2 edition of Elucidating novel biological actions of the incretin hormones GLP-1 and GIP found in the catalog.
Elucidating novel biological actions of the incretin hormones GLP-1 and GIP
Written in English
Incretins are hormones that are released from the gastrointestinal tract and potentiate glucose-stimulated insulin secretion from the endocrine pancreas. The two predominant peptides which have been identified as incretin hormones are glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Recent evidence implicates GLP-1 receptor (GLP-1R) signalling for enhancing beta-cell mass by stimulating beta-cell proliferation and islet neogenesis. We examined whether GLP-1R signalling modifies the cellular susceptibility to apoptosis both in vitro and in vivo. Our findings demonstrate that activation of GLP-1R signalling inhibits beta-cell apoptosis, and provides a novel mechanism whereby GLP-1 is able to enhance or preserve beta-cell mass.Despite the importance of the incretin hormones for glucose homeostasis, elimination of incretin receptor action in GLP-1R-/- or GIPR -/- mice produces only modest impairment in glucose tolerance, possibly due to compensatory up-regulation of the remaining incretin. To assess the consequences of disruption of incretin receptor signalling for glucose homeostasis in the absence of compensation by the complementary incretin, we generated double incretin receptor knockout (DIRKO) mice. Our data indicate that chronic disruption of incretin receptor signalling is not associated with marked perturbations in glucose homeostasis.GLP-1 and GIP regulate glucose homeostasis through overlapping actions on the islet beta-cell. However, GLP-1 also exerts important "non-incretin" effects, which contribute to its ability to lower glucose, including inhibition of gastric emptying, food intake and glucagon secretion. We examined whether disruption of dual incretin receptor signalling is associated with increased susceptibility to beta-cell metabolic stress imposed by high-fat feeding. Our results indicate that incretin receptors are essential for regulation of glucose homeostasis not only through effects on the beta-cell, but independently via modulation of the adipocyte response to excess over-nutrition.Both GLP-1 and GIP are rapidly inactivated by the protease, dipeptidyl peptidase IV (DPP-IV), which may limit their therapeutic potential. Inhibition of DPP-IV activity could thus provide a means to increase the half-life of GLP-1 and GIP. However, DPP-IV could also act on potential other substrates that are important for glucoregulation. Our studies in DIRKO mice delineate a critical role for incretin receptors as essential targets for the acute glucoregulatory actions of DPP-IV inhibitors.
|Statement||by Tanya Hansotia.|
|The Physical Object|
|Pagination||xviii, 209 leaves.|
|Number of Pages||209|
The incretin hormone glucagon-like peptide 1 (GLP-1) has been implicated in the gut–renal axis and incretin-based therapies might reduce Cited by: Glucagon-like peptide-1 (GLP-1), an incretin hormone plays an important role in regulating glucose homeostasis. The therapeutic use of native GLP-1 is inadequate due to its short in vivo half-life. We recently developed a novel GLP-1 mimetics supaglutide, and demonstrated that this formulation retained native GLP-1 biological activities and possessed long-lasting GLP-1 : Liwei Ren, Qiaoli Cui, Wenjuan Liu, Liqian Wang, Yijing Liao, Ying Feng, Wanwan Sun, Yehong Yang, Zh.
been identified as incretin hormones are glucose-dependent insulinotropic polypeptide (GP) and glucagon-like peptide4 (GLP- 1). Previous glucoregulatory studies using receptor knockout mice models suggest that the role of GIP is restncted to that of an incretin, whereas GLP-1 also exhibits non-incretin . Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the major incretin hormones that exert insulinotropic and anti-apoptotic actions Cited by:
Glucagon-like Peptide 1 (GLP-1) is a hormone produced in the small intestine that stimulates insulin production and prevents glucagon production, thereby lowering blood sugar. Learn what happens if there is too much or too little of this hormone. This deterioration of beta cells has been linked to the impaired actions of the incretin hormones, which could be aiding in the increase of beta cell mass, as well as beta cell functions. GLP-1 receptors are in high concentrations on the beta cells within the pancreas, they have many functions; a few are increasing beta-cell proliferation, and.
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GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. Recently approved therapeutic agents based on potentiation of incretin action provide new physiologically based approaches for the treatment of type 2 by: Conclusion GIP and GLP-1 are both incretin hormones secreted in response to meal ingestion that potentiate the glucose-indu- ced insulin response.
In addition, GLP-1 plays an impor- tant role in inhibiting glucagon secretion. Trophic effects of GLP-1 on pancreatic beta cells were also demonstrated in animal by: GLP-1 actions in peripheral tissues.
The majority of the effects of GLP-1 are mediated by direct interaction with GLP-1Rs on specific tissues. However, the actions of GLP-1 in liver, fat, and muscle most likely occur through indirect by: Gastric inhibitory polypeptide (GIP) and glucagon-like peptide -1 (GLP-1) are the two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic b by: Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1(GLP-1) are gut-derived incretins secreted in response to nutrient ingestion.
