertrophy. Eat more carbs, inject more insulin (because eat more carbs - insulin dose depends on carbs, you see), voila - more fat accumulation all over the place. Incidentally, when that happens, the insulin-induced lipohypertrophy becomes invisible due to the amount of fat everywhere. This suggests that insulin-induced lipohypertrophy is also a system-wide phenomenon rather than just localized to the injection site(s). Anyways, the whole thing contradicts the idea that insulin somehow causes adipocytes to go brown after a meal.

Finally, biology doesn't waste for no reason. If there's excess energy, it will be used, not merely disposed.


What they're describing here is a sort of feedback mechanism, which they posit ought to keep humans from becoming overweight. That doesn't rule out insulin being obesogenic--it just says that there are things to counter this.

Also--who says it's wasted? That sort of depends on your perspective. GCBC had a section on adolescent pigs--fed a very low protein diet the pigs just ate more. Energy was "wasted"--but maybe in the service of providing sufficient
protein and other nutrients to allow normal growth. So it would be disposed of, and the useful work that's produced might be its own disposal.

Excessive amounts of insulin in the periphery hijacking the system doesn't rule out there being other roles played by insulin when things are working right.
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  #7   ^
Old Mon, Aug-28-17, 13:33
M Levac M Levac is offline
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Wasted by brown fat. Serves no other purpose than to waste fuel as heat. Heat is produced by all other cells through normal metabolism, no need to produce more heat through waste.

We could argue that white fat cells are better at producing heat through simple insulation (not production per say, but keeps heat in, see?). We can see this with winter animals who have tons of white fat cells, then on top some fur, then on top no sweating, so there's no heat loss that way. For humans, the real problem isn't cold, it's excess heat. Even winter animals shed their fur coat comes summer. To have brown fat cells produce excess heat through waste is truly wasteful twice.

Ironically, growing fatter sorta makes us more sensitive to cold. We're not adapted to keep warm that way. It could be due to fuel partitioning. Too much gets stuck in fat tissue, not enough for normal metabolism, from which heat is actually produced. Personally, I saw this phenomenon when I first got down to 165lbs, I could now play golf all day in chilly weather (10c to 20c) no problem. Conversely, I could also play golf in very hot weather (above 30c) no problem. Today, my current illness prevents either of that.

It seems that both keeping warm and cooling off requires active metabolism in humans, which for one produces heat while for the other somehow turns this around to shed it.
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  #8   ^
Old Mon, Aug-28-17, 15:07
teaser's Avatar
teaser teaser is offline
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I guess we just disagree here. Alcohol can give a person some useful energy. Beyond a point though, it's just harmful. Best thing to do, once it's in the system, is burn it off. Some fat may be synthesized, but at that point, it really is more important to get the stuff out of the system than it is to use the energy produced efficiently. Protein--not quite like alcohol, but again, there's a limit to the rate of protein synthesis, so some gets wasted as energy, some is used to synthesize carbohydrate or fat. Carbohydrate--same thing, there's a limit to our glycogen storage, at a certain point, energy will be wasted--although in this case there's a more obvious purpose, some of the carbs being used up in the synthesis of fat, a more practical long-term energy storage.

Efficiency is important when something is scarce. Desert animals might need metabolic adaptations to spare water. In an animal that lives in the water--the same adaptations that work for a camel might be quite wasteful, optimizing for one situation is unlikely to be optimal for another.

I also doubt fat as an adaptation for insulation vs. the cold. If you look at the fattest mammals in the world, various arctic sea animals, most of them fast for long periods, some around half a year, some go through pregnancy and much of lactation during a fast--the insulation is at best secondary, they need the fat for those long fasts and to generate heat in those conditions.

One question here is how exactly the "brown" fat here is "wasting" energy. Are we talking about white adipocytes becoming brown and then becoming white again? That's some rapid cell differentiation and redifferentiation going on...

Quote:
Summary
Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure. The feeding-induced repression of hypothalamic TCPTP was defective in obesity. Mice lacking TCPTP in AgRP/NPY neurons were resistant to diet-induced obesity and had increased beige fat activity and energy expenditure. The deletion of hypothalamic TCPTP in obesity restored feeding-induced browning and increased energy expenditure to promote weight loss. Our studies define a hypothalamic switch that coordinates energy expenditure with feeding for the maintenance of energy balance.


http://www.cell.com/cell-metabolism...Fshowall%3Dtrue

Okay, we're talking about "states." One way a cell can go into "energy wasting" mode as opposed to "storage" mode is by increasing fatty acid synthesis from glucose. If you're just looking at energy in/energy out, that looks pretty good, you lose about a quarter of the calories.

Of course fasting decreases metabolic rate, but calling that "energy storage" mode really is pretty loony.

Brown fat does seem to have a role to play in fatty acid synthesis;


Quote:
Fatty acid synthesis in mouse brown adipose tissue. The influence of environmental temperature on the proportion of whole-body fatty acid synthesis in brown adipose tissue and the liver.

Trayhurn P.
Abstract
Fatty acid synthesis has been measured in vivo with 3H2O in mice acclimated at different environmental temperatures (33, 22, 4 degrees C), and the importance of brown adipose tissue and the liver to whole-body fatty acid synthesis at each temperature assessed. At 33 degrees C, when non-shivering thermogenesis is minimal, the rate of fatty acid synthesis in interscapular brown adipose tissue was lower than in the liver, but higher than in white adipose tissue and the carcass. At 4 degrees C, when non-shivering thermogenesis is maximal, the fatty acid synthesis rate in interscapular brown adipose tissue was many times greater than in any other tissue. High fatty acid synthesis rates were also found in other brown adipose tissue depots--subscapular, dorsocervical and axillary--of cold-acclimated mice. In mice maintained at 22 degrees C the rate of fatty acid synthesis was also higher in brown adipose tissue than in other tissues. Overall, the relative importance of brown adipose tissue as a site of fatty acid synthesis increased with lower environmental temperatures, while that of the liver decreased. It was calculated that brown adipose tissue in total accounted for approx. 5% of whole-body fatty acid synthesis at 33 degrees C, 10% at 22 degrees C and 30% at 4 degrees C. In contrast, hepatic synthesis amounted to 32% of whole-body fatty acid synthesis at 33 degrees C, 16% at 22 degrees C and only 11% at 4 degrees C. An estimate of the contribution that de novo synthesis makes to total fatty acid utilization by interscapular brown adipose tissue suggests that fatty acid synthesis and breakdown constitutes a significant heat-dissipating 'cycle' in brown adipose tissue of cold-acclimated mice. Such a cycle is not evident in suckling animals since fatty acid synthesis in brown adipose tissue is very low during early development.
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