Antonio Mancini1, Giuseppe Ettore Martorana2, Marinella Magini3, Roberto Festa4, Sebastiano Raimondo5, Andrea Silvestrini6, Nicola Nicolotti7, Alvaro Mordente8, Maria Cristina Mele9, Giacinto Abele Donato Miggiano10, Elisabetta Meucci11. 1. Dept. of Medical Sciences, Division of Endocrinology, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: mancini.giac@mclink.it. 2. Dept of Laboratory Medicine, Dietetic Service, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy; Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: gmartorana@rm.unicatt.it. 3. Dept of Laboratory Medicine, Dietetic Service, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: marimagini@hotmail.com. 4. Dept. of Clinical and Molecular Science, Polytechnic University of Marche, Piazza Roma, 22, 60121 Ancona, Italy. Electronic address: dott.robertofesta@gmail.com. 5. Dept. of Medical Sciences, Division of Endocrinology, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: bastio984@hotmail.com. 6. Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: asilvestrini@rm.unicatt.it. 7. Institute of Hygiene, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy; Dept. of Epidemiology and Preclinical Research L. Spallanzani, National Institute for Infectious Disease (INMI), IRCCS, Via Barberini, 3, 00187 Rome, Italy. Electronic address: nicola.nicolotti@gmail.com. 8. Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: alvaro.mordente@rm.unicatt.it. 9. Dept of Laboratory Medicine, Dietetic Service, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy; Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: mcmele@rm.unicatt.it. 10. Dept of Laboratory Medicine, Dietetic Service, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy; Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: gmiggiano@rm.unicatt.it. 11. Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8, 00168 Rome, Italy. Electronic address: emeucci@rm.unicatt.it.
Abstract
BACKGROUND & AIMS: Oxidative stress (OS) could play a role in metabolic syndrome-related manifestations contributing to insulin resistance (IR). The aim of the present study was to gain insight the relationships between OS, IR and other hormones involved in caloric balance, explaining the effects of a natural antioxidant-enriched diet in patients affected by metabolic syndrome. METHODS: We investigated the effects of dietary antioxidants on IR, studying 53 obese (20 males and 33 females, 18-66 years old, BMI 36.3 ± 5.5 kg/m2), with IR evaluated by Homeostasis Model Assessment (HOMA)-index, comparing 4 treatments: hypocaloric diet alone (group A) or plus metformin 1000 mg/daily (group B), natural antioxidants-enriched hypocaloric diet alone (group C) or plus metformin (group D). A personalized program, with calculated antioxidant intake of 800-1000 mg/daily, from fruit and vegetables, was administered to group C and D. The glycemic and insulinemic response to oral glucose load, and concentrations of total-, LDL- and HDL-cholesterol, triglycerides, uric acid, C reactive protein, fT3, fT4, TSH, insulin-like growth factor 1 were evaluated before and after 3-months. Plasma Total antioxidant capacity was determined by H2O2-metmyoglobin system, which interacting with the chromogen ABTS generates a radical with latency time (LAG) proportional to antioxidant content. RESULTS: Despite a similar BMI decrease, we found a significant decrease of HOMA and insulin peak only in group B and D. Insulin response (AUC) showed the greatest decrease in group D (25.60 ± 8.96%) and was significantly lower in group D vs B. No differences were observed in glucose response, lipid metabolism and TAC (expressed as LAG values). TSH values were significantly suppressed in group D vs B. CONCLUSIONS: These data suggest that dietary antioxidants ameliorate insulin-sensitivity in obese subjects with IR by enhancing the effect of insulin-sensitizing drugs albeit with molecular mechanisms which remain yet to be elucidated.
BACKGROUND & AIMS:Oxidative stress (OS) could play a role in metabolic syndrome-related manifestations contributing to insulin resistance (IR). The aim of the present study was to gain insight the relationships between OS, IR and other hormones involved in caloric balance, explaining the effects of a natural antioxidant-enriched diet in patients affected by metabolic syndrome. METHODS: We investigated the effects of dietary antioxidants on IR, studying 53 obese (20 males and 33 females, 18-66 years old, BMI 36.3 ± 5.5 kg/m2), with IR evaluated by Homeostasis Model Assessment (HOMA)-index, comparing 4 treatments: hypocaloric diet alone (group A) or plus metformin 1000 mg/daily (group B), natural antioxidants-enriched hypocaloric diet alone (group C) or plus metformin (group D). A personalized program, with calculated antioxidant intake of 800-1000 mg/daily, from fruit and vegetables, was administered to group C and D. The glycemic and insulinemic response to oral glucose load, and concentrations of total-, LDL- and HDL-cholesterol, triglycerides, uric acid, C reactive protein, fT3, fT4, TSH, insulin-like growth factor 1 were evaluated before and after 3-months. Plasma Total antioxidant capacity was determined by H2O2-metmyoglobin system, which interacting with the chromogen ABTS generates a radical with latency time (LAG) proportional to antioxidant content. RESULTS: Despite a similar BMI decrease, we found a significant decrease of HOMA and insulin peak only in group B and D. Insulin response (AUC) showed the greatest decrease in group D (25.60 ± 8.96%) and was significantly lower in group D vs B. No differences were observed in glucose response, lipid metabolism and TAC (expressed as LAG values). TSH values were significantly suppressed in group D vs B. CONCLUSIONS: These data suggest that dietary antioxidants ameliorate insulin-sensitivity in obese subjects with IR by enhancing the effect of insulin-sensitizing drugs albeit with molecular mechanisms which remain yet to be elucidated.