Time-restricted feeding modifies the fecal lipidome and the gut microbiota

Authors: RUST, BRENT - Washington State University; PICKLO, MATTHEW - Former ARS Employee; Yan, Lin; MEHUS, AARON - University Of North Dakota; Zeng, Huawei

Submitted to: Nutrients
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2023
Publication Date: 3/23/2023
Citation: Rust, B.M., Picklo, M.J., Yan, L., Mehus, A.A., Zeng, H. 2023. Time-restricted feeding modifies the fecal lipidome and the gut microbiota. Nutrients. 15(7):1-17. https://doi.org/10.3390/nu15071562.
DOI: https://doi.org/10.3390/nu15071562

Interpretive Summary: Diet-induced obesity is a risk factor for several chronic diseases (e.g., cardiovascular disease, diabetes, cancer), and overweight and obesity affect two-thirds of Americans and an estimated 2.3 billion people worldwide. Recent studies indicate that an effective approach to reducing obesity and its associated negative health consequences is to limit food availability to no more than 12 hours per day, known as time-restricted feeding (TRF). However, the mechanism underlying this observation remains to be determined. In this study, we demonstrate that TRF alters the bacterial composition and lipid metabolism in the colon in a mouse model. The information will be useful for scientists and health-care professionals who are interested in diet and healthy gut.

Technical Abstract: Time-restricted feeding (TRF) has been identified as an approach to reduce risk of obesity-related metabolic diseases. However, the underlying molecular mechanisms remain largely undetermined. We hypothesize that TRF reduces absorption of dietary fat (particularly high saturated fat diet) due to shortened feeding times, which subsequently changes fecal microbiome and lipidome. In this report, three groups of C57BL/6 mice were fed either a control diet with ad libitum feeding (16% energy from fat) (Ctrl-AL), a high-fat diet (48% energy from fat) with ad libitum feeding (HF-AL), or a high fat diet with time-restricted feeding (HF-TRF) for 12 weeks. No changes of microbiota at the phyla level were detected, but 8 taxonomic families were altered by either feeding timing or dietary fat content. The HF-AL diet doubled the total fecal fatty acid content of the Ctrl-AL diet while the HF-TRF doubled the total fecal fatty acid content of the HF-AL diet. Primary fecal bile acids were unaffected by diet. Total short chain fatty acids were reduced by HF-AL, but this effect was diminished by HF-TRF. Each diet produced distinct relationships between the relative abundance of taxonomic families and fecal lipids. We conclude that, in a mouse model, the mitigation of an obesogenic diet observed in TRF is in part due to the substantial increase in excretion of fat in the feces which may be attributed to insufficient bile acid secretion. Furthermore, we observe differential effects of fat content and feeding timing on the fecal microbiota and on the relationship between the microbiota and fecal lipids.