insulin secretion

GLP-1(7-36) amide (MKC 253) is a peptide hormone released from intestinal L-cells upon nutrient intake. It binds to the GLP-1 receptor in the pancreas, enhancing insulin secretion from pancreatic β-cells and increasing insulin expression, thereby exhibiting antidiabetic effects.

GIP (1-39) acetate is a gastric inhibitory peptide (GIP) purified from porcine intestine and stimulates insulin secretion.

GIP (1-30) amide, porcine acetate is an agonist of fully glucose-dependent insulinotropic polypeptide (GIP) receptor. GIP (1-30) amide, porcine acetate can weakly inhibit gastric acid secretion and strongly stimulate insulin.

Galantide acetate, a non-specific galanin receptor antagonist, is a peptide consisting of fragments of galanin and substance P. Galantide acetate recognizes two classes of galanin binding sites (KD<0.1 nM and ~6 nM) in the rat hypothalamus. Galantide acetate dose dependently (IC50=1.0 nM) antagonizes the galanin-mediated inhibition of the glucose-induced insulin secretion from mouse pancreatic islets. Galantide acetate appears to bind to a single population of SP receptors (KD~40 nM).

HAEGTFTSDVS acetate is the first N-terminal 1-11 residues of GLP-1 which stimulates insulin secretion from pancreatic β-cells.

GIP (human) acetate is a stimulator of glucose-dependent insulin secretion and a weak inhibitor of gastric acid secretion. GIP (human) acetate plays a vital role in lipid metabolism and the development of obesity.

Glucagon (19-29), human acetate a COOH-terminal fragment processed from glucagon, is a potent and efficient inhibitor of insulin secretion.

Mazdutide acetate is a potent co-agonist of glucagon-like peptide (GLP-1R) and glucagon receptor (GCGR), a gastrin-regulating hormone analog.Mazdutide acetate stimulates insulin secretion from mouse pancreatic islets, and can be used in studies of obesity and type 2 diabetes (T2D).

Glp-1(7-37) acetate is an intestinal insulin hormone that enhances glucose-induced insulin secretion.

Gastric inhibitory peptide (GIP) (1-42), an endogenous incretin hormone comprising 42 amino acids, promotes insulin secretion. Expressed in the intestinal neuroendocrine K cells and submandibular gland, it enters circulation after meals. GIP (1-42) blocks histamine, pentagastrin, and insulin-induced gastric acid and pepsin secretion, enhances glucose-stimulated insulin release, and accelerates gastric emptying in rats.

Neuromedin U (NMU) is a neuropeptide first demonstrated to drive smooth muscle contraction.1Translated as a 174 amino acid propeptide, NMU is cleaved to different lengths in different animals. It has diverse receptor-mediated rolesin vivo, as it regulates feeding, vasoconstriction, nociception, and bone remodeling and contributes to obesity, cancer and septic shock.2,2NMU-25 is the active form of NMU in humans. It binds with high affinity to receptors on human left ventricle and coronary artery (KDs = 0.26 and 0.11 nM, respectively), eliciting endothelium-independent vasoconstriction.3NMU-25 also suppresses glucose-stimulated insulin secretion in human islets, and this effect is lost in NMU R165W mutants, resulting in early-onset obesity.4 1.Mitchell, J.D., Maguire, J.J., and Davenport, A.P.Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin SBritish Journal of Pharmacology15887-103(2009) 2.Greenwood, H.C., Bloom, S.R., and Murphy, K.G.Peptides and their potential role in the treatment of diabetes and obesityRev.Diabet.Stud.8(3)355-368(2011) 3.Mitchell, J.D., Maguire, J.J., Kuc, R.E., et al.Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular systemCardiovascular Research81353-361(2009) 4.Alfa, R.W., Park, S., Skelly, K.R., et al.Suppression of insulin production and secretion by a decretin hormoneCell Metabolism21(2)323-333(2015)

(Ser8)-GLP-1 (7-36) amide, human, is a glucagon-like peptide-1 amide derived from glucagonogen, a cleavage product of the GLP-1 (1-36) amide peptide. This entero-insulinotropic hormone promotes glucose-dependent insulin secretion from pancreatic β-cells and affects gastrointestinal motility and secretion [1].

