Log in

Relevant bibliographies by topics / Insuline – Agonistes / Journal articles

To see the other types of publications on this topic, follow the link: Insuline – Agonistes.

Journal articles on the topic 'Insuline – Agonistes'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Insuline – Agonistes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Ye, Ji-Ming, Miguel A. Iglesias, David G. Watson та ін. "PPARα/γ ragaglitazar eliminates fatty liver and enhances insulin action in fat-fed rats in the absence of hepatomegaly". American Journal of Physiology-Endocrinology and Metabolism 284, № 3 (2003): E531—E540. http://dx.doi.org/10.1152/ajpendo.00299.2002.

Full text

Abstract:

Peroxisome proliferator-activated receptor (PPAR)α and PPARγ agonists lower lipid accumulation in muscle and liver by different mechanisms. We investigated whether benefits could be achieved on insulin sensitivity and lipid metabolism by the dual PPARα/γ agonist ragaglitazar in high fat-fed rats. Ragaglitazar completely eliminated high-fat feeding-induced liver triglyceride accumulation and visceral adiposity, like the PPARα agonist Wy-14643 but without causing hepatomegaly. In contrast, the PPARγ agonist rosiglitazone only slightly lessened liver triglyceride without affecting visceral adipos

APA, Harvard, Vancouver, ISO, and other styles

2

Yajima, Ken, Hiroshi Hirose, Haruhisa Fujita та ін. "Combination therapy with PPARγ and PPARα agonists increases glucose-stimulated insulin secretion in db/dbmice". American Journal of Physiology-Endocrinology and Metabolism 284, № 5 (2003): E966—E971. http://dx.doi.org/10.1152/ajpendo.00149.2002.

Full text

Abstract:

Although peroxisome proliferator-activated receptor (PPAR)γ agonists ameliorate insulin resistance, they sometimes cause body weight gain, and the effect of PPAR agonists on insulin secretion is unclear. We evaluated the effects of combination therapy with a PPARγ agonist, pioglitazone, and a PPARα agonist, bezafibrate, and a dual agonist, KRP-297, for 4 wk in male C57BL/6J mice and db/db mice, and we investigated glucose-stimulated insulin secretion (GSIS) by in situ pancreatic perfusion. Body weight gain in db/db mice was less with KRP-297 treatment than with pioglitazone or pioglitazone + b

APA, Harvard, Vancouver, ISO, and other styles

3

Kim Jun, Jeany. "Focus on New Diabetes Treatment Options with Cardiovascular Benefits." Journal of Contemporary Pharmacy Practice 66, no. 3 (2019): 34–40. http://dx.doi.org/10.37901/jcphp18-00029.

Full text

Abstract:

The landscape of diabetes treatment options has changed due to new diabetes drug approvals, changes in the Food and Drug Administration indications based on cardiovascular (CV) outcomes studies, as well as the approval of follow-on biologic insulins. Two new drugs were approved for type 2 diabetes mellitus including ertugliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, and semaglutide, a glucagon-like peptide-1 (GLP1) receptor agonist joining a number of other drugs in these classes. In addition, follow-on biologic insulins, such as long-acting Basaglar (insulin glargine), and rap

APA, Harvard, Vancouver, ISO, and other styles

4

Cresser, Justin, Arend Bonen, Adrian Chabowski та ін. "Oral administration of a PPAR-δ agonist to rodents worsens, not improves, maximal insulin-stimulated glucose transport in skeletal muscle of different fibers". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, № 2 (2010): R470—R479. http://dx.doi.org/10.1152/ajpregu.00431.2009.

Full text

Abstract:

Agonists targeting the nuclear receptor peroxisome proliferator-activated receptors (PPAR)-δ may be potential therapeutic agents for insulin-resistant related conditions, as they may be able to stimulate fatty acid (FA) oxidation and attenuate the accumulation of harmful lipid species in skeletal muscle. Several reports have demonstrated that PPAR-δ agonists improve whole body insulin sensitivity. However, whether these agonists exert their direct effects on glucose and FA metabolism in skeletal muscle, and specifically with different fiber types, is unknown. This study was undertaken to deter

APA, Harvard, Vancouver, ISO, and other styles

5

Zhang, Xianyang, Tengjiao Cui, Jinlin He, et al. "Beneficial effects of growth hormone-releasing hormone agonists on rat INS-1 cells and on streptozotocin-induced NOD/SCID mice." Proceedings of the National Academy of Sciences 112, no. 44 (2015): 13651–56. http://dx.doi.org/10.1073/pnas.1518540112.

Full text

Abstract:

Agonists of growth hormone-releasing hormone (GHRH) have been previously reported to promote growth, function, and engraftment of islet cells following transplantation. Here we evaluated recently synthesized GHRH agonists on the proliferation and biological functions of rat pancreatic β-cell line (INS-1) and islets. In vitro treatment of INS-1 cells with GHRH agonists increased cell proliferation, the expression of cellular insulin, insulin-like growth factor-1 (IGF1), and GHRH receptor, and also stimulated insulin secretion in response to glucose challenge. Exposure of INS-1 cells to GHRH ago

APA, Harvard, Vancouver, ISO, and other styles

6

Cariou, Bertrand, Narimène Belhatem, Esteban Jodar, et al. "Impact de l’IMC sur la réduction de l’HbA 1c sous IDegLira chez des diabétiques de type 2 insuffisamment contrôlés sous sulfamides, agonistes des récepteurs au GLP-1 ou insuline Glargine U100 : analyses d’études de phase IIIb." Diabetes & Metabolism 43, no. 2 (2017): A114. http://dx.doi.org/10.1016/s1262-3636(17)30437-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Chang, Feng, Linda A. Jaber, Helen D. Berlie, and Mary Beth O'Connell. "Evolution of Peroxisome Proliferator-Activated Receptor Agonists." Annals of Pharmacotherapy 41, no. 6 (2007): 973–83. http://dx.doi.org/10.1345/aph.1k013.

