Background: Hyperinsulinemia/insulin resistance and elevated plasma free fatty acids (FFA) levels are involved in the hypertension and cardiac sympathetic overactivity. Metformin improves insulin action and lower plasma FFA concentrations. We investigate the possible effect of metformin on arterial blood pressure (BP) and cardiac sympathetic nervous system. Methods: One hundred twenty overweight type 2 diabetic patients were treated by placebo (n = 60) + diet or metformin (850 mg twice daily) (n = 60) + diet for 4 months, to evaluate the effect of metformin treatment on the cardiac autonomic nervous system. Insulin resistance was measured by the Homeostasis Model Assessment (HOMA) index. Heart rate variability (HRV) assessed cardiac sympathovagal balance. Results: Metformin treatment, but not placebo treatment, was associated with a decrease in fasting plasma glucose (P < .05), insulin (P < .05), triglyceride (P < .05), and FFA (P < .03) concentrations and HOMA index (P < .03). Metformin treatment was also associated with a significant improvement in cardiac sympathovagal balance but not in mean arterial BP. Furthermore, in a multivariate analysis, delta change in sympathovagal balance index (LF/HF ratio) were associated with delta change in plasma FFA concentrations and HOMA index independently of gender and delta change in plasma triglyceride and HbA1c concentrations. Conclusions: Our study demonstrated that metformin treatment might be useful for improving cardiac sympathovagal balance in obese type 2 diabetic patients.

MANZELLA D, GRELLA R, ESPOSITO K, GIUGLIANO D, BARBAGALLO M, PAOLISSO G (2004). Blood pressure and cardiac autonomic nervous system in obese type 2 diabetic patients: Effect of metformin administration. AMERICAN JOURNAL OF HYPERTENSION, 17(3), 223-227 [10.1016/j.amjhyper.2003.11.006].

Blood pressure and cardiac autonomic nervous system in obese type 2 diabetic patients: Effect of metformin administration

BARBAGALLO, Mario;
2004-01-01

Abstract

Background: Hyperinsulinemia/insulin resistance and elevated plasma free fatty acids (FFA) levels are involved in the hypertension and cardiac sympathetic overactivity. Metformin improves insulin action and lower plasma FFA concentrations. We investigate the possible effect of metformin on arterial blood pressure (BP) and cardiac sympathetic nervous system. Methods: One hundred twenty overweight type 2 diabetic patients were treated by placebo (n = 60) + diet or metformin (850 mg twice daily) (n = 60) + diet for 4 months, to evaluate the effect of metformin treatment on the cardiac autonomic nervous system. Insulin resistance was measured by the Homeostasis Model Assessment (HOMA) index. Heart rate variability (HRV) assessed cardiac sympathovagal balance. Results: Metformin treatment, but not placebo treatment, was associated with a decrease in fasting plasma glucose (P < .05), insulin (P < .05), triglyceride (P < .05), and FFA (P < .03) concentrations and HOMA index (P < .03). Metformin treatment was also associated with a significant improvement in cardiac sympathovagal balance but not in mean arterial BP. Furthermore, in a multivariate analysis, delta change in sympathovagal balance index (LF/HF ratio) were associated with delta change in plasma FFA concentrations and HOMA index independently of gender and delta change in plasma triglyceride and HbA1c concentrations. Conclusions: Our study demonstrated that metformin treatment might be useful for improving cardiac sympathovagal balance in obese type 2 diabetic patients.
2004
MANZELLA D, GRELLA R, ESPOSITO K, GIUGLIANO D, BARBAGALLO M, PAOLISSO G (2004). Blood pressure and cardiac autonomic nervous system in obese type 2 diabetic patients: Effect of metformin administration. AMERICAN JOURNAL OF HYPERTENSION, 17(3), 223-227 [10.1016/j.amjhyper.2003.11.006].
File in questo prodotto:
File Dimensione Formato  
bloodpressure.pdf

accesso aperto

Dimensione 110.25 kB
Formato Adobe PDF
110.25 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/4869
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 72
  • ???jsp.display-item.citation.isi??? 64
social impact