Both incretins potentiate glucose-dependent insulin secretion and enhancebeta-cell mass through regulation of beta-cell proliferation, neogenesis by: The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are produced predominantly by enteroendocrine cells and have multiple blood glucose-lowering effects.
Recent years have seen a surge of interest in understanding the basic physiology and pathophysiology of incretins and in applying this knowledge to the treatment of diabetes and by: Background: Glucagon-like-peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon have important gluco-regulatory actions.
Results: Fusion of amino acid sequences of GLP-1, GIP and glucagon produces hybrid peptides with triple-acting agonist activity. Conclusion: Hybrid peptides possess beneficial biological actions equivalent, or superior to, activation of single.
GIP and GLP-1, the Two Incretin Hormones: Similarities and Differences Article Literature Review (PDF Available) in Journal of Diabetes Investigation 1(1‐2):8 - 23 April with Reads. The biological actions of GIP and GLP-1 are fundamental determinants of islet function and blood glucose homeostasis in health and type 2 diabetes.
Moreover, there is increasing recognition that GIP and GLP-1 also exert pleiotropic extra-glycaemic actions, which may represent therapeutic targets for human diseases. The incretin glucagon-like peptide-1 (GLP-1), a small peptide hormone that stimulates insulin secretion in a glucose-dependent manner [10, 11], enhances insulin release and thus plays an important.
1 mimetic exendin-4 has shown protective effects in a clinical trial in Parkinson’s disease (PD) patients. Novel GLP-1/GIP dual-agonist peptides have been developed to treat diabetes. Here, we report the neuroprotective effects of a novel dual agonist (DA-JC1) in the 1-methylphenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD.
MPTP was injected once daily (20 mg/kg. Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β cells.
GIP and GLP-1 exert their effects by binding to their specific receptors, the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R), which belong to the G-protein coupled Cited by: Incretin hormones often display inhibitory actions on gut motility.
The aim of this study was to investigate if altered responsiveness to glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) as regards insulin release and small bowel motility could bring further clarity to the pathophysiology of diabetes in the Goto-Kakizaki (GK) rat.
The incretin effect accounts for at least 50% of total insulin secreted after oral glucose administration. 1, 2 Of the two incretins, namely glucagon‐like peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic peptide (GIP), GLP‐1 has received more attention because it can increase insulin secretion and normalize blood glucose levels Cited by: Abstract: Glucagon-like peptide-1()amide (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal insulin-releasing hormones involved in the regulation of postprandial nutrient homeostasis.
These two incretin hormones are glucose-dependent stimulators of pancreatic beta-cell function, exhibiting a spectrum of. Glucagon-like peptide-1 (GLP-1) is an incretin hormone that has a wide range of effects on glucose metabolism and cardiovascular function (e.g., improving insulin sensitivity, reduction in appetite, modulation of heart rate, blood pressure and myocardial contractility).
Metabolic syndrome (MetS) is associated with an increased risk of developing atherosclerotic cardiovascular diseases. Novel Cited by: Another class of drugs called DPP-IV inhibitors also affect incretin hormone levels.
Dipeptidyl peptidase IV (or DPP-IV) is an enzyme that normally breaks down GLP-1 and GIP. DPP-IV inhibitors, which block the action of this enzyme and therefore leave more of the body’s own GLP-1 and GIP in circulation.
Frias et al. assessed the effects of NNC, a unimolecular dual agonist derived from hybridized GLP-1 and GIP, in patients with T2DM. NNC was well tolerated and significantly improved glycemic control and reduced body weight compared with placebo.
Maximum benefit was obtained by patients with the best baseline glycemic by: Other physiological actions of GLP-1 include the inhibition of gastrointestinal secretion and gastric emptying, and the reduction of food intake. In contrast with GIP, the insulinotropic action of GLP-1 has been shown to be preserved in type 2 diabetic patients.
Fig. Secretion and metabolism of GIP and GLP GIP is secreted from K cells of the upper rapidly undergoes proteolytic processing by DPP-4, and is thereby inactivated and excreted have insulinotropic effects on pancreatic b cells, whereas the DPPprocessed incretins, G - "Two incretin hormones GLP-1 and GIP: comparison of their actions in insulin secretion and β cell preservation.".
The definition an incretin hormone only refers to the ability to augment insulin secretion under physiological conditions, that is, at the incretin hormone (GIP and GLP‐1) concentrations reached after nutrient stimulation. All other effects are beyond the narrow definition of incretin function.
There are two incretins, known as glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1), that share many common actions in the pancreas but have distinct actions outside of the pancreas.
Both incretins are rapidly deactivated by an enzyme called dipeptidyl peptidase 4 (DPP4).The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), may be responsible for up to 70% of postprandial insulin secretion.
In type 2 diabetes (2DM), the incretin effect is severely by: 1.