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INS-1 combined with GLUTag cells exhibited an even higher insulin production in response to glucose stimulation

Mohammad Flood
· 3 min read
INS-1 combined with GLUTag cells exhibited an even higher insulin production in response to glucose stimulation

At  API Hormones and Regulation , the diabetes model on chip showed faster saturation of the insulin level.  Pancreatic hormones and other blood sugar regulating drugs  suggest that the endocrine system developed in this study is a useful tool for observing dynamical changes in endocrine hormones (GLP-1 and insulin) in a glucose-dependent environment. Moreover, it can potentially be used to screen GLP-1 analogues and natural insulin and GLP-1 stimulants for diabetes 10111/j365-20360125198.x. Epub 2012 Jun 28.The effects of sitagliptin on gastric emptying in healthy humans - a randomised, BACKGROUND: The rate of gastric emptying (GE) and subsequent release of the incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are critical determinants of postprandial glycaemia in health and type 2 diabetes.

Slowing of GE may be the dominant mechanism by which exogenous GLP-1, and some GLP-1 analogues, improve postprandial glycaemia.AIM: To determine the effect of sitagliptin on GE in healthy subjects, and the relationships between GE with glycaemia and incretin hormone secretion.METHODS: Fifteen volunteers (22 ± 0 years) were studied on two occasions following 2 days dosing with sitagliptin (100 mg/day) or placebo. GE (scintigraphy), glycaemia and plasma GLP-1 and GIP (total and intact), insulin and glucagon were measured for 240 min following a mashed potato meal (1808 kJ).RESULTS: There was no difference in GE between sitgaliptin and placebo [50% emptying time (T50): P = 0]. Mean blood glucose was slightly less (P = 02) on sitagliptin. Sitagliptin reduced plasma glucagon between 75 and 120 min (P < 05), and increased intact GLP-1 (P = 0002) and intact GIP (P = 0001) by approximately twofold, but reduced total GIP (P = 0003) and had no effect on total GLP-1 (P = 06) or insulin (P = 05).

On sitagliptin the initial rise in blood glucose (r = -06, P = 008) and the intact GIP response (r = -06, P = 007) were inversely related, whereas the intact GLP-1 response was related directly (r = 02, P = 05) to the T50.CONCLUSIONS: While the effects of sitagliptin on glycaemic control are unlikely to relate to slowing of GE in healthy humans, the rate of GE is a significant determinant of postprandial glycaemia on sitagliptin.Reply: Glucagon-like peptide-1 mediates cardioprotection by remote ischaemic Basalay M, Mastitskaya S, Mrochek A, Ackland GL, Arroyo AG, Sanchez J, Sjoquist Physiology & Pharmacology, University College London, London, UK; Research Physiology & Pharmacology, University College London, London, UK.10152/ajpendo0076022. Epub 2022 Jun 20.Novel roles of mTORC2 in regulation of insulin secretion by actin filament University of Miami Miller School of Medicine, Miami, Florida.Center for Diabetes Research, Department of Internal Medicine, University of Mammalian target of rapamycin (mTOR) kinase is an essential hub where nutrients and growth factors converge to control cellular metabolism.

mTOR interacts with different accessory proteins to form complexes 1 and 2 (mTORC), and each complex has different intracellular targets. Although mTORC1's role in β-cells has been extensively studied, less is known about mTORC2's function in β-cells. Here, we show that mice with constitutive and inducible β-cell-specific deletion of RICTOR (βRicKO and iβRicKO mice, respectively) are glucose intolerant due to impaired insulin secretion when glucose is injected intraperitoneally. Decreased insulin secretion in βRicKO islets was caused by abnormal actin polymerization. Interestingly, when glucose was administered orally, no difference in glucose homeostasis and insulin secretion were observed, suggesting that incretins are counteracting the mTORC2 deficiency. Mechanistically, glucagon-like peptide-1 (GLP-1), but not gastric inhibitory polypeptide (GIP), rescued insulin secretion in vivo and in vitro by improving actin polymerization in βRicKO islets. In conclusion, mTORC2 regulates glucose-stimulated insulin secretion by promoting actin filament remodeling.

NEW & NOTEWORTHY The current studies uncover a novel mechanism linking mTORC2 signaling to glucose-stimulated insulin secretion by modulation of the actin filaments. This work also underscores the important role of GLP-1 in rescuing defects in insulin secretion by modulating actin polymerization and suggests that this effect is independent of mTORC2 signaling.Conflict of interest statement: No conflicts of interest, financial or otherwise, are declared by the authors.Glucagon-like peptide-1 differentiation of primate embryonic stem cells into Reconstructive Medicine and Tissue Engineering, Shinshu University Graduate The present study was performed to determine whether glucagon-like peptide-1 (GLP-1) stimulates differentiation of nestin-selected embryonic stem cells into insulin-producing cells. Our experimental strategy began with the production of a highly enriched population of nestin-positive cells from embryoid bodies. These cells differentiated into insulin-producing cells after addition of GLP-1. Islet-like cell clusters (ICCs) formed in inducing culture.

These nestin-positive cell-derived ICCs expressed numerous beta-cell lineage genes, including insulin; Glut-2; pancreatic duodenal homebox-1 protein (PDX-1); islet amyloid polypeptide (IAPP); neurogenin 3 (ngn3); and alpha, gamma, and delta cell gene markers.