Cucurbitacin B Induces Hypoglycemic Effect in Diabetic Mice by Regulation of AMP-Activated Protein Kinase Alpha and Glucagon-Like Peptide-1 via Bitter Taste Receptor Signaling.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and in vitro mechanistic laboratory study.
PubMed 30298009 · doi:10.3389/fphar.2018.01071
What was done
Researchers investigated the hypoglycemic effects and signaling mechanism of Cucurbitacin B (CuB) using diabetic mouse models (including alpha-gustducin knockout mice and mice treated with the AMPK inhibitor dorsomorphin) and differentiated human enteroendocrine NCI-H716 cell lines. They assessed the roles of bitter taste receptor signaling (alpha-gustducin and Gbeta-gamma), intestinal AMP-activated protein kinase (AMPK) activation, plasma GLP-1, and insulin release.
What was found
The abstract reports purely directional findings without numerical values. CuB activated intestinal AMPK, induced plasma GLP-1 and insulin release, and ameliorated hyperglycemia in diabetic mice. These hypoglycemic actions were diminished in dorsomorphin-treated and alpha-gustducin null mice. In NCI-H716 cells, CuB stimulated GLP-1 secretion via AMPK activation downstream of alpha-gustducin and Gbeta-gamma taste receptor signaling.
Why it matters
This study provides mechanistic evidence that activating bitter taste receptor pathways can stimulate endogenous GLP-1 and insulin secretion, identifying a potential pathway for type 2 diabetes therapeutic exploration.
Limits
The study is restricted to in vitro and animal models with no human clinical data. The abstract omits sample sizes, quantitative effect sizes, dosages, and statistical confidence intervals.
Cited by
- supports Activation of bitter taste receptors stimulates L cells to secrete GLP-1, CCK, GIP, and PYY, and activates AMPK.