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RecruitingNCT07760883Met-SLC16A11Updated Aug 12, 2026

Metformin Effects According to SLC16A11 Carrier Status

An observational study in Diabetes Type 2, sponsored by Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran. Recruiting at 1 site in Mexico. Open to participants aged 18 Years to 65 Years. Per ClinicalTrials.gov, last updated 2026-08-12.

Sponsored by Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran · Observational

Study type
Observational
Model
Cohort
Time perspective
Prospective
Enrollment
154
Ages
18 Years to 65 Years
Sex
All
01

Study summary

This prospective observational study will evaluate whether the SLC16A11 risk variant influences the response to metformin in adults with type 2 diabetes. Participants will be classified as carriers or noncarriers and followed for 6 months while receiving extended-release metformin titrated to the maximum tolerated dose, between 1,500 and 2,250 mg/day. The primary outcome is the change in glycated hemoglobin, with additional assessment of seven-point capillary glucose profiles, liver enzymes, visceral fat, lipid profile, and lactate concentrations. The study plans to include 154 participants to compare treatment response between both genetic groups and explore the potential value of a more personalized therapeutic approach.

Read the detailed description

Type 2 diabetes (T2D) is a major global health problem and is closely associated with obesity and an increased risk of microvascular and macrovascular complications. A risk haplotype located in the SLC16A11 gene has been associated with a higher susceptibility to T2D and may contribute substantially to the increased prevalence of the disease in the Mexican population. The SLC16A11 gene encodes a bidirectional solute transporter involved in the transport of monocarboxylates such as pyruvate and lactate. However, it is not yet clear whether this genetic variation influences the metabolic response to metformin.

This prospective, analytical, observational study aims to compare the effect of metformin treatment between adults with T2D who are carriers and noncarriers of the SLC16A11 risk variant. A total of 154 participants are planned to be included. Eligible participants will be men and women aged 18 to 65 years with T2D, glycated hemoglobin of 8% or lower, and an estimated glomerular filtration rate greater than 60 mL/min. Participants may be untreated or receiving metformin alone or as part of dual pharmacological therapy.

All participants will receive extended-release metformin with gradual dose titration according to tolerance. Treatment will begin with 750 mg at night during the first week, increase to 750 mg in the morning and 750 mg at night during the second week, and may reach 750 mg three times daily from the third week onward. The target dose will be the maximum tolerated dose, ranging from 1,500 to 2,250 mg/day. Telephone follow-up will be conducted during titration to assess tolerance and guide dose adjustment.

Participants will be followed for 6 months. The primary objective is to compare the change in glycated hemoglobin between carriers and noncarriers of the SLC16A11 risk variant. Additional outcomes will include the seven-point capillary glucose profile, liver enzymes, visceral fat, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, and lactate concentrations.

The study is based on the hypothesis that carriers of the SLC16A11 risk variant will have a smaller reduction in glycated hemoglobin, estimated at 0.5 percentage points, after 6 months of metformin treatment compared with noncarriers. Understanding whether this genetic variant modifies the response to metformin may contribute to a more personalized therapeutic approach and improve knowledge of the mechanisms involved in metformin-mediated glucose regulation.

Participants receiving three glucose-lowering medications or insulin, as well as those who are pregnant, breastfeeding, have a body mass index of 45 kg/m² or higher, are participating in another study, or have selected chronic diseases such as HIV infection, cancer, or rheumatologic disease, will be excluded. Participants who cannot tolerate at least 1,500 mg/day of metformin, develop an estimated glomerular filtration rate below 30 mL/min during follow-up, or experience a serious adverse event related to metformin will be withdrawn from the study.

02

Conditions studied

  • Diabetes Type 2

Keywords

  • diabetes type 2
  • metformin
  • SLC16A11
  • glycated hemoglobin
03

Who can participate

Ages eligible
18 Years to 65 Years
Sexes eligible
All
Accepts healthy volunteers
No
Sampling method
Non-probability sample

Study population

Adults aged 18 to 65 years with type 2 diabetes and glycated hemoglobin (HbA1c) ≤8%. Participants may be treatment-naïve, receiving metformin monotherapy, or receiving dual glucose-lowering therapy, and must have an estimated glomerular filtration rate (eGFR) >60 mL/min.

