Gut microbiota is associated with dietary intake and metabolic markers in healthy individuals.

Background

Metabolic diseases have been related to gut microbiota, and new knowledge indicates that diet impacts host metabolism through the gut microbiota. Identifying specific gut bacteria associated with both diet and metabolic risk markers may be a potential strategy for future dietary disease prevention. However, studies investigating the association between the gut microbiota, diet, and metabolic markers in healthy individuals are scarce.

Objective

We explored the relationship between a panel of gut bacteria, dietary intake, and metabolic and anthropometric markers in healthy adults.

Design

Forty-nine volunteers were included in this cross-sectional study. Measures of glucose, serum triglyceride, total cholesterol, hemoglobin A1c (HbA1c), blood pressure (BP), and body mass index (BMI) were collected after an overnight fast, in addition to fecal samples for gut microbiota analyzes using a targeted approach with a panel of 48 bacterial DNA probes and assessment of dietary intake by a Food Frequency Questionnaire (FFQ). Correlations between gut bacteria, dietary intake, and metabolic and anthropometric markers were assessed by Pearson's correlation. Gut bacteria varying according to dietary intake and metabolic markers were assessed by a linear regression model and adjusted for age, sex, and BMI.

Results

Of the 48 gut bacteria measured, 24 and 16 bacteria correlated significantly with dietary intake and metabolic and/or anthropometric markers, respectively. Gut bacteria including

Conclusion

Our findings highlight the relationship between the gut microbiota, diet, and metabolic markers in healthy individuals. Further investigations are needed to address whether these findings are causally linked and whether targeting these gut bacteria can prevent metabolic diseases.

Informations de copyright

© 2022 Line Gaundal et al.

Déclaration de conflit d'intérêts

Funding for this research was provided by OsloMet, University of Oslo, Genetic Analysis, and Mills AS. Mills AS had no role in the analysis of the data. L.G., I.R., and T.G. report nothing to declare. M.G.B. is employed at Mills AS. She does not own any stocks in the company. K.R. reports research grants and/or personal fees from Akcea, Amgen, Sanofi, and Sunnovion, and none of which are related to the content of this manuscript. K.B.H. reports grants from Tine SA, Mills AS, Olympic Seafood, Amgen, Sanofi, and Kaneka, and personal fees from Amgen, Sanofi, and Pronova, outside the submitted work. S.M.U. has received research grants from Tine DA, Mills AS, and Olympic Seafood, and none of which are related to the content of this manuscript. M.C.W.M. is involved in projects with research grants from Tine SA and Olympic Seafood and has received research fund from Mills AS, and none of which are related to the content of this manuscript. V.H.T.-H. reports research grants from Mesterbakeren, Det Glutenfrie Verksted, and Norsk cøliakiforening, and none of which are related to the content of this manuscript. She has been employed at Mills AS. She does not own any stocks in the company, and the work performed in this paper was done after she left the company.