Full text

Abstract:

OBJECTIVE: To discuss the evolution of peroxisome proliferator-activated receptor (PPAR) agonists from single site to multiple subtype or partial agonists for the treatment of type 2 diabetes, dyslipidemia, obesity, and the metabolic syndrome. DATA SOURCES: Information was obtained from MEDLINE (1966-March 2007) using search terms peroxisome proliferator-activated receptor agonist, PPAR dual agonist, PPAR α/γ agonist, PPAR pan agonist, partial PPAR, and the specific compound names. Other sources included pharmaceutical companies, the Internet, and the American Diabetes Association 64th-66th Sc

APA, Harvard, Vancouver, ISO, and other styles

8

Porskjær Christensen, Lars, та Rime Bahij El-Houri. "Development of an In Vitro Screening Platform for the Identification of Partial PPARγ Agonists as a Source for Antidiabetic Lead Compounds". Molecules 23, № 10 (2018): 2431. http://dx.doi.org/10.3390/molecules23102431.

Full text

Abstract:

Type 2 diabetes (T2D) is a metabolic disorder where insulin-sensitive tissues show reduced sensitivity towards insulin and a decreased glucose uptake (GU), which leads to hyperglycaemia. Peroxisome proliferator-activated receptor (PPAR)γ plays an important role in lipid and glucose homeostasis and is one of the targets in the discovery of drugs against T2D. Activation of PPARγ by agonists leads to a conformational change in the ligand-binding domain, a process that alters the transcription of several target genes involved in glucose and lipid metabolism. Depending on the ligands, they can indu

APA, Harvard, Vancouver, ISO, and other styles

9

Montessuit, Christophe, Irène Papageorgiou, and René Lerch. "Nuclear Receptor Agonists Improve Insulin Responsiveness in Cultured Cardiomyocytes through Enhanced Signaling and Preserved Cytoskeletal Architecture." Endocrinology 149, no. 3 (2007): 1064–74. http://dx.doi.org/10.1210/en.2007-0656.

Full text

Abstract:

Insulin resistance is the failure of insulin to stimulate the transport of glucose into its target cells. A highly regulatable supply of glucose is important for cardiomyocytes to cope with situations of metabolic stress. We recently observed that isolated adult rat cardiomyocytes become insulin resistant in vitro. Insulin resistance is combated at the whole body level with agonists of the nuclear receptor complex peroxisome proliferator-activated receptor γ (PPARγ)/retinoid X receptor (RXR). We investigated the effects of PPARγ/RXR agonists on the insulin-stimulated glucose transport and on i

APA, Harvard, Vancouver, ISO, and other styles

10

Balakumar, Pitchai, Nanjaian Mahadevan та Ramanathan Sambathkumar. "A Contemporary Overview of PPARα/γ Dual Agonists for the Management of Diabetic Dyslipidemia". Current Molecular Pharmacology 12, № 3 (2019): 195–201. http://dx.doi.org/10.2174/1874467212666190111165015.

Full text

Abstract:

Background: Diabetes mellitus and concomitant dyslipidemia, being referred to as ‘diabetic dyslipidemia’, are the foremost detrimental factors documented to play a pivotal role in cardiovascular illness. Diabetic dyslipidemia is associated with insulin resistance, high plasma triglyceride levels, low HDL-cholesterol concentration and elevated small dense LDL-cholesterol particles. Maintaining an optimal glucose and lipid levels in patients afflicted with diabetic dyslipidemia could be a major task that might require a well-planned diet-management system and regular physical activity, or otherw

APA, Harvard, Vancouver, ISO, and other styles

11

Shafi, Sana, Pawan Gupta, Gopal Lal Khatik та Jeena Gupta. "PPARγ: Potential Therapeutic Target for Ailments Beyond Diabetes and its Natural Agonism". Current Drug Targets 20, № 12 (2019): 1281–94. http://dx.doi.org/10.2174/1389450120666190527115538.

Full text

Abstract:

Intense research interests have been observed in establishing PPAR gamma as a therapeutic target for diabetes. However, PPAR&#947; is also emerging as an important therapeutic target for varied disease states other than type 2 diabetes like neurodegenerative disorders, cancer, spinal cord injury, asthma, and cardiovascular problems. Furthermore, glitazones, the synthetic thiazolidinediones, also known as insulin sensitizers, are the largely studied PPAR&#947; agonists and the only ones approved for the treatment of type 2 diabetes. However, they are loaded with side effects like fluid

APA, Harvard, Vancouver, ISO, and other styles

12

Finn, Patricia D., David Rodriguez, Jill Kohler, et al. "Intestinal TGR5 agonism improves hepatic steatosis and insulin sensitivity in Western diet-fed mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 3 (2019): G412—G424. http://dx.doi.org/10.1152/ajpgi.00300.2018.

Full text

Abstract:

Takeda G protein-coupled receptor 5 (TGR5) agonists induce systemic release of glucagon-like peptides (GLPs) from intestinal L cells, a potentially therapeutic action against metabolic diseases such as nonalcoholic steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD), and Type 2 diabetes. Historically, TGR5 agonist use has been hindered by side effects, including inhibition of gallbladder emptying. Here, we characterize RDX8940, a novel, orally administered TGR5 agonist designed to have minimal systemic effects and investigate its activity in mice fed a Western diet, a model of NAF

APA, Harvard, Vancouver, ISO, and other styles

13

Meade, Lisa T., and Morgan L. Mannka. "The Effect of Glucagon-Like Peptide-1 Receptor Agonists and Sodium-Glucose Cotransporter-2 Inhibitors in Patients Prescribed Regular U-500 Insulin." Annals of Pharmacotherapy 53, no. 11 (2019): 1111–16. http://dx.doi.org/10.1177/1060028019857557.

