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  #1   ^
Old Thu, Dec-28-17, 10:59
teaser's Avatar
teaser teaser is offline
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Default internal bathroom scales.

Quote:
The body's own bathroom scales: New understanding of obesity

Researchers at Sahlgrenska Academy, University of Gothenburg, Sweden, have found evidence for the existence of an internal body weight sensing system. This system operates like bathroom scales, registering body weight and thereby fat mass. More knowledge about the sensing mechanism could lead to a better understanding of the causes of obesity as well as new anti-obesity drugs.

"We have discovered a completely new system that regulates fat mass. We hope this discovery will lead to a new direction in obesity research. The findings may also provide new knowledge about the cause of obesity and, in the long run, new treatments of obesity," says John-Olov Jansson, Professor at Sahlgrenska Academy. He explains:

"Quite simply, we have found support for the existence of internal bathroom scales. The weight of the body is registered in the lower extremities. If the body weight tends to increase, a signal is sent to the brain to decrease food intake and keep the body weight constant."

The study was performed on obese rodents that were made artificially heavier by loading with extra weights. The animals lost almost as much weight as the artificial load. The extra weights caused body fat to decrease and blood glucose levels to improve.

The body fat regulatory system discovered by the scientists in Gothenburg is the first new one since the discovery of the hormone, leptin, 23 years ago by American scientists. However, today it seems unlikely that leptin alone will become a treatment for obesity.

"The mechanism that we have now identified regulates body fat mass independently of leptin, and it possible that leptin combined with activation of the internal body scales can become an effective treatment for obesity," says Professor Claes Ohlsson at Sahlgrenska Academy, Gothenburg University.

Lately, several studies of human populations have coupled sitting with obesity and bad health. The present results could explain why.

"We believe that the internal body scales give an inaccurately low measure when you sit down. As a result you eat more and gain weight," says Claes Ohlsson.


https://www.sciencedaily.com/releas...71227150442.htm



Quote:
Significance
The only known homeostatic regulator of fat mass is the leptin system. We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin. As the body weight-reducing effect of increased loading was dependent on osteocytes, we propose that there is a sensor for body weight in the long bones of the lower extremities acting as “body scales.” This is part of a body weight homeostat, “gravitostat,” that keeps body weight and body fat mass constant.


It's an interesting idea, but where does it properly belong? There are studies with rodents on vibrating pads, these have the effect of directing certain stem cells away from differentiation into fat cells.

One of the vibration studies;

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2689082/

Quote:
Mesenchymal stem cells (MSCs) are defined by their ability to self-renew and differentiate into the cells that form mesodermal tissues such as bone and fat. Low magnitude mechanical signals (LMMS) have been shown to be anabolic to bone and have been recently reported to suppress the development of fat in normal animals fed a regular diet. Using male C57BL/6J mice, the ability of LMMS (0.2g, 90-Hz signal applied for 15 min/d, 5 d/wk) to simultaneously promote bone formation and prevent diet-induced obesity was correlated to mechanical influences on the molecular environment of the bone marrow, as indicated by the population dynamics and lineage commitment of MSCs. Six weeks of LMMS increased the overall marrow-based stem cell population by 37% and the number of MSCs by 46%. Concomitant with the increase in stem cell number, the differentiation potential of MSCs in the bone marrow was biased toward osteoblastic and against adipogenic differentiation, as reflected by upregulation of the transcription factor Runx2 by 72% and downregulation of PPARγ by 27%.


Some studies on obesity in rodents and appetite look at what the animals are willing to do to get food. Put food at the top of a slope, the steeper the slope, the less the animals will bother. The less interesting the food, the less the animals will bother. They'll work harder for more interesting food, in other words. This goes as far as the animals losing weight if the effort doesn't seem worth the reward. Adding weight to an already overweight animal seems strongly similar to increasing that slope. Maybe they'd eat more when they got to the food, but constantly running up to the dish for little snacks might decrease.

Some sort of feedback to prevent a bodyweight that puts excess strain on the skeletal system does make sense.

The full text is free, this bit shows what they've done to substantiate their proposed mechanism;

Quote:
The Suppression of Body Weight and Fat Mass by Loading Is Dependent on Osteocytes. It is known that osteocytes can sense dynamic short-term high-impact bone loading for local bone adaptation (10⇓–12). We therefore postulated that chronic static moderately increased bone loading, induced by increased body weight, also activates osteocytes, and thereby reduces fat mass via a systemic signal. To determine the role of osteocytes for the suppression of body weight by increased loading, we established an osteocyte depleted transgenic mouse model using diphtheria toxin-driven cell depletion specifically of DMP1 positive osteocytes (Fig. S2). The normal suppression of body weight by increased loading observed in mice with intact osteocytes (Fig. 3A) was lost in osteocyte-depleted mice (Fig. 3B). Increased loading decreased the weight of WAT (Fig. 3C) and serum leptin levels (Fig. 3D) in mice with intact osteocytes but not in osteocyte-depleted mice, while there was no significant differences in the skeletal muscle weight between the groups (Fig. 3E). These findings demonstrate that the suppression of body weight by loading is dependent on osteocytes. We propose that increased body weight activates a sensor dependent on the osteocytes of the weight-bearing bones. This induces an afferent signal to reduce food intake



https://www.researchgate.net/public...nd_adult_humans

Regulation of fat mass independent of leptin levels gets mentioned a few times. Leptin, the skeletal system and the central nervous system sort of come hand in hand.

