Released rapidly in response to nutrient ingestion, especially carbohydrates and fats, it enhances insulin secretion from pancreatic beta cells in a glucose-dependent manner, effectively lowering postprandial blood glucose without risking hypoglycemia
Studies have shown that protein intake increases satiety hormones, including GLP-1, leading to reduced calorie intake
The results of these experiments demonstrate that in spite of the role of mTORC1 in the control of energy metabolism, as evidenced by a significant reduction of overall glucose consumption and uptake following Rapamycin treatment
The structural argument generalizes: GLP-1s belong in the fiscal-investment portfolio alongside the major projects, R&D, AI infrastructure, and defence industrial strategy that governments are currently expanding
It mimics the endogenous hormone glucagonlike peptide-1 (GLP1)