scholarly journals Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction

2021 ◽  
Vol Volume 14 ◽  
pp. 3669-3676
Author(s):  
Otávio T Nóbrega ◽  
Alessandra M Campos-Staffico ◽  
Elayne Kelen Oliveira ◽  
Daniel B Munhoz ◽  
Filipe A Moura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Nitric Oxide Synthase ◽  
Acute Phase ◽  
Neuronal Nitric Oxide Synthase ◽  
Defective Allele ◽  
Oxide Synthase

scholarly journals Defective Allele of the Neuronal Nitric Oxide Synthase Gene Increases Insulin Resistance During Acute Phase of Myocardial Infarction.

2021 ◽  
Author(s):  
Otávio T Nóbrega ◽  
Alessandra M. Campos-Staffico ◽  
Elayne Kelen Oliveira ◽  
Daniel B Munhoz ◽  
Filipe A. Moura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Nitric Oxide Synthase ◽  
Acute Phase ◽  
Neuronal Nitric Oxide Synthase ◽  
No Production ◽  
Defective Allele ◽  
Oxide Synthase

Abstract Background: glycemia disorders are a strong predictor of mortality in ST-Elevation Myocardial Infarction (STEMI) patients. Disruption in nitric oxide (NO) production is associated with insulin-resistant states. We evaluated whether NO production in carriers of a defective allele of the neuronal nitric oxide synthase (nNOS or NOS1), whose in vivo expression is reduced by up to 50%, might influence the insulin response during acute phase of STEMI. Methods and Results: Consecutive patients with STEMI (n = 354) underwent clinical evaluations and genotyping for the promoter variation rs41279104. Blood tests were performed at admission (D1) and after five days (D5) of in-hospital follow up, with the disposition index assessed in the period. Flow-mediated dilation (FMD) was assessed by reactive hyperemia on the 30th day. Homozygotes for the defective allele (A) showed lower glycemia and insulin sensitivity at D1 while showing the highest b-cells function and no changes in the circulating NO pool, what is compatible with hyperresponsive b-cells to counteract the inherent glucose-resistant state of AA patients. At D5, glycemic scores shifted to indicate greater insulin sensitivity among A homozygotes, paralleled by a slight yet poor increase in NO bioavailability than that among G carriers. All in all, defective homozygotes showed greater insulin resistance expressed by the disposition index at admission, which was compensated 5 days after STEMI even though FMD of A carriers was lower compared to G homozygotes. Conclusion: a defective nNOS allele seems to elicit endocrine adaptation and to associate with insulin resistance during the acute phase of STEMI.

scholarly journals Role of Myocardial Neuronal Nitric Oxide Synthase–Derived Nitric Oxide in β-Adrenergic Hyporesponsiveness After Myocardial Infarction–Induced Heart Failure in Rat

Circulation ◽  
2004 ◽  
Vol 110 (16) ◽  
pp. 2368-2375 ◽  
Author(s):  
Jennifer K. Bendall ◽  
Thibaud Damy ◽  
Philippe Ratajczak ◽  
Xavier Loyer ◽  
Virginie Monceau ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase

scholarly journals Deficiency of Neuronal Nitric Oxide Synthase Increases Mortality and Cardiac Remodeling After Myocardial Infarction

Circulation ◽  
2005 ◽  
Vol 112 (22) ◽  
pp. 3415-3422 ◽  
Author(s):  
Roberto M. Saraiva ◽  
Khalid M. Minhas ◽  
Shubha V.Y. Raju ◽  
Lili A. Barouch ◽  
Eleanor Pitz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Nitric Oxide Synthase ◽  
Cardiac Remodeling ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase
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