Full text

Abstract:

Background: Only 2 small studies have examined the use of glucagon-like peptide-1 (GLP-1) receptor agonists with U-500 insulin, with mixed results. Moreover, there are no studies to our knowledge that have investigated use of sodium-glucose cotransporter-2 (SGLT-2) inhibitors with U-500 insulin therapy. Objective: This research was designed to determine the effectiveness of GLP-1 agonists and SGLT-2 inhibitors in patients already taking U-500 insulin. Methods: A retrospective chart review was conducted on patients using U-500 insulin to which a GLP-1 agonist or SGLT-2 inhibitor was added as th

APA, Harvard, Vancouver, ISO, and other styles

14

Wake, Deborah J., Roland H. Stimson, Garry D. Tan та ін. "Effects of Peroxisome Proliferator-Activated Receptor-α and -γ Agonists on 11β-Hydroxysteroid Dehydrogenase Type 1 in Subcutaneous Adipose Tissue in Men". Journal of Clinical Endocrinology & Metabolism 92, № 5 (2007): 1848–56. http://dx.doi.org/10.1210/jc.2006-2713.

Full text

Abstract:

Abstract Context: In animals, peroxisome proliferator-activated receptor-α (PPARα) and PPARγ agonists down-regulate 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) mRNA and activity in liver and adipose tissue, respectively, and PPARγ agonists reduce ACTH secretion from corticotrope cells. Objective: Our objective was to test whether PPAR agonists alter cortisol secretion and peripheral regeneration by 11β-HSD1 in humans and whether reduced cortisol action contributes to metabolic effects of PPARγ agonists. Design and Setting: Three randomized placebo-controlled crossover studies were condu

APA, Harvard, Vancouver, ISO, and other styles

15

Vikulova, O. K., Z. T. Zuraeva, O. V. Michaleva, et al. "Renal effects of glucagon-like peptide receptor agonists in patients with type 1 diabetes mellitus." Terapevticheskii arkhiv 90, no. 6 (2018): 59–64. http://dx.doi.org/10.26442/terarkh201890659-64.

Full text

Abstract:

The purpose of our study is to assess the effects of glucagon-like peptide-1 receptor agonists (GLP-1R agonists) on early markers of kidney damage in patients with type 1 diabetes mellitus (DM). Materials and methods. The study included 27 patients with type 1 diabetes with normo- (n=16) and microalbuminuria (n=11) on intensive insulin injection regimen with insulin analogs. Patients were divided into two groups: 15 patients continued insulin therapy throughout the follow-up period, 12 patients were given 1.2 mg GLP-1R agonist (Liraglutide) once a day in addition to the insulin therapy for 6 m

APA, Harvard, Vancouver, ISO, and other styles

16

Gorski, Judith N., Michele J. Pachanski, Joel Mane, et al. "GPR40 reduces food intake and body weight through GLP-1." American Journal of Physiology-Endocrinology and Metabolism 313, no. 1 (2017): E37—E47. http://dx.doi.org/10.1152/ajpendo.00435.2016.

Full text

Abstract:

G protein-coupled receptor 40 (GPR40) partial agonists lower glucose through the potentiation of glucose-stimulated insulin secretion, which is believed to provide significant glucose lowering without the weight gain or hypoglycemic risk associated with exogenous insulin or glucose-independent insulin secretagogues. The class of small-molecule GPR40 modulators, known as AgoPAMs (agonist also capable of acting as positive allosteric modulators), differentiate from partial agonists, binding to a distinct site and functioning as full agonists to stimulate the secretion of both insulin and glucago

APA, Harvard, Vancouver, ISO, and other styles

17

Nofziger, Charity, Kathleen K. Brown, Chari D. Smith та ін. "PPARγ agonists inhibit vasopressin-mediated anion transport in the MDCK-C7 cell line". American Journal of Physiology-Renal Physiology 297, № 1 (2009): F55—F62. http://dx.doi.org/10.1152/ajprenal.00090.2009.

Full text

Abstract:

PPARγ agonists are synthetic ligands for the peroxisome proliferator-activated receptor-γ (PPARγ). These agents have insulin-sensitizing properties but can cause fluid retention, thereby limiting their usefulness in patients at risk for cardiovascular disease. The side effect etiology is unknown, but the nature of presentation suggests modulation of renal salt and water homeostasis. In a well-characterized cell culture model of the principal cell type [Madin-Darby canine kidney (MDCK)-C7], PPARγ agonists inhibit vasopressin-stimulated Cl− secretion with agonist dose-response relationships that

APA, Harvard, Vancouver, ISO, and other styles

18

Hegarty, Bronwyn D., Stuart M. Furler, Nicholas D. Oakes, Edward W. Kraegen та Gregory J. Cooney. "Peroxisome Proliferator-Activated Receptor (PPAR) Activation Induces Tissue-Specific Effects on Fatty Acid Uptake and Metabolism in Vivo—A Study Using the Novel PPARα/γ Agonist Tesaglitazar". Endocrinology 145, № 7 (2004): 3158–64. http://dx.doi.org/10.1210/en.2004-0260.

Full text

Abstract:

Abstract Agonists of peroxisome proliferator-activated receptors (PPARs) have emerged as important pharmacological agents for improving insulin action. A major mechanism of action of PPAR agonists is thought to involve the alteration of the tissue distribution of nonesterified fatty acid (NEFA) uptake and utilization. To test this hypothesis directly, we examined the effect of the novel PPARα/γ agonist tesaglitazar on whole-body insulin sensitivity and NEFA clearance into epididymal white adipose tissue (WAT), red gastrocnemius muscle, and liver in rats with dietary-induced insulin resistance.

APA, Harvard, Vancouver, ISO, and other styles

19

Lacey, R. J., N. S. Berrow, N. J. M. London та ін. "Differential effects of β-adrenergic agonists on insulin secretion from pancreatic islets isolated from rat and man". Journal of Molecular Endocrinology 5, № 1 (1990): 49–54. http://dx.doi.org/10.1677/jme.0.0050049.

Full text

Abstract:

ABSTRACT The selective β2-adrenergic agonist clenbuterol was ineffective as a stimulus for insulin secretion when isolated rat pancreatic islets were incubated with glucose at concentrations between 4 and 20 mM. Inclusion of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine led to potentiation of glucose-induced insulin secretion, but did not facilitate stimulation by clenbuterol. Furthermore, maintenance of isolated rat islets for up to 3 days in tissue culture also failed to result in the appearance of a secretory response to β-agonists. By contrast, clenbuterol induced a dose-depe

APA, Harvard, Vancouver, ISO, and other styles

20

Chu, Zhi-Liang, Robert M. Jones, Hongmei He та ін. "A Role for β-Cell-Expressed G Protein-Coupled Receptor 119 in Glycemic Control by Enhancing Glucose-Dependent Insulin Release". Endocrinology 148, № 6 (2007): 2601–9. http://dx.doi.org/10.1210/en.2006-1608.

