Impact of OCT1 on Metformin Tolerance

NCT ID: NCT02586636

Last Updated: 2018-06-13

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

PHASE4

Total Enrollment

61 participants

Study Classification

INTERVENTIONAL

Study Start Date

2016-03-31

Study Completion Date

2018-04-09

Brief Summary

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Metformin is the first-line treatment for medical management of Type 2 Diabetes. Up to 25% of patients experience significant gastrointestinal symptoms and in approximate 5%, side-effects result in the discontinuation of metformin. It would be of great clinical significance if the underlying cause of this intolerance was identified.

Recent data has highlighted a metformin transporter in the gut - Organic Cation Transporter 1(OCT1) - as a potential culprit for the variability in metformin tolerance. Across a diabetic population, up to one in four people were shown to have a single reduced function allele for OCT1, with approximately 8% having two reduced function alleles. This may increase the risk of the individual experiencing metformin-associated side-effects, potentially due to accumulation within the cells lining the intestine. The investigators aim to show that loss of function of OCT1, either due to genetic variation or drug inhibition of OCT1, may lead to an increase in the symptoms associated with metformin intolerance.

The study is being undertaken at the Clinical Research Centre in Ninewells Hospital, Dundee. The investigators will recruit participants from the GoDARTS study (Genetics of Diabetes and Audit Research Tayside Study). The participants will be healthy controls, i.e. non-diabetic, and recruited according to their genotype of OCT1 (information from GoDARTS). The volunteers will then enter a matched cross-over study with two treatment periods. Metformin is taken during both treatment periods alongside either Omeprazole (a proton pump inhibitor used to prevent excess stomach acid, known to interact with OCT1) or placebo. The metformin dose is increased gradually during each period, to a maximum tolerated dose. The investigators expect to see a lower maximum tolerated dose in individuals with loss of function genotype, or in those taking concurrent omeprazole compared to placebo. The study will last approximately 9 weeks. Volunteers have 3 visits to the CRC, and weekly phone call interviews.

Detailed Description

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Conditions

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Tolerance

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

CROSSOVER

Primary Study Purpose

BASIC_SCIENCE

Blinding Strategy

DOUBLE

Participants Investigators

Study Groups

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OCT1 -/-

Cohort of patients with two loss of function alleles for OCT1. The participants within this group will receive metformin at increasing dose to a maximum tolerated dose over two distinct four week treatment periods. The concurrent treatment order of omeprazole and placebo will be randomised within the cohort.

Group Type OTHER

Metformin

Intervention Type DRUG

Metformin is given alongside omeprazole / placebo. Started at low dose and titrated gradually over four weeks according to the individual's tolerance of metformin. We anticipate that their tolerance of metformin will be reduced by loss of function variants in OCT1, and by concurrent use of OCT1 inhibiting drugs (in our study this is omeprazole).

Omeprazole

Intervention Type DRUG

Given as concurrent treatment in one of the two treatment periods. Omeprazole treatment dose is fixed at 20mg twice daily for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

Placebo

Intervention Type DRUG

Given as concurrent treatment in one of the two treatment periods. Placebo treatment dose is fixed at one tablet twice daily (to match the dosing pattern of omeprazole) for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

OCT wt/wt

Cohort of patients with two "normal" or wild type alleles for OCT1. The participants within this group will receive metformin at increasing dose to a maximum tolerated dose over two distinct four week treatment periods. The concurrent treatment order of omeprazole and placebo will be randomised within the cohort.

Group Type OTHER

Metformin

Intervention Type DRUG

Metformin is given alongside omeprazole / placebo. Started at low dose and titrated gradually over four weeks according to the individual's tolerance of metformin. We anticipate that their tolerance of metformin will be reduced by loss of function variants in OCT1, and by concurrent use of OCT1 inhibiting drugs (in our study this is omeprazole).

Omeprazole

Intervention Type DRUG

Given as concurrent treatment in one of the two treatment periods. Omeprazole treatment dose is fixed at 20mg twice daily for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

Placebo

Intervention Type DRUG

Given as concurrent treatment in one of the two treatment periods. Placebo treatment dose is fixed at one tablet twice daily (to match the dosing pattern of omeprazole) for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

Interventions

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Metformin

Metformin is given alongside omeprazole / placebo. Started at low dose and titrated gradually over four weeks according to the individual's tolerance of metformin. We anticipate that their tolerance of metformin will be reduced by loss of function variants in OCT1, and by concurrent use of OCT1 inhibiting drugs (in our study this is omeprazole).

Intervention Type DRUG

Omeprazole

Given as concurrent treatment in one of the two treatment periods. Omeprazole treatment dose is fixed at 20mg twice daily for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

Intervention Type DRUG

Placebo

Given as concurrent treatment in one of the two treatment periods. Placebo treatment dose is fixed at one tablet twice daily (to match the dosing pattern of omeprazole) for four weeks duration. Omeprazole, in our study, is used as an OCT1 inhibitor, and we hypothesise that this will reduce an individual's maximum tolerated dose of metformin during concurrent treatment. This will be compared to the other treatment period in which concurrent treatment is a placebo, and therefore, the maximum tolerated dose of metformin would not be affected.

