This is such a fascinating field of study that just following progress of their research feels like watching an Alfred Hitchcock thriller!! More news on the Amazon inside us:
"Emory's Gewirtz and his team tracked the gut microbiota in mice as the rodents experienced different kinds of metabolic disorders, such as obesity and insulin resistance. They bred mice with a genetic deficiency (specifically, the absence of Toll-like receptor 5, or TLR5, which has a hand in immune response) to see how it might change their microbial gut communities and metabolic health—and try to understand the order in which the changes were happening. "It's very much appreciated that obesity is associated with insulin resistance and type 2 diabetes," Gewirtz says. But "which comes first is not entirely clear."
They found that their mice without the TLR5
Gewirtz and others propose that inflammation—in conjunction with changes in the gut microbiome—might be driving the cycle. Inflammation can change the character of the gut microbes, in some cases allowing more calories to be extracted from food. But, Gewirtz says, "We do not know which is coming first" if inflammation is changing the microbiota or vice versa. It is likely, he notes, that whatever kicks off the process, it will start a sort of feedback loop, where one will increase accelerates the other.
How much of their findings in mice are likely to translate to humans? The stomach bacteria in mice are not found in people. But Gewirtz and his team noted that analogous species live in the human stomach. "We think it's very plausible" that the findings will carry over to humans, especially because they "fit with a lot of the ideas" currently circulating in the research community about insulin resistance and inflammation, Gewirtz says. His group has already started a new investigation comparing the human genes and microbial profiles of people with metabolic syndrome to healthy controls to see if some of the same correlations in mice appear in humans." gene—even when put on restricted diets—still showed insulin resistance, suggesting that insulin resistance might lead to obesity rather than the other way around. But if these mice were allowed to eat as they pleased, they ate 10 percent more than their peers and, by 20 weeks old, had body mass indexes that were 20 percent higher. Many researchers and public health officials have blamed the availability (and content) of contemporary foods, increasingly sedentary lifestyles and human genetics for more metabolic syndrome cases. But the mouse study suggests that there might be more to the picture. "The tendency to overeat may be underlain by changes that are more likely physiological than genetic," Gewirtz says."
"Emory's Gewirtz and his team tracked the gut microbiota in mice as the rodents experienced different kinds of metabolic disorders, such as obesity and insulin resistance. They bred mice with a genetic deficiency (specifically, the absence of Toll-like receptor 5, or TLR5, which has a hand in immune response) to see how it might change their microbial gut communities and metabolic health—and try to understand the order in which the changes were happening. "It's very much appreciated that obesity is associated with insulin resistance and type 2 diabetes," Gewirtz says. But "which comes first is not entirely clear."
They found that their mice without the TLR5
Gewirtz and others propose that inflammation—in conjunction with changes in the gut microbiome—might be driving the cycle. Inflammation can change the character of the gut microbes, in some cases allowing more calories to be extracted from food. But, Gewirtz says, "We do not know which is coming first" if inflammation is changing the microbiota or vice versa. It is likely, he notes, that whatever kicks off the process, it will start a sort of feedback loop, where one will increase accelerates the other.
How much of their findings in mice are likely to translate to humans? The stomach bacteria in mice are not found in people. But Gewirtz and his team noted that analogous species live in the human stomach. "We think it's very plausible" that the findings will carry over to humans, especially because they "fit with a lot of the ideas" currently circulating in the research community about insulin resistance and inflammation, Gewirtz says. His group has already started a new investigation comparing the human genes and microbial profiles of people with metabolic syndrome to healthy controls to see if some of the same correlations in mice appear in humans." gene—even when put on restricted diets—still showed insulin resistance, suggesting that insulin resistance might lead to obesity rather than the other way around. But if these mice were allowed to eat as they pleased, they ate 10 percent more than their peers and, by 20 weeks old, had body mass indexes that were 20 percent higher. Many researchers and public health officials have blamed the availability (and content) of contemporary foods, increasingly sedentary lifestyles and human genetics for more metabolic syndrome cases. But the mouse study suggests that there might be more to the picture. "The tendency to overeat may be underlain by changes that are more likely physiological than genetic," Gewirtz says."
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