Semaglutide achieved better blood sugar control and improved blood vessel function compared to insulin aspart in 80 type 2 diabetes patients over three months.
Target glucose reached in 3.88 vs 5.73 daysSemaglutide patients hit their blood sugar targets nearly 2 days faster than those on insulin aspart
What the researchers found
In 80 hospitalized type 2 diabetes patients, semaglutide (added to metformin) produced significantly better glycemic control than insulin aspart after three months. The semaglutide group achieved lower fasting blood glucose (6.13±0.68 vs. control, P<0.05) and 2-hour postprandial glucose (9.01±0.53 mmol/L vs. control, P<0.05). Patients on semaglutide reached target blood glucose faster (3.88±0.69 days vs. 5.73±1.01 days, P<0.05). Beyond glucose control, semaglutide lowered endothelin-1 (a vasoconstrictor), improved flow-mediated vasodilation (FMD), and improved insulin resistance as measured by HOMA-IR. C-peptide levels — a marker of the pancreas's own insulin production — were also assessed as part of the metabolic panel.
Why it matters
This study adds to the evidence that semaglutide does more than lower blood sugar. The improvements in vascular function (lower ET-1, higher FMD) suggest cardiovascular benefits beyond glycemic control. The faster time to target glucose is clinically meaningful for hospitalized patients. It also provides comparative data against a standard insulin regimen.
The numbers in context
n=80 · FBG 6.13±0.68 mmol/L · 2h-PBG 9.01±0.53 mmol/L · Target glucose in 3.88 vs 5.73 days · 3-month follow-up
How the study worked
Prospective controlled study of 80 hospitalized T2DM patients (January 2022–December 2023). All patients received oral metformin. The control group added subcutaneous insulin aspart; the observation group added subcutaneous semaglutide. Outcomes measured at baseline and 3 months included fasting blood glucose, 2-hour postprandial glucose, time to target glucose, serum endothelin-1, flow-mediated dilation, fasting C-peptide, fasting insulin, and HOMA-IR.
Who was studied
80 hospitalized type 2 diabetes patients
What this study cannot tell us
Relatively small sample size of 80 patients. Single-center study with hospitalized patients, which may not reflect outpatient populations. The abstract does not specify whether randomization was used. Published in a lower-impact journal. Three-month follow-up is relatively short for assessing long-term metabolic and vascular outcomes.
How to read the evidence
Small controlled clinical study with 80 patients. Provides real patient data but limited by small sample size, single center, short follow-up, and unclear randomization methodology.
When this study was published
Published in 2025 in the Pakistan Journal of Pharmaceutical Sciences. Reflects current clinical use of semaglutide, though larger and more rigorous trials (SUSTAIN, STEP) provide the primary evidence base.
The bigger picture
Semaglutide is already one of the most prescribed GLP-1 drugs worldwide. This study contributes to the growing evidence that its benefits extend beyond glucose control to cardiovascular protection — specifically improved vasodilation and reduced endothelin-1. As the field moves toward recognizing type 2 diabetes as a cardiometabolic disease, drugs that address both glucose and vascular function simultaneously become increasingly valuable.
Questions still open
- Do the vascular benefits of semaglutide persist beyond three months of treatment?
- Would these results hold in an outpatient population with less severe diabetes?
- How does semaglutide's effect on C-peptide levels relate to long-term preservation of beta-cell function?
Common questions
What is C-peptide and why does it matter?
How does semaglutide improve blood vessel function?
Read the original research
Effect of Semaglutide on C-peptide levels in patients with type 2 diabetes.
Pakistan journal of pharmaceutical sciences, 38(2), 457-461
Citation
Fan, Pengxiang; Ma, Xiaojun. (2025). Effect of Semaglutide on C-peptide levels in patients with type 2 diabetes.. Pakistan journal of pharmaceutical sciences, 38(2), 457-461.