Full text

Abstract:

Pancreatic β-cell dysfunction is a hallmark event in the pathogenesis of type 2 diabetes. Injectable peptide agonists of the glucagon-like peptide 1 (GLP-1) receptor have shown significant promise as antidiabetic agents by virtue of their ability to amplify glucose-dependent insulin release and preserve pancreatic β-cell mass. These effects are mediated via stimulation of cAMP through β-cell GLP-1 receptors. We report that the Gαs-coupled receptor GPR119 is largely restricted to insulin-producing β-cells of pancreatic islets. Additionally, we show here that GPR119 functions as a glucose-depend

APA, Harvard, Vancouver, ISO, and other styles

21

Downing, S. E., and J. C. Lee. "Enhanced adrenergic sensitivity of the diabetic neonatal heart." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (1985): H125—H131. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h125.

Full text

Abstract:

We have previously shown that insulin reduces inotropic responses to norepinephrine (NE) in isolated cardiac muscle and intact hearts. This inhibition also occurs in vascular smooth muscle. The present study was designed to examine inotropic sensitivity of insulin-deficient diabetic (D) hearts to mixed (NE) and pure beta 1 (isoproterenol, Iso) adrenergic agonists. Lambs were given alloxan (150 mg/kg) and studied 2 days later (glucose, 392 mg/dl). Results from eight controls (C) were compared. All animals were prepared for measurements of ventricular performance and coronary flow (CF) under con

APA, Harvard, Vancouver, ISO, and other styles

22

Zheng, Shanqing, Hilton Chiu, Jeffrey Boudreau, Tony Papanicolaou, William Bendena, and Ian Chin-Sang. "A functional study of all 40 Caenorhabditis elegans insulin-like peptides." Journal of Biological Chemistry 293, no. 43 (2018): 16912–22. http://dx.doi.org/10.1074/jbc.ra118.004542.

Full text

Abstract:

The human genome encodes 10 insulin-like genes, whereas the Caenorhabditis elegans genome remarkably encodes 40 insulin-like genes. Knockout strategies to determine the roles of all the insulin/insulin-like peptide ligands (INS) in C. elegans has been challenging due to functional redundancy. Here, we individually overexpressed each of the 40 ins genes pan-neuronally, and monitored multiple phenotypes including: L1 arrest life span, neuroblast divisions under L1 arrest, dauer formation, and fat accumulation, as readouts to characterize the functions of each INS in vivo. Of the 40 INS peptides,

APA, Harvard, Vancouver, ISO, and other styles

23

Rico, Elizabeth, Jian Zhao, Mi Chen, Ana Karin Kusnetzow, Yun Fei Zhu, and Stephen F. Betz. "Selective Somatostatin 5 (SST5) and Somatostatin 2 (SST2) Nonpeptide Agonists Potently Suppress Glucose- and Tolbutamide-Stimulated Dynamic Insulin Secretion From Isolated Human Islets." Journal of the Endocrine Society 5, Supplement_1 (2021): A325. http://dx.doi.org/10.1210/jendso/bvab048.663.

Full text

Abstract:

Abstract Congenital hyperinsulinism (HI) is the most common cause of persistent hypoglycemia in newborns and infants and arises from dysregulated insulin secretion. Rapid recognition and treatment are vital to prevent seizures, permanent developmental delays, coma, or even death. Very few medical options exist to treat congenital HI patients: the KATP channel activator diazoxide, the injectable somatostatin receptor peptide agonists octreotide and lanreotide, or chronic glucose infusions. However, side effects and/or limited efficacy render these therapies inadequate for many patients. Somatos

APA, Harvard, Vancouver, ISO, and other styles

24

Tyurenkov, Ivan N., Denis V. Kurkin, Dmitry A. Bakulin, et al. "Influence of novel GPR119 receptor agonist on plasma glucose and insulin level, as well as structural changes of pancreas islets in rats with experimental type 2 diabetes." Problems of Endocrinology 62, no. 4 (2016): 32–37. http://dx.doi.org/10.14341/probl201662432-37.

Full text

Abstract:

Background. GPR119 receptor is a promising target for novel antidiabetic drugs development because of its agonists in addition to hypoglycemic effects have cytoprotective effect on beta cells.Aim — to assess the effect of the novel GPR119 receptor agonist and sitagliptin on carbohydrate metabolism and morphological structure of the pancreas in animals with experimental type 2 diabetes.Material and methods. The study was performed in Wistar rats with streptozotocin-nicotinamide-induced diabetes. Serum insulin was determined by ELISA (Rat Insulin, (INS) ELISA Kit, 96 CSB). Immunohistochemical st

APA, Harvard, Vancouver, ISO, and other styles

25

Hu, Xinran, David Friedman, Salisha Hill та ін. "Proteomic exploration of pancreatic islets in mice null for the α2A adrenergic receptor". Journal of Molecular Endocrinology 35, № 1 (2005): 73–88. http://dx.doi.org/10.1677/jme.1.01764.

Full text

Abstract:

The present studies extend recent findings that mice null for the α2A adrenergic receptor (α2A AR KO mice) lack suppression of exogenous secretagogue-stimulated insulin secretion in response to α2 AR agonists by evaluating the endogenous secretagogue, glucose, ex vivo, and providing in vivo data that baseline insulin levels are elevated and baseline glucose levels are decreased in α2A AR KO mice. These latter findings reveal that the α2A AR subtype regulates glucose-stimulated insulin release in response to endogenous catecholamines in vivo. The changes in α2A AR responsiveness and resultant c

APA, Harvard, Vancouver, ISO, and other styles

26

Ropero, Ana B., Pablo Juan-Picó, Alex Rafacho та ін. "Rapid non-genomic regulation of Ca2+ signals and insulin secretion by PPARα ligands in mouse pancreatic islets of Langerhans". Journal of Endocrinology 200, № 2 (2008): 127–38. http://dx.doi.org/10.1677/joe-08-0397.

