GLP-1RA superior to basal insulin in control of total, LDL cholesterol

18 May 2020
Reduced dependence on insulin injections may make patients more inclined to comply with treatment and reduce adverse effects Reduced dependence on insulin injections may make patients more inclined to comply with treatment and reduce adverse effects of the injections such as local lipomas or scars.

Glucagon-like peptide-1 receptor agonists (GLP-1RA) are more effective than basal insulin in the management of total (TC) and low-density lipoprotein cholesterol (LDL-C), reveals a recent study.

Additionally, basal insulin significantly lowers serum triglycerides, while thiazolidinedione is effective in improving high-density lipoprotein cholesterol (HDL-C). Dipeptidyl peptidase–4 inhibitors (DPP4-I) and standard therapy, on the other hand, demonstrate no significant impact on lipid levels.

A meta-analysis was conducted on randomized controlled trials that reported changes in lipid parameters in type 2 diabetes (T2D) patients who were randomly assigned to basal insulin or other classes of antihyperglycaemic agents.

Therapies with GLP-1RA were associated with significant reduction in the levels of TC and LDL-C as compared with basal insulin (mean difference [MD], –3.80 mg/dL, 95 percent confidence interval [CI], –6.30 to –1.30; p<0.001 and MD, –4.17 mg/dL, 95 percent CI, –6.04 to –2.30; p<0.0001). However, there was no difference between basal insulin and DPP4-I or standard therapy (sulfonylurea ± metformin).

Treatment with thiazolidinediones correlated with significant improvement in HDL-C (MD, 3.55 mg/dL, 95 percent CI, 0.55–6.56; p=0.02) but was also associated with an increase in TC and LDL-C (MD, 16.20 mg/dL, 95 percent CI, 9.09–23.31; p<0.001 and MD, 5.19 mg/dL, 95 percent CI, –3.00 to 13.39; p=0.21). In triglyceride reduction, basal insulin showed superiority to standard therapy (MD, 3.8 mg/dL, 95 percent CI, 0.99–6.63; p=0.008).

“The lipid profile represents a driver of cardiovascular risk in T2D,” the authors said.

J Clin Endocrinol Metab 2020;105:dgaa178