Adjust T1D Study - Cardiovascular Outcomes

Document Type

Conference Proceeding

Publication Date

3-9-2026

Publication Title

Diabetes Technol Ther

Keywords

Endocrinology & Metabolism

Abstract

Cardiovascular disease (CVD) is the leading cause of death in people with type 1 diabetes, and both hyperglycemia and insulin resistance can contribute to risk. Obesity is a growing issue in people with T1D, and intensive insulin therapy can cause weight gain. Therefore, adjunctive therapies which could improve glycemic control and promote weight loss could reduce the risk of CVD in these patients. We performed a randomized controlled trial of semaglutide vs. placebo at 4 sites over 26 weeks in a sample of 72 adults with type 1 diabetes and obesity, who were treated with an automated insulin device but remained above goal for HbA1c. Semaglutide was started at 0.25 mg and titrated to 1 mg. Fasting lipids, spot urinary albumin/creatinine ratio (UACR) and blood pressure were measured after 8, 20 and 26 weeks of treatment. Arterial stiffness was measured using the Dynapulse system at baseline and after 26 weeks, with brachial artery distensibility (BrachD) as the main outcome examined. Randomized patients were similar in terms of demographics and baseline risk factors, with the exception of slightly higher total cholesterol in the semaglutide group. After 26 weeks of treatment, semaglutide treated patients experienced a significantly greater decline in total, non-HDL and LDL cholesterol, systolic blood pressure and UACR than the control group. The least square mean group difference for change in total cholesterol was -22.7 mg/dL (95% CI -34.6, -10.8, p<0.0001), for change in non-HDL cholesterol was -18.4 mg/dL (95% CI -29.1, -7.7, p<0.001), and for change in LDL cholesterol was -18.4 mg/dL (95% CI -28.7, -8.1, p<0.001). Overall, HDL cholesterol decreased by 4.3 mg/dL more in the semaglutide group than in the control group (95% CI -7.7, -0.9, p=0.01). There was no significant group difference for change in triglycerides from baseline (least square mean group difference of -2.4 mg/dL, 95% CI -20.1, 15.2, p=0.78). There was a significant group difference in the least square mean change in SBP of -6.1 mmHg (95% CI -11.1, -1.2, p=0.02)., but no significant mean group difference for diastolic blood pressure (least square mean group difference of -1.6, 95% CI -4.7, 1.4, p=0.30). There was a significantly greater decrease in log transformed UACR in the semaglutide group than the control group (-0.35 mg/g, 95% CI -0.70, -0.004, p=0.048), and there was no significant group difference for eGFR (-1.03, 95% CI -5.6, 3.57, p=0.66). Measures of central arterial stiffness improved significantly in the semaglutide compared to placebo group.The least square mean group difference for the improvement in BrachD for the semaglutide group vs. control group was 0.82%mm Hg (95% CI 0.38, 1.26, <0.001). In conclusion, treatment with semaglutide significantly improved cardiovascular risk factors, including lipids, blood pressure, UACR and arterial stiffness in obese adults with type 1 diabetes. Cardiovascular disease (CVD) is the leading cause of death in people with type 1 diabetes (T1D), and both hyperglycemia and insulin resistance can contribute to risk. Obesity is a growing issue in people with T1D, and intensive insulin therapy can cause weight gain. Therefore, adjunctive therapies which could improve glycemic control and promote weight loss could reduce the risk of CVD in these patients. We performed a randomized controlled trial of semaglutide vs. placebo at 4 sites over 26 weeks in a sample of 72 adults with type 1 diabetes and obesity, who were treated with an automated insulin device but remained above goal for HbA1c. Semaglutide was started at 0.25 mg and titrated to 1 mg. Fasting lipids, spot urinary albumin/creatinine ratio (UACR) and blood pressure were measured after 8, 20 and 26 weeks of treatment. Arterial stiffness was measured using the Dynapulse system at baseline and after 26 weeks, with brachial artery distensibility (BrachD) as the main outcome examined. Randomized patients were similar in terms of demographics and baseline risk factors, with the exception of slightly higher total cholesterol in the semaglutide group. After 26 weeks of treatment, semaglutide treated patients experienced a significantly greater decline in total, non-HDL and LDL cholesterol, systolic blood pressure and UACR than the control group. The least square mean group difference for change in total cholesterol was -22.7 mg/dL (95% CI -34.6, -10.8, p<0.0001), for change in non-HDL cholesterol was -18.4 mg/dL (95% CI -29.1, -7.7, p<0.001), and for change in LDL cholesterol was -18.4 mg/dL (95% CI -28.7, -8.1, p<0.001). Overall, HDL cholesterol decreased by 4.3 mg/dL more in the semaglutide group than in the control group (95% CI -7.7, -0.9, p=0.01). There was no significant group difference for change in triglycerides from baseline (least square mean group difference of -2.4 mg/dL, 95% CI -20.1, 15.2, p=0.78). There was a significant group difference in the least square mean change in SBP of -6.1 mmHg (95% CI -11.1, -1.2, p=0.02)., but no significant mean group difference for diastolic blood pressure (least square mean group difference of -1.6, 95% CI -4.7, 1.4, p=0.30). There was a significantly greater decrease in log transformed UACR in the semaglutide group than the control group (-0.35 mg/g, 95% CI -0.70, -0.004, p=0.048), and there was no significant group difference for eGFR (-1.03, 95% CI -5.6, 3.57, p=0.66). Measures of central arterial stiffness improved significantly in the semaglutide compared to placebo group.The least square mean group difference for the improvement in BrachD for the semaglutide group vs. control group was 0.82% mm Hg (95% CI 0.38, 1.26, <0.001). In conclusion, treatment with semaglutide significantly improved cardiovascular risk factors, including lipids, blood pressure, UACR and arterial stiffness in obese adults with type 1 diabetes.

Volume

28

First Page

23S

Last Page

24S

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