Full text

Abstract:

PPARα is a ligand-activated transcription factor belonging to the nuclear receptor superfamily. PPARα is involved in the regulation of in vivo triglyceride levels, presumably through its effects on fatty acid and lipoprotein metabolism. Some nuclear receptors have been involved in rapid effects mediated by non-genomic mechanisms. In this paper, we report the rapid non-genomic effects of PPARα ligands on the intracellular calcium concentration ([Ca2+]i), mitochondrial function, reactive oxygen species (ROS) generation, and secretion of insulin in freshly isolated mouse islets of Langerhans. The

APA, Harvard, Vancouver, ISO, and other styles

27

Carpéné, C., E. Chalaux, M. Lizarbe та ін. "β 3-adrenergic receptors are responsible for the adrenergic inhibition of insulin-stimulated glucose transport in rat adipocytes". Biochemical Journal 296, № 1 (1993): 99–105. http://dx.doi.org/10.1042/bj2960099.

Full text

Abstract:

The inhibition of insulin-stimulated glucose transport by isoprenaline, a mixed beta-adrenergic-receptor (AR) agonist, is well documented in rat adipocytes. Since it has been described that rat adipocytes possess not only beta 1- and beta 2- but also beta 3-ARs, the influence of various subtype-selective beta-AR agonists and antagonists on 2-deoxyglucose (2-DG) transport was assessed in order to characterize the beta-AR subtype involved in the adrenergic counter-regulation of the insulin effect. The stimulation of 2-DG transport by insulin was counteracted, in a dose-dependent manner, by all t

APA, Harvard, Vancouver, ISO, and other styles

28

Farese, R. V., M. L. Standaert, A. J. Francois, et al. "Effects of insulin and phorbol esters on subcellular distribution of protein kinase C isoforms in rat adipocytes." Biochemical Journal 288, no. 1 (1992): 319–23. http://dx.doi.org/10.1042/bj2880319.

Full text

Abstract:

Effects of insulin and phorbol esters on subcellular distribution of protein kinase C (PKC) isoforms were examined in rat adipocytes. Both agonists provoked rapid decreases in cytosolic, and/or increases in membrane, immunoreactive PKC-alpha, PKC-beta, PKC-gamma, and PKC-epsilon. Effects of phorbol esters on PKC-alpha redistribution to the plasma membrane, however, were much greater than those of insulin. In contrast, insulin, but not phorbol esters, stimulated the translocation of PKC-beta to the plasma membrane, and provoked changes in PKC-zeta redistribution. Neither agonist altered subcell

APA, Harvard, Vancouver, ISO, and other styles

29

Berthiaume, Magalie, Henrike Sell, Josée Lalonde та ін. "Actions of PPARγ agonism on adipose tissue remodeling, insulin sensitivity, and lipemia in absence of glucocorticoids". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, № 5 (2004): R1116—R1123. http://dx.doi.org/10.1152/ajpregu.00339.2004.

Full text

Abstract:

Peroxisome proliferator-activated receptor γ (PPARγ) agonists improve insulin sensitivity and lipemia partly through enhancing adipose tissue proliferation and capacity for lipid retention. The agonists also reduce local adipose glucocorticoid production, which may in turn contribute to their metabolic actions. This study assessed the effects of a PPARγ agonist in the absence of glucocorticoids (adrenalectomy, ADX). Intact, ADX, and intact pair-fed (PF) rats were treated with the PPARγ agonist rosiglitazone (RSG) for 2 wk. RSG increased inguinal (subcutaneous) white (50%) and brown adipose tis

APA, Harvard, Vancouver, ISO, and other styles

30

Cong, Li, Ke Chen, Ji Li, et al. "Regulation of adiponectin and leptin secretion and expression by insulin through a PI3K-PDE3B dependent mechanism in rat primary adipocytes." Biochemical Journal 403, no. 3 (2007): 519–25. http://dx.doi.org/10.1042/bj20061478.

Full text

Abstract:

Adiponectin is intimately involved in the regulation of insulin sensitivity, carbohydrate and lipid metabolism, and cardiovascular functions. The circulating concentration of adiponectin is decreased in obesity and Type 2 diabetes. The present study attempts to elucidate the mechanisms underlying the regulation of adiponectin secretion and expression in rat primary adipocytes. The β-agonist, isoprenaline, decreased adiponectin secretion and expression in a dose-dependent manner in primary adipocytes. Importantly, such an inhibitory effect could be blocked by insulin. The opposing effects of is

APA, Harvard, Vancouver, ISO, and other styles

31

Kim, Hyunsook, Patricia A. Pennisi, Oksana Gavrilova та ін. "Effect of adipocyte β3-adrenergic receptor activation on the type 2 diabetic MKR mice". American Journal of Physiology-Endocrinology and Metabolism 290, № 6 (2006): E1227—E1236. http://dx.doi.org/10.1152/ajpendo.00344.2005.

Full text

Abstract:

The antiobesity and antidiabetic effects of the β3-adrenergic agonists were investigated on nonobese type 2 diabetic MKR mice after injection with a β3-adrenergic agonist, CL-316243. An intact response to acute CL-316243 treatment was observed in MKR mice. Chronic intraperitoneal CL-316243 treatment of MKR mice reduced blood glucose and serum insulin levels. Hyperinsulinemic euglycemic clamps exhibited improvement of the whole body insulin sensitivity and glucose homeostasis concurrently with enhanced insulin action in liver and adipose tissue. Treating MKR mice with CL-316243 significantly lo

APA, Harvard, Vancouver, ISO, and other styles

32

Asrih, Mohamed, René Lerch, Irène Papageorgiou, Corinne Pellieux та Christophe Montessuit. "Differential regulation of stimulated glucose transport by free fatty acids and PPARα or -δ agonists in cardiac myocytes". American Journal of Physiology-Endocrinology and Metabolism 302, № 7 (2012): E872—E884. http://dx.doi.org/10.1152/ajpendo.00427.2011.