Inclusion criteria

  • Male and female participants
  • Aged 18 to 65 years
  • Diagnosis of type 2 diabetes
  • Estimated glomerular filtration rate (eGFR) >60 mL/min
  • Glycated hemoglobin (HbA1c) ≤8%
  • Participants who are treatment-naïve, receiving metformin monotherapy, or receiving dual glucose-lowering therapy
  • Participants who agree to take part in the study

Exclusion criteria

Exclusion Criteria:

  • Participants receiving treatment with three glucose-lowering medications
  • Participants receiving insulin therapy
  • Pregnancy
  • Breastfeeding
  • Chronic conditions such as HIV infection, cancer, or rheumatologic diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA)
  • Body mass index (BMI) ≥45 kg/m²
  • Concurrent participation in another research study
04

Study design

Observational model
Cohort
Time perspective
Prospective
Enrollment
154 participants (estimated)
Patient registry
No
Biospecimen retention
Samples with dna

Groups and cohorts

  • SLC16A11 Risk Variant Carriers

    Individuals with type 2 diabetes who carry the SLC16A11 risk variant and receive metformin treatment as part of their clinical management.

  • SLC16A11 Risk Variant Noncarriers

    Individuals with type 2 diabetes who do not carry the SLC16A11 risk variant and receive metformin treatment as part of their clinical management.

05

What researchers measure

Primary outcomes

  1. Change in Glycated Hemoglobin (HbA1c)

    Change in glycated hemoglobin (HbA1c), expressed as percentage points, from baseline to Week 12 and Week 24. Changes will be compared between participants with type 2 diabetes who are carriers and non-carriers of the SLC16A11 risk variant.

    Time frame: Baseline, Week 12, and Week 24

Secondary outcomes

  1. Change in Fasting Plasma Glucose

    Change in fasting plasma glucose concentration, measured in mg/dL, from baseline to Week 12 and Week 24. Changes will be compared between participants with type 2 diabetes who are carriers and noncarriers of the SLC16A11 risk variant.

    Time frame: Baseline, Week 12, and Week 24

  2. Change in Seven-Point Capillary Glucose Profile

    Change in capillary glucose concentrations, measured in mg/dL, using a seven-point glucose profile: fasting, 2 hours after breakfast, before lunch, 2 hours after lunch, before dinner, 2 hours after dinner, and at bedtime. Results will be compared between SLC16A11 risk variant carriers and noncarriers.

    Time frame: Baseline and Week 24

  3. Change in Alanine Aminotransferase (ALT)

    Change in serum alanine aminotransferase concentration, measured in U/L, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  4. Change in Aspartate Aminotransferase (AST)

    Change in serum aspartate aminotransferase concentration, measured in U/L, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  5. Change in Gamma-Glutamyl Transferase (GGT)

    Change in serum gamma-glutamyl transferase concentration, measured in U/L, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  6. Change in Total Cholesterol

    Change in serum total cholesterol concentration, measured in mg/dL, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  7. Change in High-Density Lipoprotein Cholesterol

    Change in serum high-density lipoprotein cholesterol concentration, measured in mg/dL, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  8. Change in Triglycerides

    Change in serum triglyceride concentration, measured in mg/dL, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  9. Change in Low-Density Lipoprotein Cholesterol

    Change in serum low-density lipoprotein cholesterol concentration, measured in mg/dL, from baseline to Week 12 and Week 24.

    Time frame: Baseline, Week 12, and Week 24

  10. Change in Apolipoprotein B

    Change in serum apolipoprotein B concentration from baseline to Week 24.

    Time frame: Baseline and Week 24

  11. Change in Blood Lactate Concentration

    Change in blood lactate concentration, measured in mmol/L, from baseline to Week 12 and Week 24. Changes will be compared between carriers and noncarriers of the SLC16A11 risk variant.

    Time frame: Baseline, Week 12, and Week 24

  12. Change in Visceral Fat Mass

    Change in visceral fat mass, measured by dual-energy X-ray absorptiometry, from baseline to Week 24. Results will be expressed in grams and compared between SLC16A11 risk variant carriers and noncarriers.

