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Nicotinic acid: Do we know how it works after 55 years of clinical experience?

World Journal of Pharmacology 2012年第3期1卷 50-54页

作者： anastazia kei Moses S Elisaf Department of Internal Medicine School of Medicine University of Ioannina 45110 Ioannina Greece

Nicotinic acid （NA） comprises the oldest hypolipidemic drug, in use since 1955. Despite its established broad spectrum effect on lipid profle and the associated re-duction in cardiovascular morbidity and mortality, the mechanisms by which NA achieves its benefcial effects remain elusive. Regarding the NA-associated reduction in triglyceride and low density lipoprotein cholesterol levels, data are controversial. The prevailing view which suggested that NA inhibits lipolysis and decreases free fatty acid （FFA） release both via activation of adipose tissue G-protein receptor-109A （GPR109A） and via inhibition of hepatic triglyceride synthesis is currently debated by the observation that the initially decreased FFA levels rebound during long-term NA treatment even though the benefcial NA effects on lipid metabo-lism are preserved, while other mechanisms involving modulation of transcription and translation pathways are emerging. In addition, NA has been demonstrated to affect high density lipoprotein （HDL） particles remod-eling in a number of ways, including reducing choles-terol ester transfer protein levels and activity, increas-ing apolipoprotein A-I levels, eliminating HDL hepatic uptake, increasing cholesterol efflux via ATP-binding cassette A1, inhibiting hepatic lipase, thereby overall in-creasing the plasma residence time of HDL and apoA-I with retention of cholesterol esters in HDL. Focus of this article is to present the mechanisms by which NA exerts its broad spectrum hypolipidemic actions.

关键词： Dyslipidemia Nicotinic acid Niacin Mechanisms GPR109A Free fatty acids

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Current role of fenofibrate in the prevention and management of non-alcoholic fatty liver disease

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World Journal of Hepatology 2013年第9期5卷 470-478页

作者： Michael S Kostapanos anastazia kei Moses S Elisaf Department of Internal Medicine School of MedicineUniversity of Ioannina45110 IoanninaGreece

Non-alcoholic fatty liver disease(NAFLD) is a common health problem with a high mortality burden due to its liver- and vascular-specific complications. It is associated with obesity, high-fat diet as well as with type 2 diabetes mellitus(T2DM) and metabolic syndrome(MetS).Impaired hepatic fatty acid(FA) turnover together with insulin resistance are key players in NAFLD pathogenesis. Peroxisome proliferator-activated receptors(PPARs)are involved in lipid and glucose metabolic *** novel concept is that the activation of the PPARαsubunit may protect from liver steatosis. Fenofibrate, by activating PPARα, effectively improves the atherogenic lipid profile associated with T2DM and MetS. Experimental evidence suggested various protective effects of the drug against liver steatosis. Namely, fenofibraterelated PPARα activation may enhance the expression of genes promoting hepatic FA β-oxidation. Furthermore, fenofibrate reduces hepatic insulin resistance. It also inhibits the expression of inflammatory mediators involved in non-alcoholic steatohepatitis *** include tumor necrosis factor-α, intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1and monocyte chemoattractant protein-1. Consequently, fenofibrate can limit hepatic macrophage infiltration. Other liver-protective effects include decreased oxidative stress and improved liver microvasculature function. Experimental studies showed that fenofibrate can limit liver steatosis associated with high-fat diet,T2DM and obesity-related insulin resistance. Few studies showed that these benefits are also relevant even in the clinical setting. However, these have certain limitations. Namely, these were uncontrolled, their sample size was small, fenofibrate was used as a part of multifactorial approach, while histological data were *** this context, there is a need for large prospective studies, including proper control groups and full assessment of liver histology.

