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Abstract
Objective We evaluated the effects of ursodeoxycholic acid (UDCA) on glucagon-like peptide-1 (GLP-1) secretion and glucose tolerance in patients with type 2 diabetes with chronic liver disease.
Research design and methods Japanese patients with type 2 diabetes (glycated hemoglobin (HbA1c) levels ≥7.0%) and chronic liver disease were included in this study. Sixteen patients (HbA1c level, 7.2%±0.6%(55.2 mmol/mol)) were randomized to receive 900 mg UDCA for 12 weeks followed by 50 mg sitagliptin add-on therapy for 12 weeks (UDCA-first group; n=8) or 50 mg sitagliptin for 12 weeks followed by 900 mg UDCA add-on therapy for 12 weeks (sitagliptin-first group; n=8). All patients underwent a liquid high-fat meal test before and after 12 or 24 weeks of treatment.
Results The baseline characteristics were similar between the UDCA-first and sitagliptin-first groups. There was a decrease in body weight (72.5±8.4 to 70.6±8.6 kg; P=0.04) and the HbA1c level (7.0%±0.3% to 6.4%±0.5%(53.0 to 46.4 mmol/mol); P=0.01) in the UDCA-first group. The HbA1c level decreased further after sitagliptin administration (6.4%±0.5% to 6.0%±0.4%(46.4 to 42.1 mmol/mol); P<0.01). Although there were no initial changes in the weight and HbA1c level in the sitagliptin-first group, the HbA1c level decreased after UDCA addition (7.1%±1.1% to 6.6%±0.9%(54.1 to 48.6 mmol/mol); P=0.04). UDCA alone increased the area under the curve0–30 for GLP-1 response (115.4±47.2 to 221.9±48.9 pmol·min/L; P<0.01), but not the glucose-dependent insulinotropic polypeptide response, in the UDCA-first group.
Conclusions UDCA treatment resulted in a greater reduction in HbA1c levels, and an increased early phase GLP-1 secretion.
Trial registration number NCT01337440.
- glp-1
- incretin hormones
- clinical studies
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Footnotes
Contributors KRS collected data and wrote the manuscript. TO, K-iK, YT and HM collected the data and reviewed the manuscript. SK contributed to the discussion and reviewed the manuscript. TT contributed to the discussion, reviewed and edited the manuscript. TT is the guarantor of this work and as such, had full access to all the study data and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding This work was supported by the Japan Society for the Promotion of Science KAKENHI (Grant Number 16K19533; KRS).
Competing interests None declared.
Patient consent Obtained.
Ethics approval Institutional Review Board of Kanazawa University Hospital.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data are available.
Presented at Parts of this article were presented (number 1169-P) at the 77th Scientific Sessions of the American Diabetes Association, San Diego, CA, 92101 in June 2017.