Potent insulinotropic hormone synthesized by duodenal K-cells. High affinity GIP receptor agonist (EC50 = 0.81 nM) that inhibits gastric acid secretion and stimulates pancreatic insulin release in response to glucose. Also affects lipid metabolism and dis

Endogenous truncated form of the incretin hormone GIP. More potent at stimulating glucose-dependent insulin secretion from rat pancreatic β-cells than GIP.

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).

GIP (1-30) amide, human acetate is a fragment of glucose-dependent insulinotropic polypeptide (GIP), an incretin hormone that plays a crucial role in stimulating insulin secretion and mitigating postprandial glycemic excursions. This compound has been shown to enhance insulin secretion in a dose-dependent manner across concentrations of 10^-9 to 10^-6 M [1].

GLP-1(7-36), amide TFA is a prominent intestinal hormone that stimulates glucose-induced insulin secretion from β cells[1].

Xenin-8 TFA, a biologically active C-terminal octapeptide derived from the 25-amino acid peptide Xenin of the neurotensin xenopsin family, enhances basal insulin secretion and amplifies glucose-stimulated insulin release in a dose-dependent manner (EC50=0.16 nM) [1].

Selective VPAC2 receptor agonist (EC50 values are 0.4, 100 and >1000 nM for VPAC2, VPAC1 and PAC1, respectively in a cAMP accumulation assay; IC50 values are 60, 8700 and >10000 nM for VPAC2, VPAC1 and PAC1, respectively in a competition binding assay). S

GIP (3-42), human acetate is an antagonist of a glucose-dependent insulinotropic polypeptide (GIP) receptor and regulates insulin secretion and GIP metabolism in vivo.

Gastric inhibitory peptide 1 (GIP-1) (3-42), a fragment of the incretin hormone GIP and antagonist to the GIP receptor, is generated through the action of serum dipeptidyl peptidase 4 (DDP-4). When administered at 25 nmol/kg to an ob/ob mouse diabetes model, GIP-1 (3-42) elevates plasma glucose levels and lowers plasma insulin levels, demonstrating its effect on reducing insulin secretion from BRIN-BD11 pancreatic cells at a concentration of 100 nM.

A-71915 (TFA) is a selective inhibitor of ANP receptor (atrial natriuretic peptide-receptor), induces apoptosis and decreases insulin secretion in RINm5F pancreatic β-cells.

Adrenocorticotropic Hormone (ACTH) (18-39), also known as the Corticotropin-like Intermediate Lobe Peptide, stimulates insulin secretion as well as amylase and protein secretion in a dose-dependent manner similar to secretin and carbamylcholine.

SDV-Exendin-3 4 is a 32-amino acid peptide. Derived from the salivary gland of the Gila monster (Heloderma suspectum), this peptide is a ligand for the GLP-1 receptor, playing a key role in glucose metabolism and insulin secretion. It exhibits significant potential for therapeutic applications in diabetes management.

Glucagon-like peptide 1 (1-37), human, is a highly potent agonist of the GLP-1 receptor and a pancreatic hormone synthesized by post-translational processing of proglucagon. Unlike truncated forms of GLP-1, it neither affects food intake in rats nor enhances pancreatic insulin secretion.

Osteocalcin (1-49) is a non-collagenous peptide that is secreted by osteoblasts and odontoblasts and comprises 1-2% of the total protein in bone. Secretion of osteocalcin (1-49) is stimulated by 1,25-dihydroxy vitamin D and plasma levels increase in diseases that induce dysregulated bone turnover such as osteoporosis, Paget's disease, and primary hyperparathyroidism. Osteocalcin (1-49) is positively correlated with insulin sensitivity and negatively correlated with high blood glucose levels in women. In vitro, osteocalcin induces chemotaxis of MDA-MB-231 breast cancer cells, human peripheral blood monocytes, and rat osteosarcoma cells with osteoblast-like characteristics. It is also expressed by vascular smooth muscle cells (VSMCs) displaying an osteoblast-like phenotype and has been positively associated with calcification of aortic tissue and heart valves in humans.

Hylambatin, a tachykinin, elevates plasma glucose and insulin levels without altering glucagon secretion, and is utilized in diabetes research [1].

