Wed, Jul-05-17, 05:29
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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gut bacteria/obesity
Quote:
Altering gut bacteria pathways may stimulate fat tissue to prevent obesity
Cleveland Clinic researchers have uncovered a biological link between gut bacteria metabolism and obesity. The team showed that blocking a specific intestinal microbial pathway can prevent obesity and insulin resistance, as well as cause fat tissue to become more metabolically active. The study was recently published in Cell Reports.
The research team, led by J. Mark Brown, Ph.D., of Cleveland Clinic's Lerner Research Institute, studied the metabolic pathway that creates trimethylamine oxide (TMAO), a chemical produced by gut bacteria during digestion of key nutrients -- choline, lecithin and carnitine -- found abundantly in animal products, such as red meat, processed meats, egg yolks and liver.
Dr. Brown's colleague on the current study -- Stanley Hazen, M.D., Ph.D. -- previously showed that high levels of TMAO are associated with a higher risk of severe cardiovascular events, such as heart attack and stroke.
Since cardiovascular disease and obesity are so closely linked, the team hypothesized that TMAO may also be involved in metabolic pathways that lead to obesity. They focused on a host enzyme called flavin-containing monooxygenase 3(FMO3), which converts TMAO into its active form. They discovered that mice that had a missing or deactivated FMO3 gene were protected from obesity, even when fed a high-fat, high-calorie diet. Furthermore, the FMO3-negative mice showed higher expression of genes associated with beige or brown fat cells, which are more metabolically active than white fat cells.
The study confirmed in 435 patients that high levels of TMAO are associated with higher incidence of Type 2 diabetes.
"Obesity, diabetes and cardiovascular disease are strongly linked. While the microbiome has been shown to affect cardiovascular disease, there is as yet no concrete evidence of precisely how gut bacteria influence obesity," Brown said. "These findings shed light on a possible way to manipulate the microbiome with therapeutics to combat our obesity and diabetes epidemic."
Brown is a member of the scientific staff in the Lerner Research Institute's Department of Cellular & Molecular Medicine. Rebecca Schugar, PhD, is first author on the publication in Cell Reports.
"Given the numerous strong associations of the gut microbe-driven TMAO pathway with human disease, this work has broad implications for drug discovery efforts targeting gut microbes themselves," said Dr. Hazen, chair of the Department of Cellular & Molecular Medicine for the Lerner Research Institute and section head of Preventive Cardiology & Rehabilitation in the Miller Family Heart & Vascular Institute at Cleveland Clinic. "However, additional work is needed to better understand the entire pathway and the links between TMA, FMO3, TMAO and human health."
TMAO is a byproduct of bacterial digestion of choline, lecithin and carnitine, nutrients that are especially abundant in animal products such as red meat, processed meats and liver. Dr. Hazen, who also holds the Jan Bleeksma Chair in Vascular Cell, has previously linked TMAO to an increased risk of cardiovascular disease and has shown it can be a powerful tool for predicting future heart attacks, stroke and death in multiple patient populations. Dr. Hazen is an inventor of a test for TMAO that was licensed to Cleveland HeartLab, Inc., a Cleveland Clinic spin-off company. Dr. Hazen and Cleveland Clinic would benefit financially from sales of the test.
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This is a fun area. A vegan might be tempted to just accept that these nutrients that meat is rich in are bad for you. Low carbers might be tempted to point out that the likely outcome of deficiency in these nutrients is fatty liver.
There is some evidence that choline deficiency can protect mice from diet induced diabetes, but they do get fatty liver in the process. And there's this;
https://www.hindawi.com/journals/jobe/2012/319172/
Abstract
Quote:
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Previous studies demonstrated that choline supply is directly linked to high-fat-diet-induced obesity and insulin resistance in mice. The aim of this study was to evaluate if choline supply could also modulate obesity and insulin resistance caused by a genetic defect. Eight-week-old male ob/ob mice were fed for two months with either choline-deficient or choline-supplemented diet. Tissue weight including fat mass and lean mass was assessed. Intracellular signaling, plasma glucagon and insulin, and glucose and insulin tolerance tests were also investigated. The choline-deficient diet slowed body weight gain and decreased fat mass. Choline deficiency also decreased plasma glucose level and improved glucose and insulin tolerance although fatty liver was exacerbated. Increased adipose lipolytic activity, decreased plasma glucagon and reduced expression of hepatic glucagon receptor were also observed with the choline-deficient diet. Our results demonstrate that a choline-deficient diet can decrease fat mass and improve glucose tolerance in obese and diabetic mice caused by a genetic defect.
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Of course if you approach this from the gut bacteria side rather than as a "bad nutrients" thing, this might yield approaches where people aren't trying to decide whether they'd rather have obesity and diabetes, or a fatty liver.
Another question is whether there's a sweet-spot for these nutrients. Also meal-timing might make a difference, keeping tmao elevated throughout the day vs. a smaller window. Since these approaches can be protective vs. diabetes and obesity, it's probably reasonable to suspect they might be protective against this potential mechanism. |
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