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* Aged 18 - 80
* White European (to limit genetic variation as much as possible)
* Non-diabetic
* No previous treatment with metformin
* No known gastrointestinal pathology e.g. inflammatory bowel disease, IBS, coeliac
* No daily treatment with PPI, anti-spasmodic, or anti-motility drugs
* No daily OCT1 inhibiting drugs
* Able to complete the symptom severity score and Bristol stool chart independently i.e. no cognitive impairment or visual impairment
* Normal renal function - eGFR\>60
* Known OCT1 genotype - either normal ("wild type") or two reduced function alleles.

* Heterozygous OCT1 genotype i.e. only one reduced function allele
* Recent involvement (\<30 days) in a CTIMP
* Pregnancy or planning to conceive
* Inability/unwillingness to comply with the protocol
Minimum Eligible Age

18 Years

Maximum Eligible Age

80 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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University of Dundee

OTHER

Sponsor Role collaborator

NHS Tayside

OTHER_GOV

Sponsor Role lead

Responsible Party

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Laura McCreight

Principal Investigator

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Ewan R Pearson, MBBCh, PhD

Role: STUDY_CHAIR

University of Dundee / NHS Tayside

Locations

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Ninewells Hospital

Dundee, Angus, United Kingdom

Site Status

Countries

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United Kingdom

References

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Koehler MR, Wissinger B, Gorboulev V, Koepsell H, Schmid M. The two human organic cation transporter genes SLC22A1 and SLC22A2 are located on chromosome 6q26. Cytogenet Cell Genet. 1997;79(3-4):198-200. doi: 10.1159/000134720.

Reference Type BACKGROUND
PMID: 9605850 (View on PubMed)

Koepsell H, Endou H. The SLC22 drug transporter family. Pflugers Arch. 2004 Feb;447(5):666-76. doi: 10.1007/s00424-003-1089-9. Epub 2003 Jul 19.

Reference Type BACKGROUND
PMID: 12883891 (View on PubMed)

Han TK, Proctor WR, Costales CL, Cai H, Everett RS, Thakker DR. Four cation-selective transporters contribute to apical uptake and accumulation of metformin in Caco-2 cell monolayers. J Pharmacol Exp Ther. 2015 Mar;352(3):519-28. doi: 10.1124/jpet.114.220350. Epub 2015 Jan 6.

Reference Type BACKGROUND
PMID: 25563903 (View on PubMed)

Proctor WR, Bourdet DL, Thakker DR. Mechanisms underlying saturable intestinal absorption of metformin. Drug Metab Dispos. 2008 Aug;36(8):1650-8. doi: 10.1124/dmd.107.020180. Epub 2008 May 5.

Reference Type BACKGROUND
PMID: 18458049 (View on PubMed)

Muller J, Lips KS, Metzner L, Neubert RH, Koepsell H, Brandsch M. Drug specificity and intestinal membrane localization of human organic cation transporters (OCT). Biochem Pharmacol. 2005 Dec 5;70(12):1851-60. doi: 10.1016/j.bcp.2005.09.011. Epub 2005 Nov 2.

Reference Type BACKGROUND
PMID: 16263091 (View on PubMed)

Han TK, Everett RS, Proctor WR, Ng CM, Costales CL, Brouwer KL, Thakker DR. Organic cation transporter 1 (OCT1/mOct1) is localized in the apical membrane of Caco-2 cell monolayers and enterocytes. Mol Pharmacol. 2013 Aug;84(2):182-9. doi: 10.1124/mol.112.084517. Epub 2013 May 16.

Reference Type BACKGROUND
PMID: 23680637 (View on PubMed)

Dujic T, Zhou K, Donnelly LA, Tavendale R, Palmer CN, Pearson ER. Association of Organic Cation Transporter 1 With Intolerance to Metformin in Type 2 Diabetes: A GoDARTS Study. Diabetes. 2015 May;64(5):1786-93. doi: 10.2337/db14-1388. Epub 2014 Dec 15.

Reference Type BACKGROUND
PMID: 25510240 (View on PubMed)

Stage TB, Brosen K, Christensen MM. A Comprehensive Review of Drug-Drug Interactions with Metformin. Clin Pharmacokinet. 2015 Aug;54(8):811-24. doi: 10.1007/s40262-015-0270-6.

Reference Type BACKGROUND
PMID: 25943187 (View on PubMed)

Christensen MM, Brasch-Andersen C, Green H, Nielsen F, Damkier P, Beck-Nielsen H, Brosen K. The pharmacogenetics of metformin and its impact on plasma metformin steady-state levels and glycosylated hemoglobin A1c. Pharmacogenet Genomics. 2011 Dec;21(12):837-50. doi: 10.1097/FPC.0b013e32834c0010.

Reference Type BACKGROUND
PMID: 21989078 (View on PubMed)

Christensen MMH, Hojlund K, Hother-Nielsen O, Stage TB, Damkier P, Beck-Nielsen H, Brosen K. Steady-state pharmacokinetics of metformin is independent of the OCT1 genotype in healthy volunteers. Eur J Clin Pharmacol. 2015 Jun;71(6):691-697. doi: 10.1007/s00228-015-1853-8. Epub 2015 May 5.

Reference Type BACKGROUND
PMID: 25939711 (View on PubMed)

Other Identifiers

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2015DM13

Identifier Type: -

Identifier Source: org_study_id

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