<i>Background</i>. Apolipoprotein (Apo) E plays a key role in the handling of lipoprotein particles with ApoE2 and ApoE4 frequently having opposite effects compared to ApoE3. Some individuals simultaneously carry both E2 and E4 alleles. The impact of the ApoE2/4 genotype on lipid concentrations and its consequences on health remain poorly documented.  <i>Objective</i>. This study compared the lipid profile between ApoE2/4 carriers and other ApoE genotypes in relation to the waist circumference.  <i>Methods</i>. Cholesterol, triglyceride (TG), and ApoB concentrations were measured among 2,680 Caucasians. Multivariate logistic regression models were used to estimate the contribution of ApoE2/4 to various dyslipidemic profiles associated with abdominal obesity.  <i>Results</i>. In presence of abdominal obesity, the lipid profile was as deteriorated in ApoE2/4 carriers as in carriers of other ApoE genotypes. There was a more pronounced effect on TG-rich lipoproteins, particularly in ApoE2/2 (a feature of type III dysbetalipoproteinemia), and non-high-density lipoprotein (HDL) cholesterol in ApoE4/4.  Compared to ApoE2/2, ApoE2/4 carriers presented lower very-low-density lipoprotein (VLDL) cholesterol concentrations and VLDL-cholesterol/TG ratios, with or without obesity, and higher low-density lipoprotein (LDL) cholesterol concentrations.  <i>Conclusion</i>. In presence of abdominal obesity, the influence of the ApoE2 allele could be less pronounced than that of ApoE4 among ApoE2/4 individuals.

Sylvia Villeneuve

Diane Brisson

Daniel Gaudet

Influence of Abdominal Obesity on the Lipid-Lipoprotein Profile in Apoprotein E2/4 Carriers: The Effect of an Apparent Duality

An anomaly in the plasma proteins of patients with multiple sclerosis detectable on SDS-PAGE has been reported. The molecular weight of the anomaly was the same as the phospholipid transfer protein. A metabolic protein was involved in lipid homeostasis and remodeling of the high density lipoproteins. We have identified the anomaly as the phospholipid  transfer protein by western blot using antiphospholipid transfer antibodies. Activity assays showed that the phospholipid transfer activity was elevated in fasted plasma samples from subjects with MS compared to controls. Sequence analysis of the gene encoding the phospholipid transfer protein did not identify any mutations in the genetic structure, suggesting that the increase in activity was not due to structural changes in the protein, but may be due to one of the other proteins with which it forms active complexes. Altered phospholipid transfer activity is important because it could be implicated in the decreased lipid uptake and abnormal myelin lipids observed in multiple sclerosis. It has been shown that alteration in myelin lipid content is an epitope for autoimmunity. Therefore, lipid changes due to a defect in phospholipid transfer and/or uptake could potentially influence the course of the disease.  Further research is needed to elucidate the role of the phospholipid transfer protein in subjects with multiple sclerosis.

Roy A. Garvin

Elevated Phospholipid Transfer Protein in Subjects with Multiple Sclerosis

Sphingolipids play a very crucial role in many diseases and are well-known as signaling mediators in many pathways. Sphingolipids are produced during the <i>de novo</i> process in the ER (endoplasmic reticulum) from the nonsphingolipid precursor and comprise both structural and bioactive lipids. Ceramide is the central core of the sphingolipid pathway, and its production has been observed following various treatments that can induce several different cellular effects including growth arrest, DNA damage, apoptosis, differentiation, and senescence. Ceramides are generally produced through the sphingomyelin hydrolysis and catalyzed by the enzyme sphingomyelinase (SMase) in mammals. Presently, there are many known SMases and they are categorized into three groups acid SMases (aSMases), alkaline SMases (alk-SMASES), and neutral SMases (nSMases). The yeast homolog of mammalians neutral SMases is inositol phosphosphingolipid phospholipase C. Yeasts generally have inositol phosphosphingolipids instead of sphingomyelin, which may act as a homolog of mammalian sphingomyelin. In this review, we shall explain the structure and function of inositol phosphosphingolipid phospholipase C1, its localization inside the cells, mechanisms, and its roles in various cell responses during replication stresses and diseases. This review will also give a new basis for our understanding for the mechanisms and nature of the inositol phosphosphingolipid phospholipase C1/nSMase.