Full text

Abstract:

Stimulation of glucose transport in response to insulin or metabolic stress is an important determinant of cardiac myocyte function and survival, particularly during ischemia-reperfusion episodes. The impact of dyslipidemia and its consequence PPAR activation on stimulated glucose transport in cardiac myocytes remains unknown. Isolated adult rat cardiac myocytes were chronically exposed to free fatty acids (FFA) or PPAR agonists. Insulin- (ISGT) and oligomycin-stimulated glucose transport (OSGT) and related cell signaling were analyzed. Exposure of cardiac myocytes to FFA reduced both ISGT and

APA, Harvard, Vancouver, ISO, and other styles

33

Ou, Horng-Yih, Hung-Tsung Wu, Hao-Chang Hung, Yi-Ching Yang, Jin-Shang Wu, and Chih-Jen Chang. "Multiple mechanisms of GW-9508, a selective G protein-coupled receptor 40 agonist, in the regulation of glucose homeostasis and insulin sensitivity." American Journal of Physiology-Endocrinology and Metabolism 304, no. 6 (2013): E668—E676. http://dx.doi.org/10.1152/ajpendo.00419.2012.

Full text

Abstract:

Activation of G protein-coupled receptor 40 (GPR40) by agonists increases insulin release in isolated islets, whereas it is inconclusive whether GPR40 antagonists decrease blood glucose and increase insulin sensitivity. Although some clinical trials indicated that administration of a GPR40 agonist shows benefits in the regulation of blood glucose homeostasis, the pharmacological mechanisms of this receptor in the improvement of glycemic control remain unclear. Therefore, we used a selective GPR40 agonist, GW-9508, to clarify the role of GPR40 in the regulation of blood glucose. Bolus intraperi

APA, Harvard, Vancouver, ISO, and other styles

34

Ackeifi, Courtney, Peng Wang, Esra Karakose та ін. "GLP-1 receptor agonists synergize with DYRK1A inhibitors to potentiate functional human β cell regeneration". Science Translational Medicine 12, № 530 (2020): eaaw9996. http://dx.doi.org/10.1126/scitranslmed.aaw9996.

Full text

Abstract:

Glucagon-like peptide-1 receptor (GLP1R) agonists and dipeptidyl peptidase 4 inhibitors are widely prescribed diabetes drugs due to their ability to stimulate insulin secretion from remaining β cells and to reduce caloric intake. Unfortunately, they fail to increase human β cell proliferation. Small-molecule inhibitors of dual-specificity tyrosine-regulated kinase 1A (DYRK1A) are able to induce adult human β cell proliferation, but rates are modest (~2%), and their specificity to β cells is limited. Here, we provide evidence that combining any member of the GLP1R agonist class with any member

APA, Harvard, Vancouver, ISO, and other styles

35

Gregoire, Francine M., Fang Zhang, Holly J. Clarke та ін. "MBX-102/JNJ39659100, a Novel Peroxisome Proliferator Activated Receptor-γ Ligand with Weak Transactivation Activity Retains Full Anti-Diabetic Properties in the Absence of Side Effects". Endocrine Reviews 30, № 4 (2009): 414. http://dx.doi.org/10.1210/edrv.30.4.9988.

Full text

Abstract:

ABSTRACT MBX-102/JNJ39659100 (MBX-102) is in clinical development as an oral glucose lowering agent for the treatment of type 2 diabetes. MBX-102 is a non-thiazolidinedione (TZD) selective partial agonist of PPAR-γ that is differentiated from the TZDs structurally, mechanistically, pre-clinically and clinically. In diabetic rodent models, MBX-102 has insulin sensitizing and glucose lowering properties comparable to TZDs without dose-dependent increases in body weight. In vitro, in contrast with full PPAR-γ agonist treatment, MBX-102 fails to drive human and murine adipocyte differentiation and

APA, Harvard, Vancouver, ISO, and other styles

36

Gregoire, Francine M., Fang Zhang, Holly J. Clarke, et al. "MBX-102/JNJ39659100, a Novel Peroxisome Proliferator-Activated Receptor-Ligand with Weak Transactivation Activity Retains Antidiabetic Properties in the Absence of Weight Gain and Edema." Molecular Endocrinology 23, no. 7 (2009): 975–88. http://dx.doi.org/10.1210/me.2008-0473.

Full text

Abstract:

Abstract MBX-102/JNJ39659100 (MBX-102) is in clinical development as an oral glucose-lowering agent for the treatment of type 2 diabetes. MBX-102 is a nonthiazolidinedione (TZD) selective partial agonist of peroxisome proliferator-activated receptor (PPAR)-γ that is differentiated from the TZDs structurally, mechanistically, preclinically and clinically. In diabetic rodent models, MBX-102 has insulin-sensitizing and glucose-lowering properties comparable to TZDs without dose-dependent increases in body weight. In vitro, in contrast with full PPAR-γ agonist treatment, MBX-102 fails to drive hum

APA, Harvard, Vancouver, ISO, and other styles

37

Iannotti, Fabio Arturo, Fabrizia De Maio, Elisabetta Panza та ін. "Identification and Characterization of Cannabimovone, a Cannabinoid from Cannabis sativa, as a Novel PPARγ Agonist via a Combined Computational and Functional Study". Molecules 25, № 5 (2020): 1119. http://dx.doi.org/10.3390/molecules25051119.

Full text

Abstract:

Phytocannabinoids (pCBs) are a large family of meroterpenoids isolated from the plant Cannabis sativa. Δ9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the best investigated phytocannabinoids due to their relative abundance and interesting bioactivity profiles. In addition to various targets, THC and CBD are also well-known agonists of peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear receptor involved in energy homeostasis and lipid metabolism. In the search of new pCBs potentially acting as PPARγ agonists, we identified cannabimovone (CBM), a structurally unique abeo

APA, Harvard, Vancouver, ISO, and other styles

38

Yang, Tianrui, B. Tate Cutshall, Alexandra Tatara, and Melanie Ruegger. "Combined Insulin and GLP-1 Receptor Agonists: Simplifying Treatment or Adding Obstacles?" Journal of Pharmacy Practice 32, no. 4 (2018): 447–49. http://dx.doi.org/10.1177/0897190017753041.

