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Nibali L.,University College London | Tatarakis N.,University College London | Needleman I.,University College London | Tu Y.-K.,National Taiwan University | And 4 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2013

Background: Several epidemiological studies have reported an association between metabolic syndrome (MetS) and periodontal diseases (PDs). The aim of this systematic review was to investigate the existence and magnitude of this association. Materials and Methods: A systematic search of the literature was conducted looking for casecontrol, cross-sectional, cohort studies and population surveys including patients with measures of MetS and PD. Ovid MEDLINE, EMBASE, LILACS, and Cochrane library databases were used for the search by 2 independent reviewers. A meta-analysis was conducted to investigate the association for coexistence of MetS and PD. Results: A total of 20 studies were included in the review, from an initial search of 3486 titles. Only 1 study reported longitudinal data on the onset of MetS components in association with periodontal measures. However, several studies investigated coexistence. A random effects meta-analysis showed that the presence of MetS is associated with the presence of periodontitis in a total of 36 337 subjects (odds ratio=1.71;95%confidence interval=1.42 to 2.03). When only studies with "secure" diagnoses wereincluded (n=16 405), themagnitudeof association increased (odds ratio=2.09;95%confidence interval = 1.28 to 3.44). Moderate heterogeneity was detected (I2 = 53.6%; P = .004). Conclusions: This review presents clear evidence for an association between MetS and periodontitis. The direction of the association and factors influencing it should be investigated by longitudinal and treatment studies. Periodontal diagnostic procedures should be routinely carried out in MetS patients. Copyright © 2013 by The Endocrine Society. Source

Nikolic D.,University of Palermo | Mikhailidis D.P.,University College London | Davidson M.H.,University of Chicago | Rizzo M.,University of Palermo | And 2 more authors.
Atherosclerosis | Year: 2014

ETC-1002 is a new investigational low density lipoprotein cholesterol (LDL-C)-lowering agent (Esperion Therapeutics, Inc.). ETC-1002 is a dicarboxylic acid derivative with a novel mechanism of action targeting two hepatic enzymes - adenosine triphosphate-citrate lyase (ACL) and adenosine monophosphate-activated protein kinase (AMPK), inhibiting sterol and fatty acid synthesis and promoting mitochondrial long-chain fatty acid oxidation. This agent is currently in phase II clinical research. Available data report that ETC-1002 significantly decreased LDL-C levels (up to 32%) in both patients with normal and elevated baseline levels of triglycerides. Such beneficial effect is superior to currently approved non-statin lipid lowering agents. The levels of apolipoprotein B (apoB) and non-high density lipoprotein cholesterol (non-HDL-C) were also reduced with beneficial effect on other cardiometabolic factors such as inflammatory markers, blood pressure and body weight. Although, the safety and tolerability of ETC-1002 needs to be confirmed in ongoing and future, larger studies, this agent has, so far, been generally safe and well tolerated. This novel, oral, once-daily, small molecule may lead to effective LDL-C lowering treatment in hypercholesterolaemic subjects who are statin intolerant or as add-on therapy in those who are unable to reach the LDL-C goals despite being on statin therapy. This agent might not only exert lipid-lowering related benefits, but also favourable cardiometabolic effects. © 2014 Elsevier Ireland Ltd. Source

Banerjee Y.,Sultan Qaboos University | Santos R.D.,University of Sao Paulo | Al-Rasadi K.,Sultan Qaboos University | Rizzo M.,University of Palermo | Rizzo M.,Euro Mediterranean Institute of Science and Technology
Atherosclerosis | Year: 2016

Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) regulates the expression of low-density lipoprotein (LDL)-receptors, through reducing their recycling by binding to the receptor along with LDL and targeting it for lysosomal destruction. PCSK9 also enhances the degradation of very-low-density-lipoprotein receptor (VLDLR) and lipoprotein receptor-related protein 1 (LRP-1) in a LDL-receptor independent manner. This role in lipid homeostasis presents PCSK9 as an attractive target for the therapeutic management of familial hypercholesterolemia as well as other refractory dyslipidaemias. However, PCSK9 mediates multifarious functions independent of its role in lipid homeostasis, which can be grouped under "pleiotropic functions" of the protein. This includes PCSK9's role in: trafficking of epithelial sodium channel; hepatic regeneration; pancreatic integrity and glucose homeostasis; antiviral activity; antimalarial activity; regulation of different cell signalling pathways; cortical neural differentiation; neuronal apoptosis and Alzheimer's disease. The question that needs to be investigated in depth is "How will the pleotropic functions of PCSK9, be affected by the therapeutic intervention of the protease's LDL-receptor lowering activity?" In this review, we appraise the different lipid lowering strategies targeting PCSK9 in light of the protein's different pleiotropic functions. Additionally, we delineate the key areas that require further examination, to ensure the long-term safety of the above lipid-lowering strategies. © 2016 Elsevier Ireland Ltd. Source

Rizzo M.,University of Palermo | Rizzo M.,Euro Mediterranean Institute of Science and Technology | Rizzo M.,University of South Carolina | Chandalia M.,University of Texas Medical Branch | And 5 more authors.
Cardiovascular Diabetology | Year: 2014

Background: Liraglutide, a long-acting glucagon-like peptide-1 (GLP-1) analog, has several non- glycemic properties, but its effect on carotid intima-media thickness (IMT), a recognized marker of subclinical atherosclerosis, is still unknown.Methods: A prospective study of 8 months duration in 64 patients with type-2 diabetes and no prior history of coronary artery disease evaluated whether adding liraglutide to metformin affects carotid IMT, measured by color doppler ultrasound.Results: After 8 months, fasting glucose decreased by 2.1 mmol/l and HbA1c by 1.9% (p < 0.01 for all). Liraglutide reduced total-cholesterol and triglycerides by 10%, and LDL-cholesterol by 19%, whereas HDL-cholesterol increased by 18% (p < 0.01 for all lipid changes). Carotid IMT decreased from 1.19 ± 0.47 to 0.94 ± 0.21 mm (p < 0.01). Yet, changes in carotid IMT did not correlate with changes in any other variable studied.Conclusions: Liraglutide decreases carotid IMT after 8 months treatment independently of its effect on plasma glucose and lipids concentrations.Trial registration: ClinicalTrials.gov: NCT01715428. © 2014 Rizzo et al.; licensee BioMed Central Ltd. Source

Tevy M.F.,Barcelona Institute for Research in Biomedicine | Giebultowicz J.,Oregon State University | Pincus Z.,Yale University | Mazzoccoli G.,IRCCS Scientific Institute and Regional General Hospital Casa Sollievo della Sofferenza | And 2 more authors.
Trends in Endocrinology and Metabolism | Year: 2013

The circadian clock machinery orchestrates organism metabolism to ensure that development, survival, and reproduction are attuned to diurnal environmental variations. For unknown reasons, there is a decline in circadian rhythms with age, concomitant with declines in the overall metabolic tissue homeostasis and changes in the feeding behavior of aged organisms. This disruption of the relationship between the clock and the nutrient-sensing networks might underlie age-related diseases; overall, greater knowledge of the molecular mediators of and variations in clock networks during lifespan may shed light on the aging process and how it may be delayed. In this review we address the complex links between the circadian clock, metabolic (dys)functions, and aging in different model organisms. © 2012 Elsevier Ltd. Source

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