Kaushlendra Tripathi

Role of Inositol Phosphosphingolipid Phospholipase C1, the Yeast Homolog of Neutral Sphingomyelinases in DNA Damage Response and Diseases

High-density lipoprotein (HDL) has protective effects against the development of atherosclerosis; these effects include reverse cholesterol transport, antioxidant ability, and anti-inflammation. Myeloperoxidase (MPO) secreted by macrophages in atherosclerotic lesions generates tyrosyl radicals in apolipoprotein A-I (apoA-I)  molecules, inducing the formation of apoA-I/apoA-II heterodimers through the tyrosine-tyrosine bond in HDL. Functional characterization of HDL oxidized by MPO could provide useful information about the significance of apoA-I/apoA-II heterodimers measurement. We investigated the effects of MPO-induced oxidation on the antiatherogenic functions of HDL as described above. The antioxidant ability of HDL, estimated as the effect on LDL oxidation induced by copper sulfate, was not significantly affected after MPO oxidation. HDL reduced THP-1 monocyte migration by suppressing the stimulation of human umbilical vein endothelial cells induced by lipopolysaccharide (LPS). MPO-oxidized HDL also showed inhibition of THP-1 chemotaxis, but the extent of inhibition was significantly attenuated compared to intact HDL. MPO treatment did not affect the cholesterol efflux capacity of HDL from [<sup>3</sup>H]-cholesterol-laden macrophages derived from THP-1 cells. The principal effect of MPO oxidation on the antiatherogenic potential of HDL would be the reduction of anti-inflammatory ability, suggesting that measurement of apoA-I/apoA-II heterodimers might be useful to estimate anti-inflammatory ability of HDL.

Takahiro Kameda

Ryunosuke Ohkawa

Kouji Yano

Yoko Usami

Akari Miyazaki

Kazuyuki Matsuda

Kenji Kawasaki

Mitsutoshi Sugano

Tetsuo Kubota

Minoru Tozuka

Effects of Myeloperoxidase-Induced Oxidation on Antiatherogenic Functions of High-Density Lipoprotein

Present review article highlights various cardiovascular risk prediction biomarkers by incorporating both traditional risk factors to be used as diagnostic markers and recent technologically generated diagnostic and therapeutic markers. This paper explains traditional biomarkers such as lipid profile, glucose, and hormone level and physiological biomarkers based on measurement of levels of important biomolecules such as serum ferritin, triglyceride to HDLp (high density lipoproteins) ratio, lipophorin-cholesterol ratio, lipid-lipophorin ratio, LDL cholesterol level, HDLp and apolipoprotein levels, lipophorins and LTPs ratio, sphingolipids, Omega-3 Index, and ST2 level. In addition, immunohistochemical, oxidative stress, inflammatory, anatomical, imaging, genetic, and therapeutic biomarkers have been explained in detail with their investigational specifications. Many of these biomarkers, alone or in combination, can play important role in prediction of risks, its types, and status of morbidity. As emerging risks are found to be affiliated with minor and microlevel factors and its diagnosis at an earlier stage could find CVD, hence, there is an urgent need of new more authentic, appropriate, and reliable diagnostic and therapeutic markers to confirm disease well in time to start the clinical aid to the patients. Present review aims to discuss new emerging biomarkers that could facilitate more authentic and fast diagnosis of CVDs, HF (heart failures), and various lipid abnormalities and disorders in the future.