Full text

Abstract:

The US Food and Drug Administration recently approved 2 combination products containing a basal insulin and a glucagon-like peptide 1 receptor agonist: insulin glargine/lixisenatide and insulin degludec/liraglutide. These agents were shown to be noninferior in lowering hemoglobin A1c compared to basal insulin and are indicated for patients inadequately controlled on basal insulin or glucagon-like peptide 1 receptor agonists alone. The clinical implications of these agents are unclear due to limitations in the clinical trials and limited recommendations in current guidelines. While these agents

APA, Harvard, Vancouver, ISO, and other styles

39

Riis-Vestergaard, Mette Ji, Bjørn Richelsen, Jens Meldgaard Bruun, Wei Li, Jacob B. Hansen, and Steen Bønløkke Pedersen. "Beta-1 and Not Beta-3 Adrenergic Receptors May Be the Primary Regulator of Human Brown Adipocyte Metabolism." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (2019): e994-e1005. http://dx.doi.org/10.1210/clinem/dgz298.

Full text

Abstract:

Abstract Purpose Brown adipose tissue (BAT) activation in humans has gained interest as a potential target for treatment of obesity and insulin resistance. In rodents, BAT is primarily induced through beta-3 adrenergic receptor (ADRB3) stimulation, whereas the primary beta adrenergic receptors (ADRBs) involved in human BAT activation are debated. We evaluated the importance of different ADRB subtypes for uncoupling protein 1 (UCP1) induction in human brown adipocytes. Methods A human BAT cell model (TERT-hBA) was investigated for subtype-specific ADRB agonists and receptor knockdown on UCP1 mR

APA, Harvard, Vancouver, ISO, and other styles

40

Sahay, Rakesh, and V. Nagesh. "Type 1 diabetes and fasting during Ramzan." Journal of Social Health and Diabetes 04, no. 01 (2016): 011–16. http://dx.doi.org/10.4103/2321-0656.176571.

Full text

Abstract:

AbstractFasting is one of the five pillars of Islam, and consequently, even the Muslims with diabetes prefer to fast fast during Ramadan, irrespective of the healthcare implications. However, this fast can be very difficult to manage in patients of Type 1 diabetes (T1DM), who are on insulin therapy. Risks of diabetic ketoacidosis, severe hypoglycaemia, hyperglycemia, dehydration and thrombotic episodes are increased. Lack of proper pre-fast assessment, management and diabetes education have been stumbling blocks in facilitating Ramadan fasting in type 1 diabetes patients. Recent developments l

APA, Harvard, Vancouver, ISO, and other styles

41

Panse, Madhura, Felicia Gerst, Gabriele Kaiser, et al. "Activation of Extracellular Signal-Regulated Protein Kinases 1 and 2 (ERK1/2) by Free Fatty Acid Receptor 1 (FFAR1/GPR40) Protects from Palmitate-Induced Beta Cell Death, but Plays no Role in Insulin Secretion." Cellular Physiology and Biochemistry 35, no. 4 (2015): 1537–45. http://dx.doi.org/10.1159/000373969.

Full text

Abstract:

Aims: GPR40/FFAR1 mediates palmitate-induced stimulation of insulin secretion but its involvement in lipotoxicity is controversial. Our previous observations suggest that FFAR1/GPR40 agonists protect against lipotoxicity although the underlying mechanism remains elusive. The present study examines the role of ERK1/2 and GPR40/FFAR1 in palmitate-induced stimulation of insulin secretion and beta cell death. Methods: Insulin secretion of INS-1E cells was measured by radioimmunoassay. Protein phosphorylation was examined on Western blots. Apoptosis was assessed by TUNEL staining. Results: Palmitat

APA, Harvard, Vancouver, ISO, and other styles

42

MOREAU, FRANCOIS, BRUNA BRANDAO, CARLY CEDERQUIST, et al. "1725-P: Viral Insulins as Agonists and Antagonists on Insulin/IGF-1 Receptors." Diabetes 69, Supplement 1 (2020): 1725—P. http://dx.doi.org/10.2337/db20-1725-p.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Inman, Taylor R., Erika Plyushko, Nicholas P. Austin, and Jeremy L. Johnson. "The role of basal insulin and GLP-1 receptor agonist combination products in the management of type 2 diabetes." Therapeutic Advances in Endocrinology and Metabolism 9, no. 5 (2018): 151–55. http://dx.doi.org/10.1177/2042018818763698.

Full text

Abstract:

The prevalence of type 2 diabetes necessitates the development of new treatment options to individualize therapy. Basal insulin has been a standard treatment option for years, while glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have grown in use over the past decade due to glucose-lowering efficacy and weight loss potential. There are two new combination injectable products that have recently been approved combining basal insulins with GLP-1 RAs in single pen-injector devices. United States guidelines recently emphasize the option to use combination injectable therapy with GLP-1 RAs an

APA, Harvard, Vancouver, ISO, and other styles

44

Milgram, S. L., J. K. McDonald, and B. D. Noe. "Neuronal influence on hormone release from anglerfish islet cells." American Journal of Physiology-Endocrinology and Metabolism 261, no. 4 (1991): E444—E456. http://dx.doi.org/10.1152/ajpendo.1991.261.4.e444.

Full text

Abstract:

Pancreatic islets in anglerfish (AF) are macroscopic collections of nearly pure endocrine cells that are densely innervated. Immunohistochemical staining for neurotransmitter biosynthetic enzymes revealed noradrenergic and cholinergic innervation of AF islets. An in vitro preparation of perifused dispersed AF islet cells was developed to study nutrient and neural control of islet hormone secretion. Glucose stimulated insulin and somatostatin-14 (SS-14) secretion in a dose-dependent manner, and 16.7 mM glucose inhibited glucagon secretion. In 2 mM glucose, norepinephrine and isoproterenol stimu

APA, Harvard, Vancouver, ISO, and other styles

45

Vilches-Flores, Alonso, Astrid C. Hauge-Evans, Peter M. Jones, and Shanta J. Persaud. "Chronic activation of cannabinoid receptors in vitro does not compromise mouse islet function." Clinical Science 124, no. 7 (2012): 467–78. http://dx.doi.org/10.1042/cs20120447.

