amibegron and Body-Weight

amibegron has been researched along with Body-Weight* in 3 studies

Other Studies

3 other study(ies) available for amibegron and Body-Weight

ArticleYear
GPR40 is partially required for insulin secretion following activation of beta3-adrenergic receptors.
    Molecular and cellular endocrinology, 2010, Aug-30, Volume: 325, Issue:1-2

    The free fatty acid (FFA) receptor GPR40, expressed by pancreatic beta-cells, may be responsible for insulin release following beta(3) adrenoceptor (Adrb3) activation. To test this hypothesis, we first studied the effects of Adrb3 agonists SR58611A and CL316,243 in GPR40 knockout (GPR40(-/-)) mice. Both drugs increased blood FFA levels in wild-type (GPR40(+/+)) and GPR40(-/-) mice, indicating that lipolysis is not GPR40-dependent. However, the magnitude of the insulin response after agonist treatment was decreased by approximately 50% in GPR40(-/-) mice. Analysis of the time-course revealed that the change in FFAs (5-10 min post-treatment) in response to SR58611A preceded insulin secretion (10-15 min post-treatment). While reduced by agonist treatment, glucose levels in GPR40(-/-) mice remained significantly higher than in GPR40(+/+) mice. Energy expenditure, food intake, or body weight was not affected in GPR40(-/-) mice, whereas SR58611A increased energy metabolism. Furthermore, CL316,243 did not potentiate glucose-stimulated insulin secretion in isolated mouse islets or activate a cAMP reporter in transgenic mice. Our data indicate that insulin secretion, a secondary event following stimulation of Adrb3 receptors, is partially mediated by GPR40 and suggest that GPR40 is integral to the anti-diabetes effects of Adrb3 agonists.

    Topics: Adrenergic beta-3 Receptor Agonists; Adrenergic beta-Agonists; Animals; Body Weight; Dioxoles; Dose-Response Relationship, Drug; Eating; Energy Metabolism; Hypoglycemic Agents; Insulin; Insulin Secretion; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Adrenergic, beta-3; Receptors, G-Protein-Coupled; Tetrahydronaphthalenes

2010
The beta3-adrenoceptor agonist SR58611A ameliorates experimental colitis in rats.
    Neurogastroenterology and motility, 2008, Volume: 20, Issue:9

    Beta(3)-adrenoceptor agonists protect against experimental gastric ulcers. We investigated the effects of the beta(3)-adrenoceptor agonist SR58611A on 2,4-dinitrobenzene sulphonic acid-induced colitis in rats and analysed the expression of beta(3)-adrenoceptors in the colonic wall. SR58611A was administered orally (1-10 mg kg(-1)) for 7 days, starting the day before induction of colitis. Colitis was assessed by macroscopic and histological scores, tissue myeloperoxidase activity, interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) levels. Reverse transcription-polymerase chain reaction and immunohistochemical analysis were used to examine the expression of beta(3)-adrenoceptors. SR58611A significantly reduced the severity of colitis as well as the tissue levels of TNF-alpha, IL-1beta and IL-6. Colitis was associated with a decreased expression of beta(3)-adrenoceptor mRNA in the mucosal/submucosal layer of distal colon and this reduction was not affected by SR58611A. Immunohistochemical analysis revealed beta(3)-adrenoceptors within the muscularis externa, in myenteric neurons and nerve fibres and in the submucosa. beta(3)-Adrenoceptor immunoreactivity was decreased in inflamed tissues compared to controls, particularly in the myenteric plexus; this reduction was counteracted by SR58611A. Amelioration of experimental colitis by the selective beta(3)-adrenoceptor agonist SR58611A suggests that beta(3)-adrenoceptors may represent a therapeutic target in gut inflammation.

    Topics: Adrenergic beta-3 Receptor Agonists; Adrenergic beta-Agonists; Animals; Body Weight; Colitis; Colon; Cytokines; Dinitrofluorobenzene; Dose-Response Relationship, Drug; Humans; Inflammation; Male; Proto-Oncogene Proteins c-kit; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, beta-3; Tetrahydronaphthalenes

2008
Sustained improvement in glucose homeostasis in lean and obese mice following chronic administration of the beta 3 agonist SR 58611A.
    British journal of pharmacology, 1999, Volume: 128, Issue:7

    1. Acute SR 58611A (0.25 mg kg-1), was effective in reducing the blood glucose response to a glucose tolerance test (GTT) in normal lean (control) and spontaneously obese/diabetic CBA/Ca mice and to be equipotent to 1.25 mg kg-1 glibenclamide in lean mice. 2. Neither brown (BAT) nor white (WAT) adipose tissue lipogenesis was altered by acute SR 58611A (2 - 8 mg kg-1) in lean mice, but both increased significantly at the higher doses in the obese mice. 3. Acute SR 58611A produced a hypoglycaemia 40 min after dosing in lean and obese animals, the duration and potency of which was less than that of glibenclamide. Plasma insulin levels increased 20 min after acute SR 58611A and glibenclamide in lean and obese mice. 4. Chronic treatment (0.25 mg kg-1, 15 days) with SR 58611A increased its effectiveness in improving glucose tolerance, but did not affect the body weight (BW) or food intake of either lean or obese mice. 5. Acute and chronic SR 58611A prolonged the hypoglycaemic effect of exogenous insulin in lean but not obese mice. 6. In fed and fasted lean mice and in fasted obese mice chronic SR 58611A produced an acute hypoglycaemia 30 min post administration which was greater than after a single dose. 7. SR 58611A maintained its effectiveness in improving glucose tolerance in lean and obese mice over a dosing period of 15 days. The improvement in glucose tolerance was achieved at a dose less than that required to stimulate adipose tissue lipogenesis and which did not affect food intake or body weight.

    Topics: Adrenergic beta-Agonists; Animals; Blood Glucose; Body Weight; Drug Administration Schedule; Eating; Glucose; Glucose Tolerance Test; Homeostasis; Insulin; Lipids; Male; Mice; Mice, Inbred CBA; Mice, Obese; Receptors, Adrenergic, beta; Receptors, Adrenergic, beta-3; Tetrahydronaphthalenes; Triglycerides

1999