Ravi Kant Upadhyay

Emerging Risk Biomarkers in Cardiovascular Diseases and Disorders

<i>Background</i>. The use of statins is essential for aggressive lipid-lowering treatment in acute coronary syndrome (ACS) patients with dyslipidemia. Recently, elevation of sitosterol, a lipid absorption marker, was reported to be associated with premature atherosclerosis. The purpose of the present study was to examine the impact of ezetimibe, a selective intestinal cholesterol transporter inhibitor, in ACS patients. <i>Methods</i>. A total of 197 ACS patients were randomized to pitavastatin + ezetimibe (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.2130003pt" id="M1" height="8.91176pt" version="1.1" viewBox="-0.0498162 -8.69876 42.0615 8.91176" width="42.0615pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><path id="g113-111" d="M495 86L479 114C446 82 419 66 409 66C401 66 401 72 406 97C420 166 436 231 453 297C489 435 454 448 428 448C406 448 384 439 354 422C305 394 222 327 161 247H159L183 345C200 415 194 448 173 448C143 448 82 410 23 351L38 325C64 349 95 371 105 371C111 371 116 365 109 336L25 -4L31 -12C50 -4 77 3 107 9C119 69 132 122 145 168C197 254 321 381 370 381C387 381 393 374 378 305L329 95C309 17 320 -12 345 -12C372 -12 430 19 495 86Z"/></g><g transform="matrix(.0135,0,0,-0.0135,10.586,0)"><path id="g117-34" d="M535 323V373H52V323H535ZM535 138V188H52V138H535Z"/></g><g transform="matrix(.0135,0,0,-0.0135,22.324,0)"><path id="g113-50" d="M384 0V27C293 34 287 42 287 114V635C232 613 172 594 109 583V559L157 557C201 555 205 550 205 499V114C205 42 199 34 109 27V0H384Z"/></g><g transform="matrix(.0135,0,0,-0.0135,28.827,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.0135,0,0,-0.0135,35.33,0)"><use xlink:href="#g113-49"/></g></svg>) or pitavastatin (<svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.2130003pt" id="M2" height="8.91176pt" version="1.1" viewBox="-0.0498162 -8.69876 35.534 8.91176" width="35.534pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><use xlink:href="#g113-111"/></g><g transform="matrix(.0135,0,0,-0.0135,10.586,0)"><use xlink:href="#g117-34"/></g><g transform="matrix(.0135,0,0,-0.0135,22.324,0)"><path id="g113-58" d="M244 635C114 635 38 519 38 422C38 317 111 240 217 240C236 240 255 244 277 256L345 292C311 140 203 39 59 15L64 -15C89 -15 150 -5 204 17C339 72 440 202 440 386C440 521 368 635 244 635ZM228 602C326 602 352 479 352 390C352 370 351 347 348 324C327 308 293 296 258 296C174 296 124 369 124 458C124 517 152 602 228 602Z"/></g><g transform="matrix(.0135,0,0,-0.0135,28.829,0)"><path id="g113-56" d="M447 623H65C61 580 56 530 47 475H76C100 541 106 550 172 550H388C308 376 196 170 91 -1L98 -12L172 -2C268 204 360 408 455 611L447 623Z"/></g></svg>). Low-density lipoprotein cholesterol (LDL-C) and sitosterol levels were evaluated on admission and after 12 weeks. <i>Results</i>. After 12 weeks, the pitavastatin + ezetimibe group showed a significantly greater decrease of sitosterol (baseline versus after 12 weeks; 2.9 &#xb1; 2.5 versus 1.7 &#xb1; 1.0&#x2009;ng/mL, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.6617603pt" id="M3" height="9.65971pt" version="1.1" viewBox="-0.0498162 -8.99795 53.2534 9.65971" width="53.2534pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><path id="g113-81" d="M600 480C600 590 528 650 384 650H143L137 622C222 614 225 607 210 531L130 127C113 41 106 36 23 28L17 0H294L300 28C204 36 195 42 212 127L243 284L314 263C327 263 339 263 352 264C465 271 600 337 600 480ZM508 481C508 351 402 304 329 304C289 304 265 311 250 317L295 559C302 594 310 606 323 611C335 616 350 619 367 619C455 619 508 573 508 481Z"/></g><g transform="matrix(.0135,0,0,-0.0135,12.15,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g><g transform="matrix(.0135,0,0,-0.0135,23.887,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,30.39,0)"><path id="g113-47" d="M113 -12C146 -12 170 11 170 46C170 78 146 103 114 103S58 78 58 46C58 11 82 -12 113 -12Z"/></g><g transform="matrix(.0135,0,0,-0.0135,33.48,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,39.983,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,46.486,0)"><use xlink:href="#g113-50"/></g></svg>) than the pitavastatin group (2.7 &#xb1; 1.5 versus 3.0 &#xb1; 1.4&#x2009;ng/mL). The baseline sitosterol level was significantly higher in patients with achieved LDL-C levels &#x2265; 70&#x2009;mg/dL than in patients with levels &#x3c; 70&#x2009;mg/dL (3.2 &#xb1; 2.5 versus 2.4 &#xb1; 1.3&#x2009;ng/mL, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-0.2129908pt" id="M4" height="9.21094pt" version="1.1" viewBox="-0.0498162 -8.99795 53.2534 9.21094" width="53.2534pt"><g transform="matrix(.0135,0,0,-0.0135,0,0)"><use xlink:href="#g113-81"/></g><g transform="matrix(.0135,0,0,-0.0135,12.15,0)"><use xlink:href="#g117-34"/></g><g transform="matrix(.0135,0,0,-0.0135,23.887,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,30.39,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.0135,0,0,-0.0135,33.48,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,39.983,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.0135,0,0,-0.0135,46.486,0)"><path id="g113-55" d="M137 343C167 482 260 545 321 574C357 591 397 603 429 609L423 641C382 634 335 622 295 608C189 570 37 457 37 238C37 84 125 -12 242 -12C362 -12 447 89 447 209C447 311 374 393 267 393C247 393 226 386 204 376L137 343ZM227 337C318 337 361 256 361 173C361 105 336 22 258 22C176 22 126 120 126 240C126 266 127 291 132 310C155 323 189 337 227 337Z"/></g></svg>). <i>Conclusions</i>. Ezetimibe plus statin therapy in ACS patients with dyslipidemia decreased LDL-C and sitosterol levels more than statin therapy solo. Sitosterol Elevation was a predictor of poor response to aggressive lipid-lowering treatment in ACS patients.