Full text

Abstract:

We have demonstrated previously that mouse and human islets express ECS (endocannabinoid system) elements, and that short-term activation of islet cannabinoid CB1r and CB2r (cannabinoid type 1 and 2 receptors respectively) stimulates insulin secretion in vitro. There is evidence that the ECS is overactive in Type 2 diabetes, impairing glucose homoeostasis, but little is known about whether it is implicated in islet dysfunction. Therefore the aim of the present study was to investigate the effect of chronic exposure of isolated mouse islets to cannabinoid receptor agonists on islet gene express

APA, Harvard, Vancouver, ISO, and other styles

46

Sato, Tetsuhiko, Emi Ohara, Chikafumi Ozone, et al. "A Possible Advantage of Glucagon-Like Peptide 1 Receptor Agonist in Kidney Transplant Recipients With Type 2 Diabetes." Journal of the Endocrine Society 5, Supplement_1 (2021): A405—A406. http://dx.doi.org/10.1210/jendso/bvab048.826.

Full text

Abstract:

Abstract Diabetic kidney disease (DKD), a devastating complication of diabetes, is one of the leading causes of end stage kidney disease (ESKD). Kidney transplantation provides superior outcomes for ESKD patients with type 2 diabetes, giving opportunities to be free from dialysis, but needs lifetime immunosuppressive medications to avoid graft kidney rejection. Post-transplant hyperglycemia, however, remains to be unsolved, because immunosuppressive agents, including glucocorticoids and calcineurin inhibitors, may result in impaired insulin secretion and sensitivity. Safe and promising anti-di

APA, Harvard, Vancouver, ISO, and other styles

47

Maida, Adriano, Julie A. Lovshin, Laurie L. Baggio та Daniel J. Drucker. "The Glucagon-Like Peptide-1 Receptor Agonist Oxyntomodulin Enhances β-Cell Function but Does Not Inhibit Gastric Emptying in Mice". Endocrinology 149, № 11 (2008): 5670–78. http://dx.doi.org/10.1210/en.2008-0336.

Full text

Abstract:

The proglucagon gene gives rise to multiple peptides that play diverse roles in the control of energy intake, gut motility, and nutrient disposal. Glucagon-like peptide-1 (GLP-1), a 30-amino-acid peptide regulates glucose homeostasis via control of insulin and glucagon secretion and by inhibition of gastric emptying and food intake. Oxyntomodulin (OXM) a 37-amino-acid peptide also derived from the proglucagon gene, binds to both the glucagon and GLP-1 receptor (GLP-1R); however, a separate OXM receptor has not yet been identified. Here we show that OXM, like other GLP-1R agonists, stimulates c

APA, Harvard, Vancouver, ISO, and other styles

48

Ruz-Maldonado, Inmaculada, Patricio Atanes, Guo Cai Huang, Bo Liu, and Shanta J. Persaud. "Direct Stimulatory Effects of the CB2 Ligand JTE 907 in Human and Mouse Islets." Cells 10, no. 3 (2021): 700. http://dx.doi.org/10.3390/cells10030700.

Full text

Abstract:

Aims: The endocannabinoid system is a complex cell-signaling network through which endogenous cannabinoid ligands regulate cell function by interaction with CB1 and CB2 cannabinoid receptors, and with the novel cannabinoid receptor GPR55. CB1, CB2, and GPR55 are expressed by islet β-cells where they modulate insulin secretion. We have previously shown that administration of the putative CB2 antagonist/inverse agonist JTE 907 to human islets did not affect the insulinotropic actions of CB2 agonists and it unexpectedly stimulated insulin secretion on its own. In this study, we evaluated whether

APA, Harvard, Vancouver, ISO, and other styles

49

Lacey, R. J., H. C. Cable, R. F. L. James, N. J. M. London, J. H. B. Scarpello, and N. G. Morgan. "Concentration-dependent effects of adrenaline on the profile of insulin secretion from isolated human islets of Langerhans." Journal of Endocrinology 138, no. 3 (1993): 555–63. http://dx.doi.org/10.1677/joe.0.1380555.

Full text

Abstract:

ABSTRACT The effects of the mixed α/β-agonist adrenaline on insulin secretion from isolated human islets of Langerhans were studied. In static incubation experiments, adrenaline (0·1 nmol/l to 10 μmol/l) caused a concentration-dependent inhibition of glucose-induced insulin secretion from isolated human islets. However, perifusion experiments revealed that the time-course of the secretory changes induced by adrenaline was complex. When employed at a high concentration (1 μmol/l), adrenaline caused a sustained inhibition of glucose-induced insulin secretion, which could be relieved by the addit

APA, Harvard, Vancouver, ISO, and other styles

50

Viby, Niels-Erik, Marie S. Isidor, Katrine B. Buggeskov, Steen S. Poulsen, Jacob B. Hansen, and Hannelouise Kissow. "Glucagon-Like Peptide-1 (GLP-1) Reduces Mortality and Improves Lung Function in a Model of Experimental Obstructive Lung Disease in Female Mice." Endocrinology 154, no. 12 (2013): 4503–11. http://dx.doi.org/10.1210/en.2013-1666.

Full text

Abstract:

The incretin hormone glucagon-like peptide-1 (GLP-1) is an important insulin secretagogue and GLP-1 analogs are used for the treatment of type 2 diabetes. GLP-1 displays antiinflammatory and surfactant-releasing effects. Thus, we hypothesize that treatment with GLP-1 analogs will improve pulmonary function in a mouse model of obstructive lung disease. Female mice were sensitized with injected ovalbumin and treated with GLP-1 receptor (GLP-1R) agonists. Exacerbation was induced with inhalations of ovalbumin and lipopolysaccharide. Lung function was evaluated with a measurement of enhanced pause

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!