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Jennifer H Stern, Gordon I Smith, Shiuwei Chen, Roger H Unger, Samuel Klein, and Philipp E Scherer

a major focus of metabolic research in obesity, glucagon is also an important regulator of glycemic control. In fact, Orci and Unger’s ‘bihormonal hypothesis’ (1975) ( Unger & Orci 1975 ) prompted decades of work that created abundant evidence

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Wanbao Yang, Hui Yan, Quan Pan, James Zheng Shen, Fenghua Zhou, Chaodong Wu, Yuxiang Sun, and Shaodong Guo

Introduction Glucagon secreted from the α-cells of pancreatic islets is a predominant counter regulatory hormone to the action of insulin in control of blood glucose homeostasis ( Habegger et al. 2010 ). This 29 animo acid peptide hormone is

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Hans Eickhoff, Teresa Louro, Paulo Matafome, Raquel Seiça, and Francisco Castro e Sousa

-dependent insulinotropic peptide (GIP) and reduced glucagon-like peptide 1 (GLP1) secretion seem to play an additional role in the development of type 2 diabetes ( Holst et al . 2009 ). Excessive or inadequate glucagon secretion promoting hepatic gluconeogenesis and

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Mingyu Li, E Danielle Dean, Liyuan Zhao, Wendell E Nicholson, Alvin C Powers, and Wenbiao Chen

Introduction Glucagon is a peptide hormone secreted by pancreatic α-cells. It is the main counter-regulatory hormone of insulin. Glucagon acts primarily on liver through glucagon receptor (GCGR) to regulate hepatic glucose production ( Mayo et al

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Sihan Lv, Xinchen Qiu, Jian Li, Jinye Liang, Weida Li, Chao Zhang, Zhen-Ning Zhang, and Bing Luan

glucose and lipid metabolism in response to hormonal signals. Dedicated transcription regulatory network is involved in the hepatic response to fasting. During the fasted state, one of the major circulating hormones required for liver function is glucagon

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Daniella B R Insuela, Julio B Daleprane, Luciana P Coelho, Adriana R Silva, Patrícia M R e Silva, Marco A Martins, and Vinicius F Carvalho

Introduction Glucagon is a 29-amino-acid peptide hormone secreted during fasting periods by the pancreatic islet α-cells into hepatic portal venous circulation in response to falling glucose levels ( Conarello et al . 2007 , Cryer 2012 ). Glucagon

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Toya M Albury-Warren, Veethika Pandey, Lina P Spinel, Michal M Masternak, and Deborah A Altomare

downregulation of the Akt1 Myr transgene reduced the non-fasted and fasted hyperglycemia to WT levels. Collectively, metabolic characterization of the AKT1 Myr mice revealed a novel glucagon-mediated mechanism by which AKT1 hyperactivation affects glucose

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L M McShane, N Irwin, D O’Flynn, Z J Franklin, C M Hewage, and F P M O’Harte

DM are present in the setting of glucagon excess ( Unger & Cherrington 2012 ). Thus, improved control of glucagon signaling represents a rational therapeutic target for T2DM. In agreement with this, early proof-of-concept studies using the orally

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Lyle Wiemerslage, Priya A Gohel, Giulia Maestri, Torfi G Hilmarsson, Michel Mickael, Robert Fredriksson, Michael J Williams, and Helgi B Schiöth

for studying a variety of molecular pathways, as well as behavior. Specifically for obesity, they have organs that function similar to the human pancreas with corresponding orthologs of insulin and glucagon: insulin-like protein 2 (Ilp2) and

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Bernard Khoo and Tricia Mei-Mei Tan

gut hormone path-finder Glucagon-like peptide 1 (GLP-1) is the most extensively studied gut hormone with translational and clinical evidence for its efficacy ( Holst 2007 ). It is an alternatively processed product of the proglucagon peptide