    Time frame: Baseline and Week 24

06

Study locations

1 of 1 sites recruiting
  • Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán
    Mexico City, Mexico City 14080, Mexico
    Recruiting
07

References and documents

Publications

  • Foretz M, Guigas B, Viollet B. Metformin: update on mechanisms of action and repurposing potential. Nat Rev Endocrinol. 2023 Aug;19(8):460-476. doi: 10.1038/s41574-023-00833-4. Epub 2023 May 2. PubMed 37130947 ↗
  • Kim H, Bae S, Yoon HY, Yee J, Gwak HS. Association of the SLC47A1 Gene Variant With Responses to Metformin Monotherapy in Drug-naive Patients With Type 2 Diabetes. J Clin Endocrinol Metab. 2022 Aug 18;107(9):2684-2690. doi: 10.1210/clinem/dgac333. PubMed 35639991 ↗
  • Rusu V, Hoch E, Mercader JM, Tenen DE, Gymrek M, Hartigan CR, DeRan M, von Grotthuss M, Fontanillas P, Spooner A, Guzman G, Deik AA, Pierce KA, Dennis C, Clish CB, Carr SA, Wagner BK, Schenone M, Ng MCY, Chen BH; MEDIA Consortium; SIGMA T2D Consortium; Centeno-Cruz F, Zerrweck C, Orozco L, Altshuler DM, Schreiber SL, Florez JC, Jacobs SBR, Lander ES. Type 2 Diabetes Variants Disrupt Function of SLC16A11 through Two Distinct Mechanisms. Cell. 2017 Jun 29;170(1):199-212.e20. doi: 10.1016/j.cell.2017.06.011. PubMed 28666119 ↗
  • Fontaine E. Metformin-Induced Mitochondrial Complex I Inhibition: Facts, Uncertainties, and Consequences. Front Endocrinol (Lausanne). 2018 Dec 17;9:753. doi: 10.3389/fendo.2018.00753. eCollection 2018. PubMed 30619086 ↗
  • SIGMA Type 2 Diabetes Consortium; Williams AL, Jacobs SB, Moreno-Macias H, Huerta-Chagoya A, Churchhouse C, Marquez-Luna C, Garcia-Ortiz H, Gomez-Vazquez MJ, Burtt NP, Aguilar-Salinas CA, Gonzalez-Villalpando C, Florez JC, Orozco L, Haiman CA, Tusie-Luna T, Altshuler D. Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico. Nature. 2014 Feb 6;506(7486):97-101. doi: 10.1038/nature12828. Epub 2013 Dec 25. PubMed 24390345 ↗
  • Pearson ER. Diabetes: Is There a Future for Pharmacogenomics Guided Treatment? Clin Pharmacol Ther. 2019 Aug;106(2):329-337. doi: 10.1002/cpt.1484. PubMed 31012484 ↗
  • Mofo Mato EP, Guewo-Fokeng M, Essop MF, Owira PMO. Genetic polymorphisms of organic cation transporter 1 (OCT1) and responses to metformin therapy in individuals with type 2 diabetes: A systematic review. Medicine (Baltimore). 2018 Jul;97(27):e11349. doi: 10.1097/MD.0000000000011349. PubMed 29979413 ↗
  • Liang H, Xu W, Zhou L, Yang W, Weng J. Differential increments of basal glucagon-like-1 peptide concentration among SLC47A1 rs2289669 genotypes were associated with inter-individual variability in glycaemic response to metformin in Chinese people with newly diagnosed Type 2 diabetes. Diabet Med. 2017 Jul;34(7):987-992. doi: 10.1111/dme.13351. Epub 2017 Apr 16. PubMed 28321905 ↗
  • Taheri R, Kazerouni F, Mirfakhraei R, Kalbasi S, Shahrokhi SZ, Rahimipour A. The influence of SLC22A3 rs543159 and rs1317652 genetic variants on metformin therapeutic efficacy in newly diagnosed patients with type 2 diabetes mellitus: 25 weeks follow-up study. Gene. 2022 May 20;823:146382. doi: 10.1016/j.gene.2022.146382. Epub 2022 Feb 28. PubMed 35240257 ↗
