Relevant bibliographies by topics / Glucagon suppression

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Glucagon suppression'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Glucagon suppression"

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Arafat, A. M., F. H. Perschel, B. Otto, et al. "Glucagon Suppression of Ghrelin Secretion Is Exerted at Hypothalamus-Pituitary Level." Journal of Clinical Endocrinology & Metabolism 91, no. 9 (2006): 3528–33. http://dx.doi.org/10.1210/jc.2006-0225.

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Abstract Context: The mechanisms underlying the well-known glucagon-induced satiety effect are unclear. Recently, we showed that glucagon induces a remarkable decrease in the orexigenic hormone ghrelin that might be responsible for this effect. Objective: The objective of this study was to evaluate the putative role of the hypothalamic pituitary axis in glucagon’s suppressive effect on ghrelin secretion. Design, Subjects, and Methods: Prospectively, we studied the endocrine and metabolic responses to im glucagon administration in 22 patients (16 males; age, 21–68 yr; body mass index, 28.1 ± 1.
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Weick, B. G., and S. Ritter. "Dose-related suppression of feeding by intraportal glucagon infusion in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 4 (1986): R676—R681. http://dx.doi.org/10.1152/ajpregu.1986.250.4.r676.

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Continuous intraportal infusion of pancreatic glucagon during a feeding test conducted in the dark phase of the circadian photoperiod produced a dose-related suppression of feeding in rats. At the end of the 30 min of infusion, food intake was suppressed 10% at the infusion rate of 0.33 micrograms X kg-1 X min-1 and 45% at the highest infusion rate studied (100 micrograms X kg-1 X min-1). At infusion rates of 33 and 100 micrograms X kg-1 X min-1, the suppression of cumulative intake persisted for 30 min after the termination of the infusion, but no effect on 24-h intake was observed. Glucagon'
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3

Urbano, Francesca, Antonino Di Pino, Roberto Scicali, et al. "Impaired glucagon suppression and reduced insulin sensitivity in subjects with prediabetes undergoing atorvastatin therapy." European Journal of Endocrinology 181, no. 6 (2019): 579–90. http://dx.doi.org/10.1530/eje-19-0173.

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Objective Statin therapy has been linked to an increased risk of type 2 diabetes in high-risk populations; however, the pathophysiology of this association remains to be clarified. We investigated glucagon suppression and its relationship with insulin resistance in prediabetic subjects undergoing atorvastatin therapy; in addition, we studied molecular insulin signaling in pancreatic α-cells exposed to atorvastatin in vitro. Design and methods Fifty subjects with prediabetes were divided into two groups based on atorvastatin therapy. All subjects underwent an oral glucose tolerance test. Early
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Lund, Asger, Tina Vilsbøll, Jonatan I. Bagger, Jens J. Holst, and Filip K. Knop. "The separate and combined impact of the intestinal hormones, GIP, GLP-1, and GLP-2, on glucagon secretion in type 2 diabetes." American Journal of Physiology-Endocrinology and Metabolism 300, no. 6 (2011): E1038—E1046. http://dx.doi.org/10.1152/ajpendo.00665.2010.

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Type 2 diabetes mellitus (T2DM) is associated with reduced suppression of glucagon during oral glucose tolerance test (OGTT), whereas isoglycemic intravenous glucose infusion (IIGI) results in normal glucagon suppression in these patients. We examined the role of the intestinal hormones glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and glucagon-like peptide-2 (GLP-2) in this discrepancy. Glucagon responses were measured during a 3-h 50-g OGTT ( day A) and an IIGI ( day B) in 10 patients with T2DM [age (mean ± SE), 51 ± 3 yr; body mass index, 33 ± 2 kg/m2;
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Bansal, Pritpal, and Qinghua Wang. "Insulin as a physiological modulator of glucagon secretion." American Journal of Physiology-Endocrinology and Metabolism 295, no. 4 (2008): E751—E761. http://dx.doi.org/10.1152/ajpendo.90295.2008.

