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Cardiac Function in Mice Lacking the Glucagon-Like Peptide-1 Receptor

Gros, Robert ; You, Xiaomang ; Baggio, Laurie L ; Kabir, M. Golam ; Sadi, Al Muktafi ; Mungrue, Imran N ; Parker, Thomas G ; Huang, Qingling ; Drucker, Daniel J ; Husain, Mansoor

Endocrinology (Philadelphia), 2003-06, Vol.144 (6), p.2242-2252 [Periódico revisado por pares]

Bethesda, MD: Endocrine Society

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Título:
Cardiac Function in Mice Lacking the Glucagon-Like Peptide-1 Receptor
Autor: Gros, Robert ; You, Xiaomang ; Baggio, Laurie L ; Kabir, M. Golam ; Sadi, Al Muktafi ; Mungrue, Imran N ; Parker, Thomas G ; Huang, Qingling ; Drucker, Daniel J ; Husain, Mansoor
Assuntos: Animals ; Biological and medical sciences ; Blood Pressure ; Body Weight ; Echocardiography ; Fundamental and applied biological sciences. Psychology ; Glucagon-Like Peptide-1 Receptor ; Heart - physiology ; Heart Diseases - diagnostic imaging ; Heart Diseases - pathology ; Heart Diseases - physiopathology ; Heart Rate ; Male ; Mice ; Mice, Mutant Strains ; Myocardium - pathology ; Receptors, Glucagon - genetics ; Signal Transduction - physiology ; Stress, Physiological - physiopathology ; Ventricular Pressure
É parte de: Endocrinology (Philadelphia), 2003-06, Vol.144 (6), p.2242-2252
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: Glucagon-like peptide-1 (GLP-1) acts via its G protein-coupled receptor (GLP-1R) to regulate blood glucose. Although the GLP-1R is widely expressed in peripheral tissues, including the heart, and exogenous GLP-1 administration increases heart rate and blood pressure in rodents, the physiological importance of GLP-1R action in the cardiovascular system remains unclear. We now show that 2-month-old mice with genetic deletion of the GLP-1R (GLP-1R−/−) exhibit reduced resting heart rate and elevated left ventricular (LV) end diastolic pressure compared with CD-1 wild-type controls. At the age of 5 months, echocardiography and histology demonstrate increased LV thickness in GLP-1R−/− mice. Although baseline hemodynamic parameters of GLP-1R−/− did not differ significantly from those of wild type, GLP-1R−/− mice displayed impaired LV contractility and diastolic function after insulin administration. The defective cardiovascular response to insulin was not attributable to a generalized defect in the stress response, because GLP-1R−/− mice responded appropriately to insulin with increased c-fos expression in the hypothalamus and increased circulating levels of glucagon and epinephrine. Furthermore, LV contractility after exogenous epinephrine infusion was also reduced in GLP-1R−/− mice. These findings provide new evidence implicating an essential role for GLP-1R in the control of murine cardiac structure and function in vivo.
Editor: Bethesda, MD: Endocrine Society
Idioma: Inglês

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Cardiac Function in Mice Lacking the Glucagon-Like Peptide-1 Receptor

Gros, Robert ; You, Xiaomang ; Baggio, Laurie L ; Kabir, M. Golam ; Sadi, Al Muktafi ; Mungrue, Imran N ; Parker, Thomas G ; Huang, Qingling ; Drucker, Daniel J ; Husain, Mansoor

Bethesda, MD: Endocrine Society

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