Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats. (Q35140228)

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English	Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats.	scientific article

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13 March 2020

Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats (English)

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13 March 2020

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13 March 2020

Paloma Alonso Magdalena

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13 March 2020

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13 March 2020

Sebastião R. Taboga

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13 March 2020

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13 March 2020

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13 March 2020

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Luiz M Gonçalves-Neto

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13 March 2020

Junia C Santos-Silva

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13 March 2020

Everardo M Carneiro

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13 March 2020

Antonio C Boschero

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13 March 2020

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4 April 2014

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13 March 2020

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13 March 2020

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13 March 2020

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13 March 2020

e93531

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13 March 2020

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Creative Commons Attribution 4.0 International

4 April 2014

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11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC3976288/fullTextXML

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11β-Hydroxysteroid dehydrogenase type 1: relevance of its modulation in the pathophysiology of obesity, the metabolic syndrome and type 2 diabetes mellitus.

1 reference

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13 July 2018

Optimal elevation of β-cell 11β-hydroxysteroid dehydrogenase type 1 is a compensatory mechanism that prevents high-fat diet-induced β-cell failure.

1 reference

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Diminished glucagon suppression after β-cell reduction is due to impaired α-cell function rather than an expansion of α-cell mass

1 reference

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13 July 2018

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1 reference

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Glucose intolerance induced by glucocorticoid excess is further impaired by co-administration with β-hydroxy-β-methylbutyrate in rats.

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1 reference

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Dual glucagon recognition by pancreatic beta-cells via glucagon and glucagon-like peptide 1 receptors

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1 reference

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1 reference

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10.1371/JOURNAL.PONE.0093531

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13 March 2020

2014PLoSO...993531R

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13 March 2020

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13 March 2020

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