关键词： Fenofibrate Non-alcoholic fatty liver disease Steatohepatitis Peroxisome proliferator-activated receptors

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Dysbetalipoproteinemia: Two cases report and a diagnostic algorithm

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World Journal of Clinical Cases 2015年第4期3卷 371-376页

作者： anastazia kei Moses Elisaf George Miltiadous Marilena Hadjivassiliou Marios Cariolou Eleni Bairaktari Department of Internal Medicine University of Ioannina Medical School Department of Cardiovascular Genetics and the Laboratory of Forensic Genetics Cyprus Institute of Neurology and Genetics Department of Biochemistry University of Ioannina Medical School

Dysbetalipoproteinemia is a rare familial dyslipidemia characterized by approximately equally elevated serum cholesterol and triglyceride levels due to accumulated remnant lipoproteins in apolipoprotein E2/E2 *** is associated with an increased risk for premature cardiovascular disease. Thus, making a diagnosis of dysbetalipoproteinemia aids in assessing cardiovascular risk correctly and allows for genetic counseling. However, the diagnostic work-up can be challenging. Diagnosis of dysbetalipoproteinemia should be considered in patients mixed dyslipidemia when the apolipoprotein B concentration is relatively low in relation to the total cholesterol concentration or when there is significant disparity between the calculated low density lipoprotein(LDL) and directly measured LDL cholesterol concentrations. Other indices are also informative in the diagnostic process. We present herein two phenotypically different cases(a 44-year-old man with severe hypertriglyceridemia and a 49-year-old woman with mixed dyslipidemia) of genotypically proven familial dysbetalipoproteinemia and a diagnostic algorithm of the disease.

关键词： Dysbetalipoproteinemia Chylomicronemia Hyperlipoproteinemia typeⅢ Hypertriglyceridemia

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Effect of hypolipidemic treatment on glycemic profile in patients with mixed dyslipidemia

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World Journal of Diabetes 2013年第6期4卷 365-371页

作者： anastazia kei Evangelos Liberopoulos Moses Elisaf Department of Internal Medicine University of Ioannina Medical School

AIM:To assess the effect of different hypolipidemic treatment strategies on glycemic profile in mixed dyslipidemia ***:This is a prespecified analysis of a prospective,randomized,open-label,blinded end point(PROBE)study(*** identifier:NCT01010516).Patients(n=100)with mixed dyslipidemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin(40 mg/d)or to add-on-statin extended release nicotinic acid(ER-NA)/laropiprant(LRPT)or to addon-statin micronised fenofibrate for a total of 3 *** plasma glucose(FPG),glycosylated hemoglobin(HbA1c),homeostasis model assessment of insulin resistance(HOMA-IR)index and lipid profile were evaluated at baseline and 3 mo after treatment ***:FPG increased in add-on ER-NA/LRPT and rosuvastatin monotherapy groups by 9.7%and 4.4%,respectively(P<0.01 between the 2 groups and compared with baseline),while it did not significantly change in the add-on fenofibrate ***,HbA1c increased by 0.3%in add-on ER-NA/LRPT group and by 0.2%in the rosuvastatin monotherapy group(P<0.01 for all comparisons vs baseline and for the comparison between the 2 groups),while no significant change was reported in the add-on fenofibrate ***-IR increased by 65%in add-on ER-NA/LRPT and by 14%in rosuvastatin monotherapy group,while it decreased by 6%in the add-on fenofibrate group(P<0.01 vs baseline and for all comparisons among the groups).Non-HDL-C decreased in all groups(by 237%,247%and 7%in the rosuvastatin,ER-NA/LRPT and fenofibrate group,respectively,P<0.01 for all vs baseline and P<0.01 for all vs with fenofibrate group).CONCLUSION:Both addition of ER-NA/LRPT and switch to the highest dose of rosuvastatin deteriorated glycemic profile in patients with mixed dyslipidemia,while add-on fenofibrate seems to increase insulin sensitivity.

关键词： Diabetes mellitus Fasting plasma glucose Fenofibrate Insulin Nicotinic acid/laropiprant Rosuvastatin

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