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  #1   ^
Old Thu, Sep-20-18, 02:46
Demi's Avatar
Demi Demi is offline
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Default Anti-inflammatory protein promotes healthy gut bacteria to curb obesity

Quote:
From Science Daily
September, 2018


Anti-inflammatory protein promotes healthy gut bacteria to curb obesity

Summary

Scientists have discovered that the anti-inflammatory protein NLRP12 normally helps protect mice against obesity and insulin resistance when they are fed a high-fat diet. The researchers also reported that the NLRP12 gene is underactive in people who are obese, making it a potential therapeutic target for treating obesity and diabetes, both of which are risk factors for cardiovascular disease and other serious conditions.


https://www.sciencedaily.com/releas...80919133616.htm
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  #2   ^
Old Thu, Sep-20-18, 06:48
whynot18 whynot18 is offline
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Reading more from this study is interesting:

"The scientists fed mice that lacked the NLRP12 gene (NLRP12-knockout mice) and ordinary mice a high-fat diet for several months. The NLRP12-knockout mice ate and drank no more than their healthy cousins but accumulated significantly more fat and became heavier. The knockout mice also showed signs of insulin resistance, which involves a reduced ability to clear glucose from the bloodstream and tends to follow the development of obesity.

"The absence of NLRP12 in these mice led to increased signs of inflammation in the gut and in fat deposits, but it wasn't clear how this led to extra weight gain until the researchers moved the animals from one facility to another. Following standard safety protocols to prevent disease spread, the researchers dosed the mice with antibiotics before the move.

"We noticed that the mice treated with antibiotics gained less weight than the mice that stayed in the old facility," said study co-first author Agnieszka Truax, PhD, a postdoctoral researcher in the Ting lab during the study. "That led us to suspect that gut bacteria were involved in promoting obesity."

Further tests showed that when NLRP12-knockout mice were kept in a bacteria-free condition, the mice did not gain weight because there were no bacteria. The deficiency of NLRP12 didn't matter as much. This suggested that "bad" bacteria had been driving the excess weight gain during a high-fat diet.

Scientists have known that high-fat diets, as compared to low-fat diets, tend to reduce the diversity of bacterial species in the gut by suppressing some species and allowing a few others to proliferate abnormally. The UNC researchers confirmed this in their high-fat-eating mice, and they observed that the loss of bacterial diversity was much worse in the Nlrp12-knockout mice.

The experiments suggested that inflammation caused by a high-fat diet and worsened by the absence of NLRP12 was a major cause of this shift. Killing off rival bacterial species allowed a sharp rise in the levels of a bacterial family called Erysipelotrichaceae. These microbes became more prominent as gut inflammation worsened and exacerbated the weight-gain from a high-fat diet when put into the guts of otherwise germ-free mice.

By contrast, the Lachnospiraceae family of bacteria, which tended to die off in mice fed a high-fat diet, appeared to be highly beneficial. The researchers fed Lachnospiraceae to NLRP12-knockout mice prior to and during three weeks of high-fat eating and found that these "good" bacteria reduced gut inflammation, eliminated the hegemony of harmful Erysipelotrichaceae, and promoted more bacterial diversity. The Lachnospiraceae also significantly protected the animals against obesity and associated insulin-resistance.

Lachnospiraceae contain enzymes that convert carbs and fiber into small molecules called short-chain fatty acids (SCFAs). The scientists observed that two in particular, butyrate and propionate, appeared in significantly greater abundance when Lachnospiracea levels rose. Butyrate and propionate are known to have anti-inflammatory properties that promote gut health. ...
treating people with "good" bacteria or the beneficial SCFAs they produce might one day be a relatively inexpensive strategy to combat obesity as well as diabetes and other obesity-driven conditions.
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  #3   ^
Old Thu, Sep-20-18, 06:56
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teaser teaser is offline
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From what I've seen in mouse studies, when fermentable fibers are effective, they may prevent obesity, but they don't reverse it. But they do result in a less insulin resistant mouse, obese or not.

https://researchdiets.com/formulas/d12451

Of course the high fat diet was high in sucrose.


.... but the low fat diet was even higher in sucrose.

https://researchdiets.com/formulas/d12450b

Which doesn't show that sucrose is "innocent"--only shows that the combination of high fat with high sucrose is worse than high sucrose in and of itself--all else being equal.

Fat sources here were lard and soybean oil. Studies with various diets, low or high in fat, show 8 percent linoleic (omega 6) fatty acid is fattening versus 1 percent which is not. This is shown to work through the endocannabinoid system at least in part, the endocannabinoids in question are produced from arachidonic acid which is produced from the linoleic--and this is also substrate for inflammatory eicosanoids. And cannabinoids have an anti-inflammatory effect... lots of temptation to speculate, here. Like, if promotion of resolution of inflammation is a function of endocannabinoids, but increased appetite is also a function...
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Old Thu, Sep-20-18, 07:07
whynot18 whynot18 is offline
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https://www.healthline.com/nutritio...ds-101#section9

More on short chain fatty acids ...
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