Abstract
Background The extract of Andrographis paniculata (Burm. F.) Wall. Ex. Nees. (sambiloto) (穿心蓮 chuān xīn lián) has been reported to have an antidiabetic effect on mice models and has been used traditionally in the community. The exact mechanism of sambiloto extract in decreasing plasma glucose is unclear, so we investigated the role of sambiloto extract in the incretin pathway in healthy and prediabetic subjects. Methods This study was a randomized, placebo-controlled, crossover, double-blind trial. It included 38 people who were healthy and 35 people who had prediabetes. All subjects were randomly assigned to receive either the intervention sambiloto extract or a placebo. All subjects were randomly assigned to receive the first intervention for 14 days. There was a washout period between subsequent interventions. The primary outcome was glucagon-like peptide 1 (GLP-1) concentration, and secondary outcomes were fasting insulin, 2-hour postprandial insulin, homeostasis model assessment of insulin resistance (HOMA-IR), fasting blood glucose, 2-hour postprandial blood glucose, dipeptidyl peptidase-4 (DPP-4), and glycated albumin before and after the intervention. Result After the intervention, GLP-1 concentration significantly increased in prediabetes by 19.6% compared to the placebo (p=0.043). There were no significant differences in the changes of fasting insulin, 2-hour postprandial insulin, HOMA-IR, fasting blood glucose, 2-hour postprandial blood glucose, DPP-4, and glycated albumin levels after the intervention. Sambiloto extract did not inhibit the DPP-4 enzyme in healthy and prediabetic subjects. Conclusion Sambiloto extract increased GLP-1 concentration without inhibiting the DPP-4 enzyme in prediabetic subjects. This trial is registered with ClinicalTrials.gov (ID: NCT03455049), registered on 6 March 2018—retrospectively registered (https://clinicaltrials.gov/ct2/show/NCT03455049).
Highlights
Type 2 diabetes mellitus (T2DM) affects approximately 8.5 percent of the global population or 415 million people
Incretins are hormones released from the small intestine into the bloodstream in response to food intake, especially carbohydrates. e main incretin hormones produced in the intestine are glucagon-like peptide 1 (GLP-1) and glucosedependent insulinotropic peptide (GIP), which are produced mainly in ileal L cells and jejunum K cells, respectively
From the perspective of incretin activity, there is robust evidence regarding the decrease of the incretin effect in T2DM, but the exact mechanism remains unknown. ere are several strategies to increase the incretin effect, such as administering exogenous subcutaneous GLP-1, oral administration of dipeptidyl peptidase-4 (DPP-4) enzyme inhibitors, and oral administration of small-molecule GLP-1 receptor ligands
Summary
Type 2 diabetes mellitus (T2DM) affects approximately 8.5 percent of the global population or 415 million people. Incretins are hormones released from the small intestine into the bloodstream in response to food intake, especially carbohydrates. Incretin hormones mediate the insulinotropic response of intestinal nutrients [2]. From the perspective of incretin activity, there is robust evidence regarding the decrease of the incretin effect in T2DM, but the exact mechanism remains unknown. Ere are several strategies to increase the incretin effect, such as administering exogenous subcutaneous GLP-1, oral administration of dipeptidyl peptidase-4 (DPP-4) enzyme inhibitors, and oral administration of small-molecule GLP-1 receptor ligands. A GLP-1 receptor ligand is a small molecule that can bind to a part of the GLP-1 receptor (GLP-1R); the biological effect due to GLP-1 and GLP-1 receptor binding becomes more optimal, increasing insulin secretion. The number of evidence is limited [3]
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