We know from studies on jet lag and night shifts that metabolism — how bodies use energy from food — is linked to the body’s circadian rhythms. These rhythms, regular daily fluctuations in mental and bodily functions, are communicated and carried out via signals sent from the brain and liver. Light and dark signals guide circadian rhythms, but it appears that microbes have a role to play as well.
All humans have a set of bacteria, viruses and fungi living in our guts, called the gut microbiome, which helps us digest food — and also interacts with the body in a number of other ways: there is evidence they affect allergies, mental health, weight and other metabolic conditions.
Researchers found that mice with a normal set of gut microbes showed evidence of a regular daily microbial cycle, with different species flourishing in different parts of the day and producing different compounds as a result. These compounds appear to act on the liver — they affected how circadian clock genes were expressed in the liver.
A high-fat diet reduced the variation in the microbial cycle; the circadian clock genes were disrupted, and the mice gained weight.
Meanwhile, “germ-free” mice raised without a normal gut microbiome showed evidence of a disrupted circadian clock cycle, but did not gain weight even on a high-fat diet.
The researchers hypothesize that high-fat diets change the compounds that microbes produce, thus disrupting the liver’s circadian clock signaling.
“The earlier explanation for microbiome-related weight gain was that some bacteria make calories from food more available to your body, but this is a fundamental alternative explanation,” said Jack Gilbert, an Argonne microbial ecologist who co-authored the study.
Next, Gilbert said, “we’d like to more rigorously explore what kinds of diets trigger this response.”
The study, “Effects of Diurnal Variation of Gut Microbes and High-Fat Feeding on Host Circadian Clock Function and Metabolism,” was published in Cell Host & Microbe.
The research, performed at Argonne, the University of Chicago, and the University of Wisconsin in Madison, was supported by the National Institute of Health’s (NIH) National Institute of Diabetes and Digestive and Kidney Diseases; the Peter and Carol Goldman Family Research Fund; the Washington University in St. Louis’s Digestive Diseases Research Core Center; and the Environmental Protection Agency’s STAR graduate fellowship program.
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