Quote:
Abstract
The present investigation was carried out to analyse, immunohistochemically, in vivo leptin expression in cartilage and bone cells, the latter restricted to the elements of the osteogenic system (stromal cells, osteoblasts, osteocytes, bone lining cells). Observations were performed on the first lumbar vertebra, tibia and femur of four rats and on the humerus, femur and acromion of four patients. Histological sections of paraffin-embedded bone samples were immunostained using antibody to leptin. The results showed that, in growing rat bone, leptin is expressed in chondrocytes and stromal cells, but not in osteoblasts; bone lining cells were not found in the microscopic fields examined. In adult human bone, leptin is expressed in chondrocytes, stromal cells and bone lining cells; osteoblasts were not found in the microscopic fields examined. Osteocytes were found to be leptin positive only occasionally and focally in both rat and human bone. The in vivo findings reported show, for the first time, that leptin appears to be expressed only in the cells of the osteogenic lineage (stromal cells, bone lining cells, osteocytes) that, with respect to osteoblasts, are permanent and inactive, i.e. in those cells that according to our terminology constitute the bone basic cellular system (BBCS). Because the BBCS seems to be primarily involved in sensing and integrating mechanical strains and biochemical factors and then in triggering and driving bone formation and/or bone resorption, it appears that leptin seems to be mainly involved in modulating the initial phases of bone modelling and remodelling processes.


You can make mice lose most of their body fat by injecting leptin into their brains--but they suffer a loss of bone mass. Maybe a result of the loss of peripheral leptin rather than a direct effect of central leptin? This is one of the problems with making body weight regulation entirely a central thing. Insulin is anti-obesogenic, because it reduces bodyweight when injected into the hypothalamus? What happens to the rest of the body? Circumventing peripheral signals might be okay, as long as those peripheral signals don't actually serve a purpose. What are the odds of that?
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  #2   ^
Old Thu, Dec-28-17, 13:21
M Levac M Levac is offline
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Lately, several studies of human populations have coupled sitting with obesity and bad health.

I wrote something smarty, changed my mind. That quote illustrates everything wrong about the experiment result interpretation - assumed premise is biased, i.e. sitting is the cause, obesity and bad health is the effect.
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  #3   ^
Old Thu, Dec-28-17, 13:40
dcc0455 dcc0455 is offline
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We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin.

I'm not dismissing their hypothesis, but could we also assume a simpler hypothesis that carrying extra weight make us burn more calories?
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  #4   ^
Old Thu, Dec-28-17, 13:59
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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I don't want to jump to the conclusion that they're wrong though, either.

One thing the study doesn't really look at is time spent on the animal's feet. If you look at another area where standing vs. not standing definitely makes a difference, in lean mass, the actual amount of time that needs to be spent weight-loaded vs. not to increase lean mass/prevent loss is fairly short.

The mice were loaded with 15 percent of their bodyweight. One thing here, weight loading isn't much of a thing with mice. For me 15 percent is like 24 pounds, it's a rare day where I wouldn't be loaded at some point with a lot more weight than that. Even if this applies to both mice and humans, a lot of us might already be bearing enough weight on a regular basis that any benefit to be had by weight bearing has already been had.

If you look at the vibrating platform study I posted

Quote:
Using male C57BL/6J mice, the ability of LMMS (0.2g, 90-Hz signal applied for 15 min/d, 5 d/wk)


These mice were also used for the added weight study, and it only took 15 minutes of stimulus a day, cute little weighted vests for short periods of time daily might have been just as effective as the permanently implanted weight pellets.
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  #5   ^
Old Thu, Dec-28-17, 14:03
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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Originally Posted by dcc0455
We hypothesized that there is a second homeostat regulating body weight with an impact on fat mass. In this study we have added and removed weight loads from experimental animals and measured the effects on the biological body weight. The results demonstrate that there is a body weight homeostat that regulates fat mass independently of leptin.

I'm not dismissing their hypothesis, but could we also assume a simpler hypothesis that carrying extra weight make us burn more calories?


They produced mice with compromised osteocytes/weight sensing to rule this out. Also--burning more calories isn't what happened, because the mice ate considerably less calories. Pair fed mice had similar results. Nobody asked if any of the mice were happy about the whole situation.
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  #6   ^
Old Fri, Dec-29-17, 09:43
Zei Zei is offline
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I tend to buy into the weight set point theory because that's what I've observed happen in myself and others, that the body "defends" a certain weight (whether it's higher than the amount we'd ideally like or not) despite varying amounts of daily food, activity, etc. So the discovery of yet another method the body uses to monitor its own parameters in regard to weight makes sense to me. The trick seems to be to find ways to tell the body it's okay to lower its defended set point so that it will automatically work to maintain the new weight. I lost a bunch of weight and was maintaining extremely well until I thought it was alright to add back a bit more carbs from healthy things like low-carb vegetables and nuts. For my body, not a good plan. My weight started climbing and now having a lot of trouble trying to control it. I think the increase in carbs, while still pretty low, was too much for my body and triggered metabolic changes that raised my weight set point. So yeah, it's an interesting idea that in addition to hormones, the body may also use its own bones to sense how much weight its carrying so it can make needed adjustments to meet its perceived set point. You know there are some kind of mechanisms going on in there sensing and regulating things where you can pay no attention to energy intake/output and still weigh the same amount for long periods of time.
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