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Fat Mouse

  • Categories:News Center
  • Author:JBH Biotech
  • Origin:Henan Jinbaihe Biotechnology Co.,LTD
  • Time of issue:2022-03-03 16:13
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(Summary description)the causal relationship between gut bacteria obesity and diabetes

Fat Mouse

(Summary description)the causal relationship between gut bacteria obesity and diabetes

  • Categories:News Center
  • Author:JBH Biotech
  • Origin:Henan Jinbaihe Biotechnology Co.,LTD
  • Time of issue:2022-03-03 16:13
  • Views:

Since 2004, a series of important papers have clarified the causal relationship between gut bacteria obesity and diabetes. Gut bacteria control fat metabolism in animals, and when they are out of kilter, they can lead to low and chronic inflammation throughout the body, leading to obesity and insulin resistance. Today, The author of JBH Bio tells you the story of Fat Mouse.

Professor Gordon, of the University of Washington and a member of the National Academy of Sciences, is the world's first to study the physiological effects of gut bacteria using germ-free mice. Time magazine wrote twice in July and November 2009 about their study of obese mice.
First, Gordon's team bred germ-free mice to eat 30 percent more, had a 27 percent lower metabolic rate and had 40 percent less total body fat than normal mice with the bacteria. It seems that gut bacteria make mice eat less, get fatter and more active. On the other hand, the gut bacteria seemed to help the mice digest food more efficiently, absorb calories more efficiently and become more energetic, yet become fatter and less likely to lose weight.
To prove it further, they transplanted gut bacteria from infected mice into the intestines of germ-free mice and found that the bacteria reduced the amount of food the mice ate to the same level as normal mice and increased their total fat mass by up to 50 percent. There is strong evidence that gut bacteria help animals use food more efficiently and store more fat.

More interesting, Gordon raised a group of genetically obese mice called OB and fed them with gut bacteria from both ob and normal mice. As you might expect, if you gave fat mice gut bacteria, they became fat. When normal mice were given intestinal bacteria, their weight was normal. When analyzing the quantity of heat contained in fat and thin rat defecate, discover fat rat defecate quantity of heat is far under thin rat defecate, that is to say, fat rat stays more quantity of heat inside body, so the quantity of heat that defecate educates is low -- really not fat also difficult.
Professor Gordon even experimented on people. They compared identical twins of different weights and found that heavier twins had more thick intestinal walls than thinner twins. Obese volunteers were then given a low-calorie diet and some exercise, and as they lost weight, their gut bacteria became less and less firmicutes.
I'm not going to tell you what Firmicutes and coagulants are, but I'm going to tell you why gut bacteria affect weight.
The amount of microvessels under the villi of the intestine of the bacteria mice was twice as much as that of the germ-free mice, and the natural efficiency of nutrient absorption was high. Many gut bacteria break down dietary fiber and ferment to produce short-chain fatty acids (lactic acid, acetic acid... Etc.), can not only promote the growth of intestinal cells, inhibit inflammatory response, and is an important source of heat. In other words, gut bacteria convert unusable fiber into high-calorie, recyclable fatty acids, and firmicutes are better at this recycling job than clos, so fat people have more firmicutes

Intestinal bacteria not only affect the recovery of intestinal heat, they even control the master switch of the resource recovery and storage system. There is a gene called ghRELin in the body. When you are hungry, the ghrelin turns on, turning on the fat burning system in the body, burning fat inside the body, and turning off the fat decomposition and recycling system in the intestine. When a big meal is eaten, the hunger factor is turned off, so the fat-burning system is switched on and the gut fat recovery system is switched on.
Certain member of fat person intestinal tract bacterium, can do without authorization turn off hunger factor, it is belly hungry obviously, hunger factor can not be opened however, cannot start the adipose combustion system inside body of method, cannot switch intestinal tract adipose decomposes recovery system, no matter how diet, also thin not come down.
Aseptic mice intestinal tract without the kind of bacteria that will shut off hunger factor without authorization, so the use of high fat feed is not fat, and there are bacteria mice, especially fat mice, there will be this kind of bacteria will shut off hunger factor, fat utilization rate is naturally high, the mice will be fat.
We all know that when it comes to weight control, 'diet, exercise, genetics', but Now Professor Gordon's research suggests that gut bacteria may be the ninja behind the scenes. Intestinal bacteria affect the fat decomposition and recovery system in the intestinal tract. Obesity is also an inflammatory disease, and intestinal bacteria are an important factor affecting inflammation. They are interlinked, and now obesity is involved.

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