Search Results

You are looking at 61 - 70 of 249 items for :

  • "insulin secretion" x
  • All content x
Clear All
Free access

Ana Luiza R Rolim, Susan C Lindsey, Ilda S Kunii, Felipe Crispim, Regina Célia M S Moisés, Rui M B Maciel, and Magnus R Dias-da-Silva

-stimulated insulin secretion result in reduced outward K + efflux in skeletal muscle, which causes hypokalaemia and culminates in the depolarisation-induced acute loss of muscle excitability ( Kung 2006 , Rolim et al . 2010 , Maciel et al . 2011 ). Among seven

Free access

Juliane Dinter, Jessica Mühlhaus, Simon Friedrich Jacobi, Carolin Leonie Wienchol, Maxi Cöster, Jaroslawna Meister, Carolin Stephanie Hoefig, Anne Müller, Josef Köhrle, Annette Grüters, Heiko Krude, Jens Mittag, Torsten Schöneberg, Gunnar Kleinau, and Heike Biebermann

et al . 2007 ). Therefore, we additionally examined the long-term effect of 3-T1AM application in vivo in order to examine whether insulin secretion remains blocked after 3-T1AM stimulation of Adra2a. Finally, our analysis revealed important

Free access

Kayla A Boortz, Kristen E Syring, Lynley D Pound, Huan Mo, Lisa Bastarache, James K Oeser, Owen P McGuinness, Joshua C Denny, and Richard M O’Brien

shift in the dose–response curve for glucose-stimulated insulin secretion (GSIS) ( Pound et al . 2013 ). Under fasting conditions, where insulin levels are the same in WT and G6pc2 KO mice, this shift results in reduced fasting blood glucose (FBG) in

Free access

G A Martens, E Motté, G Kramer, G Stangé, L W Gaarn, K Hellemans, J H Nielsen, J M Aerts, Z Ling, and D Pipeleers

been reported to have a lower glucose-stimulated insulin secretion (GSIS) than adult β cells ( Asplund et al . 1969 , Grill et al . 1981 , Hellerstrom & Swenne 1991 ). Both their higher propensity to proliferate and their lower functional glucose

Restricted access

R. D. Hurst and N. G. Morgan


The mechanisms involved in inhibition of insulin secretion by somatostatin and noradrenaline were compared in order to establish whether the receptors for these agents are coupled to similar effector systems in the pancreatic B cell. Both agents significantly reduced forskolin-induced adenylate cyclase activity in islet homogenates, although noradrenaline was more effective than somatostatin. The capacity of noradrenaline to inhibit insulin secretion was largely unaffected by agents that increase intracellular cyclic AMP, whereas the effect of somatostatin as an inhibitor was markedly reduced under these conditions. Both noradrenaline and somatostatin inhibited the stimulation of insulin secretion induced by K+ depolarization, but different mechanism were involved. Somatostatin significantly inhibited K+-stimulated 45Ca2+ efflux and influx in islets, while noradrenaline exerted only a minor influence on these processes. The data indicate that noradrenaline controls insulin secretion by a mechanism which operates beyond the level of intracellular messenger generation. In contrast, somatostatin exerts at least part of its inhibitory effect on insulin secretion by directly controlling islet cell Ca2+ influx in a manner which may be regulated by cyclic AMP.

Free access

Xianjie Wen and Yisheng Yang

-type littermates ( Kang et al . 2009 b ). SUR1 is a sensor of intracellular levels of the nucleotides ATP and ADP to initiate insulin secretion in response to the sulfonylurea class of antidiabetic drugs ( Yang & Chan 2016 ). These data suggested that in addition

Restricted access

Karin J Bosma, Mohsin Rahim, Kritika Singh, Slavina B Goleva, Martha L Wall, Jing Xia, Kristen E Syring, James K Oeser, Greg Poffenberger, Owen P McGuinness, Anna L Means, Alvin C Powers, Wen-hong Li, Lea K Davis, Jamey D Young, and Richard M O’Brien

glucose and was thought to be the key factor that determines the rate of beta cell glycolytic flux ( Iynedjian 2009 , Matschinsky & Wilson 2019 ). This glycolytic rate determines the sensitivity of glucose-stimulated insulin secretion (GSIS) to glucose

Free access

Inge Seim, Amy A Lubik, Melanie L Lehman, Nadine Tomlinson, Eliza J Whiteside, Adrian C Herington, Colleen C Nelson, and Lisa K Chopin

functions, including regulation of adipogenesis, insulin secretion and pancreatic homeostasis and cancer cell progression ( Zhang et al . 2005 , Seim et al . 2011 b ). Following cleavage of the signal peptide, the 94 amino acid proghrelin peptide is post

Restricted access

Takumi Nakamura, Kazuki Harada, Taichi Kamiya, Mai Takizawa, Jim Küppers, Kazuo Nakajima, Michael Gütschow, Tetsuya Kitaguchi, Kunihiro Ohta, Tadafumi Kato, and Takashi Tsuboi

Introduction Glucagon-like peptide-1 (GLP-1) is a member of the incretin family and is secreted by the gastrointestinal endocrine L cells ( Harada et al. 2017 , 2018 a , b , Drucker 2018 ). GLP-1 regulates the increase in insulin

Free access

R Perfetti, H Hui, K Chamie, S Binder, M Seibert, J McLenithan, K Silver, and JD Walston

The Arg64 beta(3)-adrenergic receptor (beta(3)AR) variant is associated with an earlier age of onset of diabetes and lower levels of insulin secretion in humans. The aims of this study were to investigate whether beta(3)AR is expressed by islet cells, if receptor binding affects insulin secretion and, finally, if the beta(3)AR Arg64 variant induces abnormal insulin secretory activity. Human pancreas extracts were subjected to RT-PCR, Western blotting and immunostaining analyses. DNA sequencing and Western blotting demonstrated that the beta(3)AR gene is transcribed and translated in the human pancreas; immunostaining showed that it is expressed by the islets of Langerhans. Cultured rat beta-cells responded to human beta(3)AR agonists in a dose- and time-dependent manner. Transfection of cultured rat beta-cells with the wild-type human beta(3)AR produced an increased baseline and ligand-dependent insulin secretion compared with parental cells. On the other hand, cells transfected with the Arg64 variant of the beta(3)AR secreted less insulin, both spontaneously and after exposure to human beta(3)AR agonists. Furthermore, while transfection with the wild-type beta(3)AR preserved the glucose-dependent secretion of insulin, expression of the variant receptor rendered the host cells significantly less responsive to glucose. In summary, cells express the beta(3)AR, and its activation contributes to the regulation of insulin secretion. These findings may help explain the low levels of insulin secretion in response to an i.v. glucose tolerance test observed in humans carrying the Arg64 polymorphism.