It has been suggested that the actual obesity epidemy is related to chronic overconsumption of added or free sugars. The increasing popularity of artificial sweeteners attest the population willingness to reduce added sugars intake and to use alternatives to alleviate health impact of free sugar overconsumption. However, recent findings suggest that artificial sweeteners may rather contribute to obesity epidemy and its associated adverse health effects, potentially via a negative impact on gut microbiota. It has been shown in various studies that, for the same amount of sucrose, unrefined sugars (such as maple syrup) are associated with favorable metabolic effects. The polyphenols contained in maple syrup, especially lignans, could contribute to these positive effects. Indeed, the strong impact of those biomolecules on the modulation of gut microbiota and on gastro-intestinal and metabolic health has been demonstrated in several studies. It is therefore highly relevant to test the hypothesis that the substitution of refined sugar by an equivalent amount of maple syrup (5% of daily energy intake) result in a lesser metabolic deterioration, by the modulation of maple syrup on gut microbiota, than the one observed with refined sugar.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
QUADRUPLE
Enrollment
47
Substitution of refined sugar by an equivalent quantity of maple syrup (5% of daily energy intake) in the participant diet. A dietitian will help study subjects to target added sugar sources in their usual diet and suggest ways to substitute it with maple syrup.
Substitution of refined sugar by an equivalent quantity of maple-flavored sucrose syrup (5% of daily energy intake) in the participant diet. A dietitian will help study subjects to target added sugar sources in their usual diet and suggest ways to substitute it with the placebo (sucrose syrup).
INAF, Université Laval
Québec, Canada
Change in Glucose homeostasis
Evaluation of plasma glucose, insulin and c-peptide concentration using a 3-hour oral glucose tolerance test
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Endotoxemia
Plasma Lipopolysaccharides (LPS) and Lipopolysaccharide Binding Protein (LBP)
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Intestinal permeability
Plasma zonulin
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Inflammation state of the tissue
Fecal calprotectin and chromogranin
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Short chain fatty acids in the feces
Measure short chain fatty acids in the feces
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Gut health and stool consistency
Evaluation of gastrointestinal symptoms and stool consistency using standardized questionnaires (the gastrointestinal symptom rating scale (GSRS) and Bristol stool chart)
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in fat accumulation in the liver
Evaluation of fat accumulation by magnetic resonance imaging (MRI)
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Glucose homeostasis
Evaluation of glycated haemoglobin
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Lipid profile
Evaluation of plasma triglycerides (TG), Total cholesterol, LDL, HDL, Apolipoprotein B and free fatty acids end of two dietary treatment
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in anthropometric measurements
Evaluation of bmi with weight and height measurements
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in anthropometric measurements
Evaluation of waist circumference
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in body composition
Evaluation of body composition by osteodensitometry
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in chronic inflammation
Evaluation of plasma high sensitive C-Reactive Protein (hs-CRP)
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in gene expression levels
Transcriptomic analyses to investigate underlying mechanisms of action
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in circulating levels of plasma metabolites
Metabolomic analyses to investigate underlying mechanisms of action
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in maple-derived metabolites present in stool
Evaluation of metabolome: camu-camu derived metabolites, short chain fatty acids, branched chain fatty acids, bile acids, phenolic compounds
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in blood pressure
Evaluation of systolic and diastolic blood pressure
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Gut Microbiota Composition
Gut microbiota composition will be evaluated by 16S rRNA amplicon sequencing (V3-V4 region)
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Gut Microbiota Composition
Gut microbiota composition will also be evaluated by whole genome sequencing
Time frame: Change between the beginning and the end of maple syrup treatment (8 weeks)
Change in Gut Microbiota alpha Diversity
To quantify bacterial alpha diversity, Shannon's reciprocal index will be calculated
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Gut Microbiota alpha Diversity
To quantify bacterial alpha diversity, Simpson's reciprocal index will be calculated
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
Change in Gut Microbiota beta Diversity
Principal component analysis (PCA) will be performed on the Aitchison distance matrix to measure beta diversity.
Time frame: Change between the beginning and the end of each treatment (8 weeks each)
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