C-Peptide 2, rat, a 31-amino-acid peptide, serves as a constituent in proinsulin. It possesses the ability to hinder glucose-triggered insulin secretion.

neurotensin-like peptide that modulate pancreatic insulin and glucagon secretion/effects

GLP-1(7-36) Acetate is a major intestinal hormone that stimulates glucose-induced insulin secretion from β cells.

increases glucose stimulated insulin secretion and glucose metabolism

Somatostatin, also known as growth hormone-inhibiting hormone, is a naturally-occurring peptide hormone of 14 or 28 amino acid residues that regulates the endocrine system. It is secreted by the D cells of the islets to inhibit the release of insulin and

GIP (1-30) amide, porcine TFA is a high-affinity full agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor, with potency comparable to native GIP(1-42) [1]. It also exhibits potent insulin-stimulating properties and weakly inhibits gastric acid secretion.

GRPP (human), a 30-amino-acid peptide derived from Gcg, modestly elevates plasma insulin levels while reducing plasma glucagon concentrations. However, GRPP (human) has no impact on insulin secretion within rat islets [1].

Human glucagon-like peptide-1-(7-36)-Lys(Biotin) amide, a biotin-labeled variant of glucagon-like peptide-1-(7-36), is a gastrointestinal peptide known for its antidiabetogenic properties, including enhancing insulin secretion [1] [2].

CPF-7 (Caerulein precursor fragment), an insulinotropic peptide, promotes insulin secretion and drives epithelial-mesenchymal transition via Snai1 upregulation in PANC-1 ductal cells. Moreover, it induces exocrine plasticity through Ngn3 upregulation, with applications in type 2 diabetes research [1] [2].

C-Peptide 2, rat acetate is a proinsulin component of inhibiting glucose-induced insulin secretion, consisting of acetate and a polypeptide composed of 31 amino acid residues [1] [2].

Urocortin III is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin II , frog sauvagine, and piscine urotensin I.1 Human urocortin III shares 90, 40, 37, and 21% identity to mouse urocortin III , mouse urocortin II , human urocortin , and mouse urocortin, respectively. Urocortin III selectively binds to type 2 CRF receptors (Kis = 21.7, 13.5, and >100 nM for rat CRF2α, rat CRF2β, and human CRF1, respectively). It stimulates cAMP production in CHO cells expressing rat CRF2α and mouse CRF2β (EC50s = 0.16 and 0.12 nM, respectively) as well as cultured anterior pituitary cells expressing endogenous CRF2β. Urocortin III is co-released with insulin to potentiate glucose-stimulated somatostatin release in vitro in human pancreatic β-cells.2 In vivo, urocortin III reduces food intake in a dose- and time-dependent manner in mice with a minimum effective dose (MED) of 0.3 nmol/animal.3 It increases swimming time in a forced swim test in mice, indicating antidepressant-like activity.4References1. Lewis, K., Li, C., Perrin, M.H., et al. Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor. Proc. Natl. Acad. Sci. U.S.A. 98(13), 7570-7575 (2001).2. van der Meulen, T., Donaldson, C.J., Cáceres, E., et al. Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion. Nat. Med. 21(7), 769-776 (2015).3. Pelleymounter, M.A., Joppa, M., Ling, N., et al. Behavioral and neuroendocrine effects of the selective CRF2 receptor agonists urocortin II and urocortin III. Peptides 25(4), 659-666 (2004).4. Tanaka, M., Kádár, K., Tóth, G., et al. Antidepressant-like effects of urocortin 3 fragments. Brain Res. Bull. 84(6), 414-418 (2011). Urocortin III is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin II , frog sauvagine, and piscine urotensin I.1 Human urocortin III shares 90, 40, 37, and 21% identity to mouse urocortin III , mouse urocortin II , human urocortin , and mouse urocortin, respectively. Urocortin III selectively binds to type 2 CRF receptors (Kis = 21.7, 13.5, and >100 nM for rat CRF2α, rat CRF2β, and human CRF1, respectively). It stimulates cAMP production in CHO cells expressing rat CRF2α and mouse CRF2β (EC50s = 0.16 and 0.12 nM, respectively) as well as cultured anterior pituitary cells expressing endogenous CRF2β. Urocortin III is co-released with insulin to potentiate glucose-stimulated somatostatin release in vitro in human pancreatic β-cells.2 In vivo, urocortin III reduces food intake in a dose- and time-dependent manner in mice with a minimum effective dose (MED) of 0.3 nmol/animal.3 It increases swimming time in a forced swim test in mice, indicating antidepressant-like activity.4 References1. Lewis, K., Li, C., Perrin, M.H., et al. Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor. Proc. Natl. Acad. Sci. U.S.A. 98(13), 7570-7575 (2001).2. van der Meulen, T., Donaldson, C.J., Cáceres, E., et al. Urocortin3 mediates somatostatin-dependent negative feedback control of insulin secretion. Nat. Med. 21(7), 769-776 (2015).3. Pelleymounter, M.A., Joppa, M., Ling, N., et al. Behavioral and neuroendocrine effects of the selective CRF2 receptor agonists urocortin II and urocortin III. Peptides 25(4), 659-666 (2004).4. Tanaka, M., Kádár, K., Tóth, G., et al. Antidepressant-like effects of urocortin 3 fragments. Brain Res. Bull. 84(6), 414-418 (2011).

