ObesityNCT02795559
Acute Effects of Dietary Fiber on Postprandial Responses in Lean and Overweight Subjects
A study testing Glucose, Inulin and Resistant starch in people with Obesity and Diabetes, run by University of Toronto at 1 site in Canada.
Trial 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. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- What is being tested?
- Glucose, Inulin and Resistant starch
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 25 participants
- Where
- 1 siteCanada
- Study dates
- Mar 2012to Jul 2012
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- over 18 years of age
Who cannot join
- 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)
Show all 13Show fewer
- 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
Trial locations and contacts
1 site in 1 country.
About this study
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
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.
Read the 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:
- 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
- determine the types of bacteria in the stools of lean and overweight subjects
- 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.
- Being tested
- Glucose, Inulin, Resistant starch
- Keywords
- Nutrition, Humans, Obesity, Blood glucose, Dietary fiber, Appetite, Short chain fatty acids
- Medical subject headings
- Obesity, Diabetes Mellitus
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
GlucoseOther
75g glucose dissolved in 300ml water
InulinOther
75g glucose plus 24g inulin dissolved in 300ml water
Resistant starchOther
75g glucose plus 28g resistant starch in 300ml water
| Study group | Role | What they receive |
|---|---|---|
| Lean | Other | Subjects within the range of desirable body weight (BMI<25) Receives: Other: Glucose; Other: Inulin; Other: Resistant starch |
| OWO | Other | Subjects who are overweight or obese (BMI between 25 and 40) Receives: Other: Glucose; Other: Inulin; Other: Resistant starch |
What is being measured
The primary outcome is the main question the study is designed to answer.
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)
Measured: 0 to 6 hours after the intervention
Secondary outcomes (27)
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)
Measured: 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)
Measured: 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)
Measured: 0 to 6 hours after the intervention
Energy intake
From 3-day diet record, mean energy intake.
Measured: 3 days
Fat intake
From 3-day diet record, mean total fat intake.
Measured: 3 days
Protein intake
From 3-day diet record, mean protein intake.
Measured: 3 days
Carbohydrate intake
From 3-day diet record, mean available carbohydrate intake.
Measured: 3 days
Dietary fiber intake
From 3-day diet record, mean dietary fiber intake.
Measured: 3 days
Fecal microbiota
Ion Torrent V6 16S-rRNA sequencing for comparison of phyla
Measured: 1 day
0-2 hour Glucose response
Incremental area under the curve of the serum glucose response from fasting to 2 hours.
Measured: 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.
Measured: 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.
Measured: 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
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 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.
Measured: 0 to 2 hours after consuming lunch
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted10 Jun 2016 (estimated)
- Study startMar 2012
- Primary completionJul 2012
- Study completionJul 2012
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for ObesityStudies of the same condition, open and under way.
- More trials run by University of TorontoThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Enrolment
- 25 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Toronto
- Sponsor type
- University, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR)
- Responsible party
- Principal investigator, Thomas Wolever, University of Toronto
- Investigators
- Thomas MS Wolever, MD, PhD, Principal investigator, University of Toronto
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02795559
- Sponsor's protocol ID
- Protocol Reference # 27112
- Status last verified
- Jun 2016
- First submitted
- 6 Jun 2016
- Last updated
- 13 Jun 2016
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 13 Jun 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- 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
- ClinicalTrials.gov ID
- NCT02795559
- Acronym / sponsor ID
- Protocol Reference # 27112
- Keywords
- Nutrition, Humans, Obesity, Blood glucose, Dietary fiber, Appetite, Short chain fatty acids
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 25 participants (actual)
- Lead sponsor
- University of TorontoUniversity, hospital or other
- Collaborators
- Canadian Institutes of Health Research (CIHR)
- Study start
- Mar 2012
- Primary completion
- Jul 2012 (actual)
- Study completion
- Jul 2012 (actual)
- First posted
- 10 Jun 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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:
- 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
- determine the types of bacteria in the stools of lean and overweight subjects
- 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 design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Lean | Other | Other: Glucose, Other: Inulin, Other: Resistant starchSubjects within the range of desirable body weight (BMI<25) |
| OWO | Other | Other: Glucose, Other: Inulin, Other: Resistant starchSubjects who are overweight or obese (BMI between 25 and 40) |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- over 18 years of age
Key exclusion criteria (13 listed)
- Pregnant
- BMI<18 or >39.9
- diabetes
- anaemia
- use of diuretics of beta-blockers
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Glucose75g glucose dissolved in 300ml water | Other | Lean, OWO |
| Inulin75g glucose plus 24g inulin dissolved in 300ml water | Other | Lean, OWO |
| Resistant starch75g glucose plus 28g resistant starch in 300ml water | Other | Lean, OWO |
Primary outcome
Serum acetate response
Time frame: 0 to 6 hours after the intervention
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)
27 secondary outcomes
Serum propionate response
Time frame: 0 to 6 hours after the intervention
Serum butyrate response
Time frame: 0 to 6 hours after the intervention
Breath hydrogen response
Time frame: 0 to 6 hours after the intervention
Energy intake
Time frame: 3 days
Fat intake
Time frame: 3 days
Protein intake
Time frame: 3 days
Carbohydrate intake
Time frame: 3 days
Dietary fiber intake
Time frame: 3 days
Fecal microbiota
Time frame: 1 day
0-2 hour Glucose response
Time frame: 0 to 2 hours after consuming treatment
2-4 hour Glucose response
Time frame: 2 to 4 hours after consuming treatment
Second-meal glucose response
Time frame: 0 to 2 hours after lunch
0-2 hour Insulin response
Time frame: 0 to 2 hours after consuming treatment
2-4 hour Insulin response
Time frame: 2-4 hours after consuming treatment
Second-meal Insulin response
Time frame: 0-to 2 hours after lunch
0-2 hour c-peptide response
Time frame: 0 to 2 hours after consuming treatment
2-4 hour c-peptide response
Time frame: 2 to 4 hours after consuming treatment
Second-meal c-peptide response
Time frame: 0-2 hours after lunch
Free-fatty acid rebound
Time frame: 0 to 4 hours after consuming intervention
Acute total glucagon-like peptide-1 response
Time frame: 0 to 4 hours after consuming intervention
Post-lunch total glucagon-like peptide-1 response
Time frame: 0 to 2 hours after consuming lunch
Acute active glucagon-like peptide-1 response
Time frame: 0 to 4 hours after consuming intervention
Post-lunch active glucagon-like peptide-1 response
Time frame: 0 to 2 hours after consuming lunch
Acute peptide tyrosine tyrosine response
Time frame: 0 to 4 hours after consuming intervention
Post-lunch peptide tyrosine tyrosine response
Time frame: 0 to 2 hours after consuming lunch
Acute ghrelin response
Time frame: 0 to 4 hours after consuming intervention
Post-lunch ghrelin response
Time frame: 0 to 2 hours after consuming lunch
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Jun 2016.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Thomas MS Wolever, MD, PhD principal investigator
University of Toronto
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Glucose, Inulin and Resistant starch in people with Obesity and Diabetes, run by University of Toronto at 1 site in Canada.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 13 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 13 Jun 2016. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Canada. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Serum acetate response (time frame: 0 to 6 hours after the intervention). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 13 Jun 2016.