  • Dujic T, Zhou K, Yee SW, van Leeuwen N, de Keyser CE, Javorsky M, Goswami S, Zaharenko L, Hougaard Christensen MM, Out M, Tavendale R, Kubo M, Hedderson MM, van der Heijden AA, Klimcakova L, Pirags V, Kooy A, Brosen K, Klovins J, Semiz S, Tkac I, Stricker BH, Palmer C, 't Hart LM, Giacomini KM, Pearson ER. Variants in Pharmacokinetic Transporters and Glycemic Response to Metformin: A Metgen Meta-Analysis. Clin Pharmacol Ther. 2017 Jun;101(6):763-772. doi: 10.1002/cpt.567. Epub 2017 Feb 3. PubMed 27859023 ↗
  • Li X, Yang Y, Zhang B, Lin X, Fu X, An Y, Zou Y, Wang JX, Wang Z, Yu T. Lactate metabolism in human health and disease. Signal Transduct Target Ther. 2022 Sep 1;7(1):305. doi: 10.1038/s41392-022-01151-3. PubMed 36050306 ↗
  • Abrahams-October Z, Johnson R, Benjeddou M, Cloete R. The determination of the effect(s) of solute carrier family 22-member 2 (SLC22A2) haplotype variants on drug binding via molecular dynamic simulation systems. Sci Rep. 2022 Oct 8;12(1):16936. doi: 10.1038/s41598-022-21291-4. PubMed 36209293 ↗
  • He L, Wondisford FE. Metformin action: concentrations matter. Cell Metab. 2015 Feb 3;21(2):159-162. doi: 10.1016/j.cmet.2015.01.003. PubMed 25651170 ↗
  • LaMoia TE, Shulman GI. Cellular and Molecular Mechanisms of Metformin Action. Endocr Rev. 2021 Jan 28;42(1):77-96. doi: 10.1210/endrev/bnaa023. PubMed 32897388 ↗
  • Resendiz-Abarca CA, Flores-Alfaro E, Suarez-Sanchez F, Cruz M, Valladares-Salgado A, Del Carmen Alarcon-Romero L, Vazquez-Moreno MA, Wacher-Rodarte NA, Gomez-Zamudio JH. Altered Glycemic Control Associated With Polymorphisms in the SLC22A1 (OCT1) Gene in a Mexican Population With Type 2 Diabetes Mellitus Treated With Metformin: A Cohort Study. J Clin Pharmacol. 2019 Oct;59(10):1384-1390. doi: 10.1002/jcph.1425. Epub 2019 Apr 23. PubMed 31012983 ↗
  • Brooks GA. Lactate shuttles in nature. Biochem Soc Trans. 2002 Apr;30(2):258-64. doi: 10.1042/bst0300258. PubMed 12023861 ↗
  • Brooks GA. The Science and Translation of Lactate Shuttle Theory. Cell Metab. 2018 Apr 3;27(4):757-785. doi: 10.1016/j.cmet.2018.03.008. PubMed 29617642 ↗
  • Foretz M, Guigas B, Viollet B. Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus. Nat Rev Endocrinol. 2019 Oct;15(10):569-589. doi: 10.1038/s41574-019-0242-2. Epub 2019 Aug 22. PubMed 31439934 ↗
  • Gong L, Goswami S, Giacomini KM, Altman RB, Klein TE. Metformin pathways: pharmacokinetics and pharmacodynamics. Pharmacogenet Genomics. 2012 Nov;22(11):820-7. doi: 10.1097/FPC.0b013e3283559b22. No abstract available. PubMed 22722338 ↗
08

Registry details

Key details

Study ID
NCT07760883
Lead sponsor
Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran
Responsible party
Paloma Almeda-Valdés (Staff Physician and Investigator at the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran) — Principal investigator
First posted
Aug 12, 2026
Start date
Sep 23, 2020
Primary completion
Jul 2027 (estimated)
Completion
Dec 2027 (estimated)
Last update
Aug 12, 2026

Study contacts

Paloma Almeda Valdés, MD, PhD
Contact
paloma.almedav@incmnsz.mx
525554870900 ext. 2405

Oversight

Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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