[Tyr0] Gastric Inhibitory Peptide (23-42), human, is a glucose-dependent insulinotropic polypeptide (GIP) that modestly inhibits gastric acid secretion while enhancing insulin secretion, making it relevant for research on diabetes and obesity [1] [2].

A-71915 (TFA) is a selective atrial natriuretic peptide-receptor (ANP receptor) inhibitor that induces apoptosis and decreases insulin secretion in RINm5F pancreatic β-cells [1].

Urocortin III (human) is a corticotropin-releasing factor (CRF)-related peptide that primarily interacts with and activates the CRF receptor type 2 (CRF-R2), showing a specific distribution in the central nervous system and periphery. It selectively binds to type 2 CRF receptors with dissociation constants (Ki values) of 13.5 nM for mouse CRF2β, 21.7 nM for rat CRF2α, and >100 nM for human CRF1, indicating a strong preference for CRF-R2 over CRF1. Additionally, Urocortin III (human) plays a crucial role in the somatostatin-dependent negative feedback mechanism regulating the secretion of Insulin (human).

GIP (3-42), human (Gastric Inhibitory Polypeptide (3-42) (human)) is a peptide that acts as a glucose-dependent proinsulinotropic polypeptide (GIP) receptor antagonist and regulates insulin secretion and the metabolic effects of GIP in vivo, which can be used to study type 2 diabetes.

GIP (1-30) amide (Human) is an insulin-dependent glucose-dependent polypeptide.The sugar-dependent insulin polypeptide (GIP) is an insulin secreting hormone, which can stimulate the secretion of insulin and reduce the occurrence of postpranal-glycemic dis

Endogenous peptide product of human prepro-VIP and analog of porcine PHI-27; potent agonist for the human calcitonin receptor (EC50 = 11 nM). Transgenic mice expressing the human VIP/PHM 27 gene in pancreatic β-islets display enhanced glucose-induced insu

GIP, human TFA, a 42-amino acid peptide hormone, functions as a glucose-dependent insulin secretion stimulator and a weak gastric acid secretion inhibitor. Released from intestinal K cells following nutrient ingestion, it serves as an incretin hormone [1] [2] [3].

Phoenixin-14 TFA (PNX-14) is a blood-brain barrier (BBB)-penetrable neuropeptide with anxiolytic, cardioprotective, and neuroprotective properties. It modulates pituitary gonadotrophin release by enhancing gonadotropin-releasing hormone (GnRH) receptor mRNA expression and promotes insulin secretion. Additionally, PNX-14 TFA protects against ischemia reperfusion (IR) injury in mice and combats oxidative stress by diminishing reactive oxygen species (ROS) and elevating glutathione (GSH) levels [1] [2] [3].

Amylin (IAPP), feline TFA, a 37-amino acid polypeptide derived from felines, is a principal secretion product of the pancreatic islets' β-cells. This regulatory peptide notably inhibits the secretion of insulin and glucagon [1].

Amylin, amide, human TFA, a 37-amino acid polypeptide, functions as a pancreatic hormone cosecreted with insulin, playing distinct roles in metabolism and glucose homeostasis by regulating blood sugar through inhibiting glucagon secretion, delaying gastric emptying, and promoting satiety [1].

HNGF6A TFA, a humanin analogue, enhances glucose-stimulated insulin secretion and glucose metabolism, offering potential for diabetes research. It also inhibits ROS (Reactive Oxygen Species) production under oxidative stress and may prevent endothelial dysfunction and atherosclerosis in vivo [1] [2].

Insulin Detemir, an artificial insulin, effectively controls blood sugar levels by stimulating GLP-1 secretion through enhanced Gcg expression via the activation of Akt- and/or extracellular signal-regulated kinase (ERK)-dependent-cat and CREB signaling pathways. It is applicable for type 2 diabetes research [1] [2].