Clinical trial NCT02795559: Acute Effects of Dietary Fiber on Postprandial Responses in Lean and Overweight Subjects
Official title: Role of Colonic Short Chain Fatty Acids in Obesity: Acute Effects of Inulin and Resistant Starch on Postprandial Short Chain Fatty Acid, Glucose, Insulin, Free-fatty Acid and Gut Hormone Responses
Study type: INTERVENTIONAL
Overall status: COMPLETED
Phase: NA
Conditions: Obesity
Diabetes
Keywords: Nutrition
Humans
Obesity
Blood glucose
Dietary fiber
Appetite
Short chain fatty acids
Lead sponsor: University of Toronto
Sponsor class: OTHER
Collaborators: name: Canadian Institutes of Health Research (CIHR)
First posted: 2016-06-10
Enrollment: 25
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Allocation: RANDOMIZED
Intervention model: CROSSOVER
Primary purpose: BASIC_SCIENCE

Brief summary: It has been suggested that obesity occurs because the colonic microbes in obese individuals, compared to those who are lean, produce more short chain fatty acids during the fermentation of dietary fiber; this means that obese individuals obtain more energy from dietary fiber than lean. On the other hand, it is possible that the ability of colonic short chain fatty acids to improve glycemic control and suppress appetite may be reduced in obese subjects. The aim of this study was to determine the acute effects of 2 fibers commonly used as food ingredients, inulin and resistant starch, on postprandial serum responses of short chain fatty acids, glucose, insulin, free-fatty acids and selected gut hormones in lean and overweight or obese subjects.

Detailed description: The human colon (large intestine) contains hundreds of species of bacteria which exist in a symbiotic (mutually beneficial) relationship with their human host. The number and type of colonic bacteria varies in different people. Recent studies show that overweight individuals have different types of bacteria in their colons than lean subjects, and that as overweight subjects lose weight their colonic bacteria change to resemble those in lean subjects. It was suggested that this was because the bacteria in overweight people more efficiently ferment dietary fiber thus producing more SCFAs and providing more energy to the body. However, this is not consistent with other studies showing that high fiber intakes are associated with reduced risk of obesity.

Some studies have shown that overweight people have higher concentrations of SCFA in their stool samples. But the reasons for the difference in stool concentrations of SCFA have not been studied. Stool concentrations of SCFA may differ in lean and overweight people because of differences in type of bacteria in their colons, differences in dietary intakes or maybe because lean and overweight people absorb SCFA produced by bacteria differently.

Therefore, the objectives of this study were to:

1. determine the relationship between SCFA production and the acute effects of consuming an unabsorbed carbohydrate on blood SCFA, FFA, glucose, insulin, c-peptide and gut hormone responses in lean and overweight subjects
2. determine the types of bacteria in the stools of lean and overweight subjects
3. to see if the types of bacteria are correlated with body weight, the composition of the diet, breath gases, fecal SCFA and other demographic and lifestyle factors.

Healthy subjects with a BMI \<25 (lean) or between 25 and 35 (overweight or obese; OWO) took part in a 2 phase study. In phase 1 subjects recorded their dietary intake for 3 days and then provided a stool sample for analysis of micro-organisms and short chain fatty acids. In phase 2 overnight fasted subjects were studied on 3 occasions separated by about a week. On each occasion subjects consumed a control test meal of dextrose, or dextrose plus inulin or dextrose plus resistant start and had breath and blood samples taken at intervals over 4 hours. Subjects were then given a standardized lunch and had more blood and breath samples taken over the next 2 hours.

Eligibility criteria: Inclusion Criteria:

* over 18 years of age

Exclusion Criteria:

* Pregnant
* BMI\<18 or \>39.9
* diabetes
* anaemia
* use of diuretics of beta-blockers
* regular user of antibiotics (≥1 course per year over the last 5 years)
* any use of antibiotics within 3 months
* use of laxatives, weight reducing agents, pre/probiotics or supplements known to influence gastrointestinal function within 3 months
* presence of inflammatory bowel disease, malabsorption, motility disorder, gastrointestinal infection, short bowel, or other condition affecting gastrointestinal function
* liver or kidney disease or major medical or surgical event (within the last 6 months) requiring hospitalization
* high fibre intake (\>30g/day) or other abnormal dietary pattern
* on a weight-loss diet or not on their habitual diet in the two months prior to the study
* unwilling or unable to give informed consent and/or comply with study protocol

Primary outcomes:
measure: Serum acetate response
timeFrame: 0 to 6 hours after the intervention
Secondary outcomes:
measure: Serum propionate response
timeFrame: 0 to 6 hours after the intervention
measure: Serum butyrate response
timeFrame: 0 to 6 hours after the intervention
measure: Breath hydrogen response
timeFrame: 0 to 6 hours after the intervention
measure: Energy intake
timeFrame: 3 days
measure: Fat intake
timeFrame: 3 days
measure: Protein intake
timeFrame: 3 days
measure: Carbohydrate intake
timeFrame: 3 days
measure: Dietary fiber intake
timeFrame: 3 days
measure: Fecal microbiota
timeFrame: 1 day
measure: 0-2 hour Glucose response
timeFrame: 0 to 2 hours after consuming treatment
measure: 2-4 hour Glucose response
timeFrame: 2 to 4 hours after consuming treatment
measure: Second-meal glucose response
timeFrame: 0 to 2 hours after lunch
measure: 0-2 hour Insulin response
timeFrame: 0 to 2 hours after consuming treatment
measure: 2-4 hour Insulin response
timeFrame: 2-4 hours after consuming treatment
measure: Second-meal Insulin response
timeFrame: 0-to 2 hours after lunch
measure: 0-2 hour c-peptide response
timeFrame: 0 to 2 hours after consuming treatment
measure: 2-4 hour c-peptide response
timeFrame: 2 to 4 hours after consuming treatment
measure: Second-meal c-peptide response
timeFrame: 0-2 hours after lunch
measure: Free-fatty acid rebound
timeFrame: 0 to 4 hours after consuming intervention
measure: Acute total glucagon-like peptide-1 response
timeFrame: 0 to 4 hours after consuming intervention
measure: Post-lunch total glucagon-like peptide-1 response
timeFrame: 0 to 2 hours after consuming lunch
measure: Acute active glucagon-like peptide-1 response
timeFrame: 0 to 4 hours after consuming intervention
measure: Post-lunch active glucagon-like peptide-1 response
timeFrame: 0 to 2 hours after consuming lunch
measure: Acute peptide tyrosine tyrosine response
timeFrame: 0 to 4 hours after consuming intervention
measure: Post-lunch peptide tyrosine tyrosine response
timeFrame: 0 to 2 hours after consuming lunch
measure: Acute ghrelin response
timeFrame: 0 to 4 hours after consuming intervention
measure: Post-lunch ghrelin response
timeFrame: 0 to 2 hours after consuming lunch
Other outcomes:
Locations:
city: Toronto
country: Canada
facility: Glycemic Index Laboratories
state: Ontario
Study officials:
affiliation: University of Toronto
name: Thomas MS Wolever, MD, PhD
role: PRINCIPAL_INVESTIGATOR
References: