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Страница 1 от 270 полученные результаты
Metabolic effects of sub-chronic ablation of the incretin receptors by daily administration of (Pro3)GIP and exendin(9-39)amide in obese diabetic (ob/ob) mice.
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Effects of chemical ablation of the GIP and GLP-1 receptors on metabolic aspects of obesity-diabetes were investigated using the stable receptor antagonists (Pro3)GIP and exendin(9-39)amide. Ob/ob mice received a daily i.p. injection of saline vehicle, (Pro3)GIP, exendin(9-39)amide or a combination
Spiroindane based amides as potent and selective MC4R agonists for the treatment of obesity.
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We report a series of potent and selective MC4R agonists based on spiroindane amide privileged structures for potential treatments of obesity. Among the synthetic methods used, Method C allows rapid synthesis of the analogs. The series of compounds can afford high potency on MC4R as well as good
New amide derivatives as melanin-concentrating hormone receptor 1 antagonists for the treatment of obesity.
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Melanin-concentrating hormone (MCH) is a recently discovered central nervous system (CNS) target for treating obesity. Two novel series of amide derivatives were synthesized and evaluated biologically as MCH-R1 (melanin-concentrating hormone receptor 1) antagonists. The results showed that diphenyl
Overweight and obesity associated with a missense polymorphism in fatty acid amide hydrolase (FAAH).
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BACKGROUND
The brain endogenous cannabinoid system modulates reward and craving pathways and consequently may affect body weight. A naturally occurring missense polymorphism in the gene encoding fatty acid amide hydrolase (FAAH), the primary enzyme for inactivation of endocannabinoids, is associated
The influence of the fatty acid amide hydrolase 385C>A single nucleotide polymorphisms on obesity susceptibility.
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The chronic over-activation of the endogenously produced cannabinoids in obesity has been demonstrated in several studies. A common 385C>A single nucleotide polymorphism of the fatty acid amide hydrolase, one the most important inactivating enzymes of endogenous cannabinoids, has been shown to be
Mutation screen and association studies for the fatty acid amide hydrolase (FAAH) gene and early onset and adult obesity.
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BACKGROUND
The orexigenic effects of cannabinoids are limited by activation of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH). The aim of this study was to analyse whether FAAH alleles are associated with early and late onset obesity.
METHODS
We initially assessed association
Comparison of the anti-diabetic effects of GIP- and GLP-1-receptor activation in obese diabetic (ob/ob) mice: studies with DPP IV resistant N-AcGIP and exendin(1-39)amide.
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BACKGROUND
The two major incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are being actively explored as anti-diabetic agents because they lower blood glucose through multiple mechanisms. The rapid inactivation of GIP and GLP-1 by the
Degradation and glycemic effects of His(7)-glucitol glucagon-like peptide-1(7-36)amide in obese diabetic ob/ob mice.
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Glucagon-like peptide-1(7-36)amide (tGLP-1) has attracted considerable potential as a possible therapeutic agent for type 2 diabetes. However, tGLP-1 is rapidly inactivated in vivo by the exopeptidase dipeptidyl peptidase IV (DPP IV), thereby terminating its insulin releasing activity. The present
Effect of chronic central administration of glucagon-like peptide-1 (7-36) amide on food consumption and body weight in normal and obese rats.
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Glucagon-like peptide (7-36) amide (GLP-1) acutely inhibits food and water consumption in rats after intracerebroventricular (icv) administration. To assess the potential for desensitization of these effects, we investigated the effects of chronic icv administration of GLP-1 on food consumption and
Unexpected responses of the obese "cafeteria" rat to the peptide FMRF-amide.
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The relationship between the acute effects of FMRF-amide on central monoamines and feeding effects were investigated simultaneously in normophagic and "cafeteria" rats. This tetrapeptide is considered as being representative of an endogenous related peptides family with antagonistic properties on
Glucagon-like peptide-1 (7-36) amide response to low versus high glycaemic index preloads in overweight subjects with and without type II diabetes mellitus.
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OBJECTIVE
Glucagon-like-peptide-1 (7-36) amide (GLP-1) is an insulin secretagogue and potential treatment for type II diabetes mellitus. An alternative to GLP-1 administration is endogenous dietary stimulation. We described a greater GLP-1 release following ingestion of liquids versus solids. We add
Chronic treatment with exendin(9-39)amide indicates a minor role for endogenous glucagon-like peptide-1 in metabolic abnormalities of obesity-related diabetes in ob/ob mice.
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Glucagon-like peptide-1 (GLP-1) is a potent insulinotropic hormone proposed to play a role in both the pathophysiology and treatment of type 2 diabetes. This study has employed the GLP-1 receptor antagonist, exendin-4(9-39)amide (Ex(9-39)) to evaluate the role of endogenous GLP-1 in genetic
C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females.
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BACKGROUND
Recently, it has been shown that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. Visfatin has been identified as a protein expressed in visceral adipose tissue with contradictory functions in glucose metabolism.
OBJECTIVE
The aim
Effects of the novel (Pro3)GIP antagonist and exendin(9-39)amide on GIP- and GLP-1-induced cyclic AMP generation, insulin secretion and postprandial insulin release in obese diabetic (ob/ob) mice: evidence that GIP is the major physiological incretin.
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OBJECTIVE
This study examined the biological effects of the GIP receptor antagonist, (Pro3)GIP and the GLP-1 receptor antagonist, exendin(9-39)amide.
METHODS
Cyclic AMP production was assessed in Chinese hamster lung fibroblasts transfected with human GIP or GLP-1 receptors, respectively. In vitro
Inhibition of dipeptidyl peptidase IV with NVP-DPP728 increases plasma GLP-1 (7-36 amide) concentrations and improves oral glucose tolerance in obese Zucker rats.
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OBJECTIVE
The potent incretin hormone glucagon-like peptide 1 (GLP-1) plays a pivotal role in prandial insulin secretion. In the circulation GLP-1 (7-36) amide is, however, rapidly (t(1/2):1-2 min) inactivated by the protease dipeptidyl peptidase IV (DPP-IV). We therefore investigated whether DPP-IV
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