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Montalto, Giuseppe

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  • Montalto, Giuseppe (5)
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Author's Bibliography

Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study

Rizzo, Manfredi; Abate, Nicola; Chandalia, Manisha; Rizvi, Ali A.; Giglio, Rosaria V.; Nikolić, Dragana; Gammazza, Antonella Marino; Barbagallo, Ignazio; Isenović, Esma R.; Banach, Maciej; Montalto, Giuseppe; Volti, Giovanni Li

(2015)

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Abate, Nicola
AU  - Chandalia, Manisha
AU  - Rizvi, Ali A.
AU  - Giglio, Rosaria V.
AU  - Nikolić, Dragana
AU  - Gammazza, Antonella Marino
AU  - Barbagallo, Ignazio
AU  - Isenović, Esma R.
AU  - Banach, Maciej
AU  - Montalto, Giuseppe
AU  - Volti, Giovanni Li
PY  - 2015
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/508
AB  - Context: Liraglutide is a glucagon-like peptide-1 analog and glucose-lowering agent whose effects on cardiovascular risk markers have not been fully elucidated. Objective: We evaluated the effect of liraglutide on markers of oxidative stress, heme oxygenase-1 (HO-1), and plasma ghrelin levels in patients with type-2 diabetes mellitus (T2DM). Design and Setting: A prospective pilot study of 2 months duration has been performed at the Unit of Diabetes and Cardiovascular Prevention at University of Palermo, Italy. Patients and Intervention(s): Twenty subjects with T2DM (10 men and 10 women; meanage: 57 +/- 13 y) were treated with liraglutide sc (0.6 mg/d for 2 wk, followed by 1.2 mg/d) in addition to metformin (1500 mg/d orally) for 2 months. Patients with liver disorders or renal failure were excluded. Main Outcome Measure(s): Plasma ghrelin concentrations, oxidative stress markers, and heat-shock proteins, including HO-1 were assessed. Results: The addition of liraglutide resulted in a significant decrease in glycated hemoglobin (HbA1c) (8.5 +/- 0.4 vs 7.5 +/- 0.4%, P LT .0001). In addition, plasma ghrelin and glutathione concentrations increased (8.2 +/- 4.1 vs 13.6 +/- 7.3 pg/ml, P = .0007 and 0.36 +/- 0.06 vs 0.44 +/- 0.07 nmol/ml, P = .0002, respectively), whereas serum lipid hydroperoxides and HO-1 decreased (0.11 +/- 0.05 vs 0.04 +/- 0.07 pg/ml, P = .0487 and 7.7 +/- 7.7 vs 3.6 +/- 1.8 pg/ml, P = .0445, respectively). These changes were not correlated with changes in fasting glycemia or HbA1c. Conclusions: In a 2-months prospective pilot study, the addition of liraglutide to metformin resulted in improvement in oxidative stress as well as plasma ghrelin and HO-1 concentrations in patients with T2DM. These findings seemed to be independent of the known effects of liraglutide on glucose metabolism.
T2  - Journal of Clinical Endocrinology and Metabolism
T1  - Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study
VL  - 100
IS  - 2
SP  - 603
EP  - 606
DO  - 10.1210/jc.2014-2291
ER  - 
@article{
author = "Rizzo, Manfredi and Abate, Nicola and Chandalia, Manisha and Rizvi, Ali A. and Giglio, Rosaria V. and Nikolić, Dragana and Gammazza, Antonella Marino and Barbagallo, Ignazio and Isenović, Esma R. and Banach, Maciej and Montalto, Giuseppe and Volti, Giovanni Li",
year = "2015",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/508",
abstract = "Context: Liraglutide is a glucagon-like peptide-1 analog and glucose-lowering agent whose effects on cardiovascular risk markers have not been fully elucidated. Objective: We evaluated the effect of liraglutide on markers of oxidative stress, heme oxygenase-1 (HO-1), and plasma ghrelin levels in patients with type-2 diabetes mellitus (T2DM). Design and Setting: A prospective pilot study of 2 months duration has been performed at the Unit of Diabetes and Cardiovascular Prevention at University of Palermo, Italy. Patients and Intervention(s): Twenty subjects with T2DM (10 men and 10 women; meanage: 57 +/- 13 y) were treated with liraglutide sc (0.6 mg/d for 2 wk, followed by 1.2 mg/d) in addition to metformin (1500 mg/d orally) for 2 months. Patients with liver disorders or renal failure were excluded. Main Outcome Measure(s): Plasma ghrelin concentrations, oxidative stress markers, and heat-shock proteins, including HO-1 were assessed. Results: The addition of liraglutide resulted in a significant decrease in glycated hemoglobin (HbA1c) (8.5 +/- 0.4 vs 7.5 +/- 0.4%, P LT .0001). In addition, plasma ghrelin and glutathione concentrations increased (8.2 +/- 4.1 vs 13.6 +/- 7.3 pg/ml, P = .0007 and 0.36 +/- 0.06 vs 0.44 +/- 0.07 nmol/ml, P = .0002, respectively), whereas serum lipid hydroperoxides and HO-1 decreased (0.11 +/- 0.05 vs 0.04 +/- 0.07 pg/ml, P = .0487 and 7.7 +/- 7.7 vs 3.6 +/- 1.8 pg/ml, P = .0445, respectively). These changes were not correlated with changes in fasting glycemia or HbA1c. Conclusions: In a 2-months prospective pilot study, the addition of liraglutide to metformin resulted in improvement in oxidative stress as well as plasma ghrelin and HO-1 concentrations in patients with T2DM. These findings seemed to be independent of the known effects of liraglutide on glucose metabolism.",
journal = "Journal of Clinical Endocrinology and Metabolism",
title = "Liraglutide Reduces Oxidative Stress And Restores Heme Oxygenase-1 and Ghrelin Levels in Patients with Type 2 Diabetes: A Prospective Pilot Study",
volume = "100",
number = "2",
pages = "603-606",
doi = "10.1210/jc.2014-2291"
}
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59

Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome

Rizzo, Manfredi; Obradović, Milan M.; Labudović-Borović, Milica; Nikolić, Dragana; Montalto, Giuseppe; Rizvi, Ali A.; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2014)

TY  - JOUR
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Labudović-Borović, Milica
AU  - Nikolić, Dragana
AU  - Montalto, Giuseppe
AU  - Rizvi, Ali A.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2014
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/290
AB  - In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
T2  - Current Vascular Pharmacology
T1  - Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome
VL  - 12
IS  - 4
SP  - 572
EP  - 585
DO  - 10.2174/1570161111999131205160756
ER  - 
@article{
author = "Rizzo, Manfredi and Obradović, Milan M. and Labudović-Borović, Milica and Nikolić, Dragana and Montalto, Giuseppe and Rizvi, Ali A. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2014",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/290",
abstract = "In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.",
journal = "Current Vascular Pharmacology",
title = "Uric Acid Metabolism in Pre-hypertension and the Metabolic Syndrome",
volume = "12",
number = "4",
pages = "572-585",
doi = "10.2174/1570161111999131205160756"
}
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Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches

Nikolić, Dragana; Katsiki, Niki; Montalto, Giuseppe; Isenović, Esma R.; Mikhailidis, Dimitri P.; Rizzo, Manfredi

(2013)

@article{
author = "Nikolić, Dragana and Katsiki, Niki and Montalto, Giuseppe and Isenović, Esma R. and Mikhailidis, Dimitri P. and Rizzo, Manfredi",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5380",
abstract = "Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk.",
journal = "Nutrients",
title = "Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches",
volume = "5",
number = "3",
pages = "928-948",
doi = "10.3390/nu5030928"
}
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93
95

PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?

Banach, Maciej; Rizzo, Manfredi; Obradović, Milan M.; Montalto, Giuseppe; Rysz, Jacek; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2013)

TY  - JOUR
AU  - Banach, Maciej
AU  - Rizzo, Manfredi
AU  - Obradović, Milan M.
AU  - Montalto, Giuseppe
AU  - Rysz, Jacek
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2013
UR  - http://vinar.vin.bg.ac.rs/handle/123456789/5502
AB  - Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.
T2  - Current Pharmaceutical Design
T1  - PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?
VL  - 19
IS  - 21
SP  - 3869
EP  - 3877
DO  - 10.2174/13816128113199990303
ER  - 
@article{
author = "Banach, Maciej and Rizzo, Manfredi and Obradović, Milan M. and Montalto, Giuseppe and Rysz, Jacek and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5502",
abstract = "Plasma low-density lipoprotein cholesterol (LDL-C) is one of the biomarkers of cardiovascular disease (CVD) risk. LDL is cleared from the circulation preferentially through the LDL receptor (LDLR) pathway. Proprotein convertase subtilisin/kexin 9 (PCSK9) promotes the degradation of the LDLR. PCSK9 inhibition is attractive as a new strategy for lowering LDL-C levels, especially in combination with lipid lowering drugs such as statins. We review data from the available studies which focus on PCSK9 as a potential target in the treatment of hyperlipidemia. Further studies are still necessary to investigate the potential underlying mechanisms involved.",
journal = "Current Pharmaceutical Design",
title = "PCSK9 Inhibition - A Novel Mechanism to Treat Lipid Disorders?",
volume = "19",
number = "21",
pages = "3869-3877",
doi = "10.2174/13816128113199990303"
}
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37
39

A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin

Rizzo, Manfredi; Rizvi, Ali A.; Sudar, Emina; Soskić, Sanja S.; Obradović, Milan M.; Montalto, Giuseppe; Boutjdir, Mohamed; Mikhailidis, Dimitri P.; Isenović, Esma R.

(2013)

@article{
author = "Rizzo, Manfredi and Rizvi, Ali A. and Sudar, Emina and Soskić, Sanja S. and Obradović, Milan M. and Montalto, Giuseppe and Boutjdir, Mohamed and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2013",
url = "http://vinar.vin.bg.ac.rs/handle/123456789/5565",
abstract = "Ghrelin is a peptide hormone produced mainly in the stomach that has widespread tissue distribution and diverse hormonal, metabolic and cardiovascular activities. The circulating ghrelin concentration increases during fasting and decreases after food intake. Ghrelin secretion may thus be initiated by food intake and is possibly controlled by nutritional factors. Lean subjects have increased levels of circulating ghrelin compared with obese subjects. Recent reports show that low plasma ghrelin is associated with elevated fasting insulin levels, insulin resistance and type 2 diabetes mellitus. Factors involved in the regulation of ghrelin secretion have not yet been defined; however, it is assumed that blood glucose levels represent a significant regulator. Recent evidence indicates that ghrelin can increase myocardial contractility, enhance vasodilatation, and has protective effect from myocardial damage. It has been shown that ghrelin may improve cardiac function through growth hormone (GH)-dependent mechanisms but there is also evidence to suggest that ghrelins cardioprotective activity is independent of GH. Recent data demonstrate that ghrelin can influence key events in atherogenesis. Thus, ghrelin may be a new target for the treatment of some cardiovascular diseases. In this review, we consider the current literature focusing on ghrelin as a potential antiatherogenic agent in the treatment of various pathophysiological conditions.",
journal = "Current Pharmaceutical Design",
title = "A Review of the Cardiovascular and Anti-Atherogenic Effects of Ghrelin",
volume = "19",
number = "27",
pages = "4953-4963",
doi = "10.2174/1381612811319270018"
}
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