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Glucose homeostasis is regulated primarily by the opposing actions of insulin and glucagon, hormones that are secreted by pancreatic islets from β-cells and α-cells, respectively. Insulin secretion is increased in response to elevated blood glucose to maintain normoglycemia by stimulating glucose transport in muscle and adipocytes and reducing glucose production by inhibiting gluconeogenesis in the liver. Whereas glucagon secretion is suppressed by hyperglycemia, it is stimulated during hypoglycemia, promoting hepatic glucose production and ultimately raising blood glucose levels. Diabetic hyp
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Le Marchand, Sylvain J., and David W. Piston. "Glucose Suppression of Glucagon Secretion." Journal of Biological Chemistry 285, no. 19 (2010): 14389–98. http://dx.doi.org/10.1074/jbc.m109.069195.

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Shah, Pankaj, Ananda Basu, Rita Basu, and Robert Rizza. "Impact of lack of suppression of glucagon on glucose tolerance in humans." American Journal of Physiology-Endocrinology and Metabolism 277, no. 2 (1999): E283—E290. http://dx.doi.org/10.1152/ajpendo.1999.277.2.e283.

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People with type 2 diabetes have defects in both α- and β-cell function. To determine whether lack of suppression of glucagon causes hyperglycemia when insulin secretion is impaired but not when insulin secretion is intact, twenty nondiabetic subjects were studied on two occasions. On both occasions, a “prandial” glucose infusion was given over 5 h while endogenous hormone secretion was inhibited. Insulin was infused so as to mimic either a nondiabetic ( n = 10) or diabetic ( n = 10) postprandial profile. Glucagon was infused at a rate of 1.25 ng ⋅ kg−1 ⋅ min−1, beginning either at time zero t
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Chen, Xi, Enrique Maldonado, Ralph A. DeFronzo, and Devjit Tripathy. "Impaired Suppression of Glucagon in Obese Subjects Parallels Decline in Insulin Sensitivity and Beta-Cell Function." Journal of Clinical Endocrinology & Metabolism 106, no. 5 (2021): 1398–409. http://dx.doi.org/10.1210/clinem/dgab019.

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Abstract Aim To examine the relationship between plasma glucagon levels and insulin sensitivity and insulin secretion in obese subjects. Methods Suppression of plasma glucagon was examined in 275 obese Hispanic Americans with varying glucose tolerance. All subjects received a 2-hour oral glucose tolerance test (OGTT) and a subset (n = 90) had euglycemic hyperinsulinemic clamp. During OGTT, we quantitated suppression of plasma glucagon concentration, Matsuda index of insulin sensitivity, and insulin secretion/insulin resistance (disposition) index. Plasma glucagon suppression was compared betwe
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Lewis, Gary F., Mladen Vranic, and Adria Giacca. "Role of free fatty acids and glucagon in the peripheral effect of insulin on glucose production in humans." American Journal of Physiology-Endocrinology and Metabolism 275, no. 1 (1998): E177—E186. http://dx.doi.org/10.1152/ajpendo.1998.275.1.e177.

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We have shown previously that the greater suppression of endogenous glucose production (GP) with equimolar peripheral vs. portal insulin cannot be detected or is minimally reversed when the insulin-induced suppression of either free fatty acids (FFA) or glucagon alone is prevented. The present experiments were designed to minimize the insulin suppression of both glucagon and FFA in an attempt to further examine the mechanism of insulin’s peripheral effect on GP. In nine healthy men, we investigated the effect of limiting the insulin suppression of both FFA and glucagon by infusing heparin (250
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10

Schrader, Henning, Bjoern A. Menge, Thomas G. K. Breuer, et al. "Impaired Glucose-Induced Glucagon Suppression after Partial Pancreatectomy." Journal of Clinical Endocrinology & Metabolism 94, no. 8 (2009): 2857–63. http://dx.doi.org/10.1210/jc.2009-0826.

