Antonio Mancini1, Chantal Di Segni2, Carmine Bruno2, Giulio Olivieri2, Francesco Guidi3, Andrea Silvestrini4, Elisabetta Meucci5, Patrick Orlando6, Sonia Silvestri6, Luca Tiano6, Alfredo Pontecorvi2. 1. Operative Unit of Endocrinology, Catholic University of the Sacred Heart, Largo A. Gemelli 8, Rome, 00168, Italy. mancini.giac@mclink.it. 2. Operative Unit of Endocrinology, Catholic University of the Sacred Heart, Largo A. Gemelli 8, Rome, 00168, Italy. 3. Department of Obstetrics and Gynecology, Catholic University of the Sacred Heart, Largo A. Gemelli 8, Rome, 00168, Italy. 4. Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo F. Vito 1, Rome, 00168, Italy. andrea.silvestrini@unicatt.it. 5. Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo F. Vito 1, Rome, 00168, Italy. 6. Department of Life and Environmental Sciences, Polytechnic University of Marche, Via Brecce Bianche, Ancona, 60131, Italy.
Abstract
BACKGROUND AND AIMS: Growth hormone deficiency (GHD) is a condition associated with increased cardiovascular risk and insulin-resistance. Oxidative stress (OS) could be a mechanism underlying both these phenomena. In order to investigate plasma antioxidant defenses in such condition, we evaluated adults with GHD, compared with controls and metabolic syndrome patients (MetS), studying plasma total antioxidant capacity (TAC) and coenzyme Q10 (CoQ10, lipophilic antioxidant) levels, both in its oxidized and reduced forms, correlating this data with metabolic and hormonal pattern. MATERIALS AND METHODS: In this case-control study, 51 GHD, 36 controls, and 35 MetS were enrolled. An evaluation of hormonal and metabolic parameters was performed. TAC was measured using the system metmyoglobin -H202 and the chromogen ABTS, whose radical form is spectroscopically revealed; latency time (LAG) in the appearance of ABTS● is proportional to antioxidant in sample. CoQ10 was assayed by electrochemical method. RESULTS: Despite HOMA index was higher in both GHD and MetS (2.2 ± 0.3 and 3.1 ± 0.3 vs. 1.2 ± 0.2 in controls), only in MetS we observed lower LAG levels (64.5 ± 3.1 s vs. 82.8 ± 5.8 in GHD and 80.6 ± 6.6 in controls), suggesting an increased consumption of antioxidants. LAG significantly correlated with uric acid only in MetS (r 2 = 0.65, p < 0.001), suggesting a different pattern of antioxidants. CoQ10 exhibited a trend toward lower levels in GHD, although not significant. CONCLUSIONS: Our data indicate that GHD, although sharing with MetS various metabolic features, including increased HOMA levels, showed a different pattern of plasma antioxidants, suggesting inadequate reactivity toward radical production rather than an antioxidants consumption as in MetS.
BACKGROUND AND AIMS: Growth hormone deficiency (GHD) is a condition associated with increased cardiovascular risk and insulin-resistance. Oxidative stress (OS) could be a mechanism underlying both these phenomena. In order to investigate plasma antioxidant defenses in such condition, we evaluated adults with GHD, compared with controls and metabolic syndromepatients (MetS), studying plasma total antioxidant capacity (TAC) and coenzyme Q10 (CoQ10, lipophilic antioxidant) levels, both in its oxidized and reduced forms, correlating this data with metabolic and hormonal pattern. MATERIALS AND METHODS: In this case-control study, 51 GHD, 36 controls, and 35 MetS were enrolled. An evaluation of hormonal and metabolic parameters was performed. TAC was measured using the system metmyoglobin -H202 and the chromogen ABTS, whose radical form is spectroscopically revealed; latency time (LAG) in the appearance of ABTS● is proportional to antioxidant in sample. CoQ10 was assayed by electrochemical method. RESULTS: Despite HOMA index was higher in both GHD and MetS (2.2 ± 0.3 and 3.1 ± 0.3 vs. 1.2 ± 0.2 in controls), only in MetS we observed lower LAG levels (64.5 ± 3.1 s vs. 82.8 ± 5.8 in GHD and 80.6 ± 6.6 in controls), suggesting an increased consumption of antioxidants. LAG significantly correlated with uric acid only in MetS (r 2 = 0.65, p < 0.001), suggesting a different pattern of antioxidants. CoQ10 exhibited a trend toward lower levels in GHD, although not significant. CONCLUSIONS: Our data indicate that GHD, although sharing with MetS various metabolic features, including increased HOMA levels, showed a different pattern of plasma antioxidants, suggesting inadequate reactivity toward radical production rather than an antioxidants consumption as in MetS.
Entities:
Keywords:
Antioxidants; Coenzyme Q10; Insulin-resistance; Metabolic syndrome; Pituitary; Precision medicine
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