MD+VOO Mediterranean diet + Virgin Olive Oil, MD+nuts Mediterranean diet + Nuts, CD Control diet, BMI body mass index, GLP-1 glucagon-like peptide 1, GIP glucose-dependent insulinotropic polypeptide; IL-6 interleukin-6, PAI-1 plasminogen activator inhibitor-1, TNF-α tumor necrosis factor-α.
Bioactive peptides generated from whey protein have been demonstrated to stimulate the release of several gut hormones including cholecystokinin, peptide YY and the incretins glucose-dependent insulinotropic polypeptide 1 (GIP-1) and glucagon-like peptide (GLP-1) that potentiate insulin secretion [33, 39, 40].
Bioactive peptides generated from whey protein have been demonstrated to stimulate the release of several gut hormones including cholecystokinin, peptide YY and the incretins glucose-dependent insulinotropic polypeptide 1 (GIP-1) and glucagon-like peptide (GLP-1) that potentiate insulin secretion [ 33, 39, 40].
Besides, since all possible values of the topological similarity proposed in GIP falls into (0, 1], GIP is an incomplete similarity metric which may not adequately characterize the dissimilarity between those very different drugs/targets.
Besides GPR119, GPR40, GLP1R and GIP are also involved in glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells22, 30, 31.
GLP-1, GIP, exendin-4 and [ d-Ala2]GIP 1-30) d-Ala2]GIP 1-30ssolved in PBS and stored at −80°C.
Plasma for glucagon, GLP-1, GIP, PYY, CCK and triglyceride analyses was stored at −20 °C and plasma for insulin and C-peptide analyses was stored at −80 °C until analysis.
Our objective was to determine acute (hours) and chronic (1 week) effects of increased abomasal supply of protein, carbohydrate, or fat to the small intestine on dry matter intake (DMI) and plasma concentrations of GLP-1, GIP, CCK, and insulin.
Whereas (Abu8 GLP-1 was completely stable to human plasma (half-life >12 h), GLP-1, GIP, and (Abu2 GIP were rapidly degraded (half-lives: 6.2, 6.0, and 7.1 h, respectively).
TLQP-21 prevents islet cell apoptosis by a pathway similar to that used by GLP-1, but independent of the GLP-1, GIP, or VIP receptors.
They engineered a protein that takes structural pieces of GLP-1, GIP, and glucagon and merges them into a single molecule.