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Introduction: The glucose-induced decline in glucagon levels is often lost in patients with type 2 diabetes. It is unclear whether this is due to an independent defect in α-cell function or secondary to the impairment in insulin secretion. We examined whether a partial pancreatectomy in humans would also impair postchallenge glucagon concentrations and, if so, whether this could be attributed to the reduction in insulin levels. Patients and Methods: Thirty-six patients with pancreatic tumours or chronic pancreatitis were studied before and after approximately 50% pancreatectomy with a 240-min
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Dissertations / Theses on the topic "Glucagon suppression"

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Neumann, Ursula Hope. "The metabolic effects of leptin therapy and glucagon suppression therapy in mouse models of diabetes." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62127.

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It has long been thought that the only hormone capable of reversing the catabolic consequences of diabetes is insulin. However, various studies have demonstrated that the adipocyte-derived hormone leptin can potently lower blood glucose levels in rodent models of insulin-deficient diabetes. In addition, the hormone glucagon is elevated in type 1 and type 2 diabetes, and glucagon suppression therapy has shown promise as an agent to treat diabetes in mice. Given the interest in both of these therapies, leptin treatment and glucagon antagonism were propelled into clinical trials for patients with
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2

Arafat, Ayman M. [Verfasser]. "The impact of insulin-independent, glucagon-induced suppression of total ghrelin on satiety in obesity and type 1 diabetes mellitus / Ayman M. Arafat." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1058105094/34.

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Ikedo, Taichi. "Dipeptidyl Peptidase-4 Inhibitor Anagliptin Prevents Intracranial Aneurysm Growth by Suppressing Macrophage Infiltration and Activation." Kyoto University, 2018. http://hdl.handle.net/2433/232101.

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Huang, Ya-Chi. "Glucagon-like peptide-1-induced suppression on glucagon secretion in pancreatic alpha-cells: A study using phosphoinositol 3-kinasegamma deficient mice." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=450646&T=F.

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Aziz, Alfred. "The role of glucagon-like peptide-1 receptors in protein-induced suppression of food intake in rats." 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=94780&T=F.

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Books on the topic "Glucagon suppression"

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Tucker, J. Devin. Suppression of pancreatic glucagon production in mice carrying proglucagon-expressing tumours, and elucidation of the tumoural patterns of proglucagon processing. National Library of Canada, 1994.

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Weatherford, Sally Crinean. Neural substrates mediating glucagon-induced suppression of food intake. 1987.

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Huang, Ya-Chi. Glucagon-like peptide-1-induced suppression on glucagon secretion in pancreatic alpha-cells: A study using phosphoinositol 3-kinasegamma deficient mice. 2006.

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Aziz, Alfred. The role of glucagon-like peptide-1 receptors in protein-induced suppression of food intake in rats. 2004.

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Book chapters on the topic "Glucagon suppression"

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Cousins, Robert J., and Daphne E. Coppen. "Regulation of Liver Zinc Metabolism and Metallothionein by Camp, Glucagon and Glucocorticoids and Suppression of Free Radicals by Zinc." In Experientia Supplementum. Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-6784-9_56.

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A. Ochola, Lucy, and Eric M. Guantai. "Prevention of Hyperglycemia." In Metformin - Pharmacology and Drug Interactions. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99342.

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Hyperglycemia is the elevation of blood glucose concentrations above the normal range. Prolonged uncontrolled hyperglycemia is associated with serious life-threatening complications. Hyperglycemia arises from an imbalance between glucose production and glucose uptake and utilization by peripheral tissues. Disorders that compromise pancreatic function or affect the glucose counter-regulatory hormones cause hyperglycemia. Acute or serious illness or injury may also bring about hyperglycemia, as can many classes of drugs. Metformin lowers blood glucose levels by inhibiting the production of gluco
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Vasist, LS, J. Lin, JS Stuart, et al. "Effectiveness of GSK1362885, a Novel Glycogen Phosphorylase Inhibitor, Demonstrated in Single Dose Suppression of a Glucagon Stimulated Glucose Rise in Healthy Volunteers." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.or1.or24-5.

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Conference papers on the topic "Glucagon suppression"

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Henriques Forsythe, Marshaleen, Zvezdana Vuk-Pavlovic, and Andrew H. Limper. "Possible Activity Of Macrophages In Suppression Of Fungal B-Glucan-Induced Lung Inflammation By A Glycosphingolipid Synthesis Inhibitor." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6178.

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Journal articles
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