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CompletedNCT02562014Updated Sep 29, 2015

Role of Colonic Short Chain Fatty Acids in Obesity

An interventional study of Glucose and Inulin in Obesity, sponsored by University of Toronto. Completed. Open to participants aged 18 Years to 65 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2015-09-29.

Sponsored by University of Toronto · Not applicable, Interventional, and Basic science

Phase
Not applicable
Study type
Interventional
Enrollment
25
Allocation
Randomized
Ages
18 Years to 65 Years
Sex
All
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Study summary

The excess production of colonic short-chain-fatty-acids (SCFA) has been implicated in the promotion of obesity, but colonic fermentation of dietary-fiber to SCFA may also play a role in preventing diabetes. The investigators aimed to compare the effects of two fermentable fibers (inulin and resistant-starch) on postprandial SCFA, glucose, insulin, free-fatty acids (FFA) and gut hormone responses and to compare the responses in healthy overweight and obese (OWO) vs lean (LN) participants. Methods: Using a randomized, single blind, crossover design, 13 OWO and 12 LN overnight fasted participants were studied on 3 separate occasions. On each day they consumed a 300 mL drink containing 75g glucose (Control) or 75g glucose plus 24g inulin (IN), or 28.2g resistant-starch (RS). A standard lunch was served 4 h after the test drink.

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Conditions studied

  • Obesity

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03

In context

Obesity

6,296 studies on the registry are indexed under Obesity; 1,692 are open to participants now.

This study's enrollment of 25 is below the median of 78 across 4,878 interventional studies indexed under Obesity.

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Lead sponsor

University of Toronto is the lead sponsor of 397 studies on the registry; 59 are open to participants now.

Counted across the registry records on this site, refreshed daily.

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Who can participate

Ages eligible
18 Years to 65 Years
Sexes eligible
All
Accepts healthy volunteers
Yes

Inclusion criteria

  • non-pregnant
  • body mass index >=20 and \<=35

Exclusion criteria

Exclusion Criteria:

  • history of diabetes mellitus
  • history of cardiovascular disease
  • history of bowel disease
  • history of kidney disease
  • history of liver disease
  • use of antibiotics within 3 months of enrolment
  • unusual dietary habits
  • fasting glucose >6.9mmol/L
  • hematocrit below normal range for age and sex
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Study design

Phase
Not applicable
Primary purpose
Basic science
Allocation
Randomized
Intervention model
Crossover assignment
Masking
None (open label)
Enrollment
25 participants (actual)

Study arms

  • Other
    Lean

    Participants with body mass index \<=25

    Other: Glucose · Other: Inulin · Other: Resistant Starch

  • Other
    Overweight

    Participants with body mass index \>25

    Other: Glucose · Other: Inulin · Other: Resistant Starch

Interventions

  • OtherGlucose

    75g glucose

  • OtherInulin

    75g glucose plus 24g inulin

  • OtherResistant Starch

    75g glucose plus 28.2g resistant starch

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What researchers measure

Primary outcomes

  1. Incremental area under the serum acetate response curve

    Time frame: For 6 hours after consuming the test meal

Secondary outcomes

  1. Incremental area under the serum propionate response curve

    Time frame: For 6 hours after consuming the test meal

  2. Incremental area under the serum butyrate response curve

    Time frame: For 6 hours after consuming the test meal

  3. Incremental area under the breath hydrogen response curve

    Time frame: For 6 hours after consuming the test meal

  4. Incremental area under the breath methane response curve

    Time frame: For 6 hours after consuming the test meal

  5. Incremental area under the serum glucose response curve

    Time frame: For 4 hours after consuming the test meal

  6. Incremental area under the serum glucose response curve

    Time frame: For 2 hours after consuming the standard lunch

  7. Incremental area under the serum insulin response curve

    Time frame: For 4 hours after consuming the test meal

  8. Incremental area under the serum insulin response curve

    Time frame: For 2 hours after consuming the standard lunch

  9. Incremental area under the serum c-peptide response curve

    Time frame: For 4 hours after consuming the test meal

  10. Incremental area under the serum c-peptide response curve

    Time frame: For 2 hours after consuming the standard lunch

  11. Total area under the serum free-fatty acid response curve

    Time frame: For 4 hours after consuming the test meal

  12. Total area under the serum free-fatty acid response curve

    Time frame: For 2 hours after consuming the standard lunch

Other outcomes

  1. Incremental area under the serum glucagon-like peptide-1 response curve

    Time frame: For 4 hours after consuming the test meal

  2. Incremental area under the serum glucagon-like peptide-1 response curve

    Time frame: For 2 hours after consuming the standard lunch

  3. Incremental area under the serum peptide-YY response curve

    Time frame: For 4 hours after consuming the test meal

  4. Incremental area under the serum peptide-YY response curve

    Time frame: For 2 hours after consuming the standard lunch

  5. Incremental area under the serum ghrelin response curve

    Time frame: For 4 hours after consuming the test meal

  6. Incremental area under the serum ghrelin response curve

    Time frame: For 2 hours after consuming the standard lunch

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Study locations

No study locations are listed for this record.

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References and documents

Publications

  • Rahat-Rozenbloom S, Fernandes J, Cheng J, Wolever TMS. Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans. Eur J Clin Nutr. 2017 Aug;71(8):953-958. doi: 10.1038/ejcn.2016.249. Epub 2016 Dec 14. PubMed 27966574 ↗
  • Rahat-Rozenbloom S, Fernandes J, Cheng J, Gloor GB, Wolever TM. The acute effects of inulin and resistant starch on postprandial serum short-chain fatty acids and second-meal glycemic response in lean and overweight humans. Eur J Clin Nutr. 2017 Feb;71(2):227-233. doi: 10.1038/ejcn.2016.248. Epub 2016 Dec 14. PubMed 27966565 ↗
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Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Sep 29, 2015, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
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Registry details

Key details

Study ID
NCT02562014
Lead sponsor
University of Toronto
Responsible party
Thomas Wolever (Professor, University of Toronto) — Principal investigator
First posted
Sep 29, 2015
Start date
Feb 2012
Primary completion
Jul 2012
Completion
Jan 2013
Last update
Sep 29, 2015

Study contacts

Thomas MS Wolever, MD, PhD
principal investigator · University of Toronto

Oversight

Data monitoring committee
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is completed, as verified in Sep 2015. You cannot join it, but the record below documents what was studied.

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