Erisa Watanabe

Junichi Yamaguchi

Hiroyuki Arashi

Hiroshi Ogawa

Nobuhisa Hagiwara

Effects of Statin versus the Combination of Ezetimibe plus Statin on Serum Lipid Absorption Markers in Patients with Acute Coronary Syndrome

Diabetes, obesity, and metabolic syndrome are becoming epidemic both in developed and developing countries in recent years. Complementary and alternative medicines have been used since ancient era for the treatment of diabetes and cardiovascular diseases. Bitter melon is widely used as vegetables in daily food in Bangladesh and several other countries in Asia. The fruits extract of bitter melon showed strong antioxidant and hypoglycemic activities in experimental condition both <i>in vivo</i> and <i>in vitro</i>. Recent scientific evaluation of this plant extracts also showed potential therapeutic benefit in diabetes and obesity related metabolic dysfunction in experimental animals and clinical studies. These beneficial effects are mediated probably by inducing lipid and fat metabolizing gene expression and increasing the function of AMPK and PPARs, and so forth. This review will thus focus on the recent findings on beneficial effect of <i>Momordica charantia</i> extracts on metabolic syndrome and discuss its potential mechanism of actions.

Md Ashraful Alam

Riaz Uddin

Nusrat Subhan

Md Mahbubur Rahman

Preeti Jain

Hasan Mahmud Reza

Beneficial Role of Bitter Melon Supplementation in Obesity and Related Complications in Metabolic Syndrome

About this journal

<p><em>Journal of Lipids</em> provides a forum for scientists, physicians, and nutritionists working in all aspects of lipids research. Topics covered include their biochemistry, synthesis, function in health and disease, and nutrition.</p>


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<p><em>Journal of Lipids</em> maintains an Editorial Board of practicing researchers from around the world, to ensure manuscripts are handled by editors who are experts in the field of study.</p>


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Journal of Lipids - Table of contents 2015

title

Journal of Lipids provides a forum for scientists, physicians, and nutritionists working in all aspects of lipids research. Topics covered include their biochemistry, synthesis, function in health and disease, and nutrition.

Journal of Lipids