Acute Effects of Dietary Fiber on Postprandial Responses in Lean and Overweight Subjects

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

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.

Study Overview

• Status: Completed
• Conditions: Obesity; Diabetes
• Intervention / Treatment: Other: Glucose; Other: Inulin; Other: Resistant starch

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.

• Study Type: Interventional
• Enrollment (Actual): 25
• Phase: Not Applicable

Contacts and Locations

Study Locations

• Canada
  • Ontario
    • Toronto, Ontario, Canada, M5C 2X3
      • Glycemic Index Laboratories

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years and older (Adult, Older Adult)
• Accepts Healthy Volunteers: No
• Genders Eligible for Study: All

Description

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

Study Plan

How is the study designed?

Design Details

• Primary Purpose: Basic Science
• Allocation: Randomized
• Interventional Model: Crossover Assignment
• Masking: None (Open Label)

Number of Arms

2

Arms and Interventions

Participant Group / Arm	Intervention / Treatment
Other: Lean; Subjects within the range of desirable body weight (BMI<25)	Other: Glucose; 75g glucose dissolved in 300ml water; Other: Inulin; 75g glucose plus 24g inulin dissolved in 300ml water; Other: Resistant starch; 75g glucose plus 28g resistant starch in 300ml water
Other: OWO; Subjects who are overweight or obese (BMI between 25 and 40)	Other: Glucose; 75g glucose dissolved in 300ml water; Other: Inulin; 75g glucose plus 24g inulin dissolved in 300ml water; Other: Resistant starch; 75g glucose plus 28g resistant starch in 300ml water

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Serum acetate response	Incremental area under the curve of the serum acetate response from the lowest concentration achieved during the first 3 hours to the end of the study (6hr)	0 to 6 hours after the intervention

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
Serum propionate response	Incremental area under the curve of the serum propionate response from the lowest concentration achieved during the first 3 hours to the end of the study (6hr)	0 to 6 hours after the intervention
Serum butyrate response	Incremental area under the curve of the serum butyrate response from the lowest concentration achieved during the first 3 hours to the end of the study (6hr)	0 to 6 hours after the intervention
Breath hydrogen response	Incremental area under the curve of the breath hydrogen response from the lowest concentration achieved during the first 3 hours to the end of the study (6hr)	0 to 6 hours after the intervention
Energy intake	From 3-day diet record, mean energy intake.	3 days
Fat intake	From 3-day diet record, mean total fat intake.	3 days
Protein intake	From 3-day diet record, mean protein intake.	3 days
Carbohydrate intake	From 3-day diet record, mean available carbohydrate intake.	3 days
Dietary fiber intake	From 3-day diet record, mean dietary fiber intake.	3 days
Fecal microbiota	Ion Torrent V6 16S-rRNA sequencing for comparison of phyla	1 day
0-2 hour Glucose response	Incremental area under the curve of the serum glucose response from fasting to 2 hours.	0 to 2 hours after consuming treatment
2-4 hour Glucose response	Incremental area under the curve of the serum glucose response from 2 to 4 hours.	2 to 4 hours after consuming treatment
Second-meal glucose response	Total area under the curve of the serum glucose response for 2 hours after lunch.	0 to 2 hours after lunch
0-2 hour Insulin response	Incremental area under the curve of the serum insulin response from fasting to 2 hours	0 to 2 hours after consuming treatment
2-4 hour Insulin response	Incremental area under the curve of the serum insulin response from 2 to 4 hours.	2-4 hours after consuming treatment
Second-meal Insulin response	Total area under the curve of the serum insulin response for 2 hours after lunch.	0-to 2 hours after lunch
0-2 hour c-peptide response	Incremental area under the curve of the serum c-peptide response from fasting to 2 hours.	0 to 2 hours after consuming treatment
2-4 hour c-peptide response	Incremental area under the curve of the serum c-peptide response from 2 to 4 hours.	2 to 4 hours after consuming treatment
Second-meal c-peptide response	Total area under the curve of the serum c-peptide response for 2 hours after lunch.	0-2 hours after lunch
Free-fatty acid rebound	Increase in serum free-fatty acid concentration from the lowest to the subsequent highest concentration before consuming lunch	0 to 4 hours after consuming intervention
Acute total glucagon-like peptide-1 response	Incremental area under the curve of the serum total glucagon-like peptide-1 response from 0 to 4 hours.	0 to 4 hours after consuming intervention
Post-lunch total glucagon-like peptide-1 response	Incremental area under the curve of the serum total glucagon-like peptide-1 response from 0 to 2 hours after lunch.	0 to 2 hours after consuming lunch
Acute active glucagon-like peptide-1 response	Incremental area under the curve of the serum active glucagon-like peptide-1 response from 0 to 4 hours.	0 to 4 hours after consuming intervention
Post-lunch active glucagon-like peptide-1 response	Incremental area under the curve of the serum active glucagon-like peptide-1 response from 0 to 2 hours after lunch.	0 to 2 hours after consuming lunch
Acute peptide tyrosine tyrosine response	Incremental area under the curve of the serum PYY response from 0 to 4 hours.	0 to 4 hours after consuming intervention
Post-lunch peptide tyrosine tyrosine response	Incremental area under the curve of the serum PYY response from 0 to 2 hours after lunch.	0 to 2 hours after consuming lunch
Acute ghrelin response	Incremental area under the curve of the serum ghrelin response from 0 to 4 hours.	0 to 4 hours after consuming intervention
Post-lunch ghrelin response	Incremental area under the curve of the serum ghrelin response from 0 to 2 hours after lunch.	0 to 2 hours after consuming lunch

Collaborators and Investigators

• Sponsor: University of Toronto
• Collaborators: Canadian Institutes of Health Research (CIHR)
• Investigators: Principal Investigator: Thomas MS Wolever, MD, PhD, University of Toronto

Study record dates

Study Major Dates

• Study Start: March 1, 2012
• Primary Completion (Actual): July 1, 2012
• Study Completion (Actual): July 1, 2012

Study Registration Dates

• First Submitted: June 6, 2016
• First Submitted That Met QC Criteria: June 6, 2016
• First Posted (Estimate): June 10, 2016

Study Record Updates

• Last Update Posted (Estimate): June 13, 2016
• Last Update Submitted That Met QC Criteria: June 9, 2016
• Last Verified: June 1, 2016

More Information

Terms related to this study

• Keywords: Humans; Obesity; Nutrition; Appetite; Short chain fatty acids; Dietary fiber; Blood glucose
• Additional Relevant MeSH Terms: Overnutrition; Nutrition Disorders; Overweight; Body Weight; Obesity
• Other Study ID Numbers: Protocol Reference # 27112

Plan for Individual participant data (IPD)

• Plan to Share Individual Participant Data (IPD)?: No