In this preliminary cross-sectional study, high intake of saturated fats was negatively related to sperm concentration whereas higher intake of omega-3 fats was positively related to sperm morphology. Further, studies with larger samples are now required to confirm these findings.

Background Here, we aim to identify defects of apolipoprotein (apo) B lipoprotein metabolism that characterize hypertriglyceridemia, focusing on apoC-III and apoE. Methods and Results We studied the transport of plasma apoB within 21 distinct subfractions as separated by anti–apoC-III and anti–apoE immunoaffinity chromatography and ultracentrifugation in 9 patients with moderate hypertriglyceridemia and 12 normotriglyceridemic control subjects. Hypertriglyceridemia was characterized by a 3-fold higher liver secretion of very low-density lipoprotein (VLDL) that had apoC-III but not apoE and a 50% lower secretion of VLDL with both apoC-III and apoE (both P<0.05). This shift in VLDL secretion pattern from apoE to apoC-III resulted in significantly reduced clearance of light VLDL (−39%; P<0.05), compatible with the antagonizing effects of apoC-III on apoE-induced clearance of triglyceride-rich lipoproteins. In addition, rate constants for clearance were reduced for apoE-containing triglyceride-rich lipoproteins in hypertriglyceridemia, associated with increased apoC-III contents of these particles. LDL distribution shifted from light and medium LDL to dense LDL in hypertriglyceridemia through a quartet of kinetic perturbations: increased flux from apoC-III–containing triglyceride-rich lipoproteins, a shift in liver LDL secretion pattern from light to dense LDL, an increased conversion rate from light and medium LDL to dense LDL, and retarded catabolism of dense LDL. Conclusions These results support a central role for apoC-III in metabolic defects leading to hypertriglyceridemia. Triglyceride-rich lipoprotein metabolism shifts from an apoE-dominated system in normotriglyceridemic participants characterized by rapid clearance from circulation of VLDL to an apoC-III–dominated system in hypertriglyceridemic patients characterized by reduced clearance of triglyceride-rich lipoproteins and the formation of the dense LDL phenotype.

Objective-We aimed to clarify the influence of apolipoprotein C-III (apoCIII) on human apolipoprotein B metabolism. Methods and Results-We studied the kinetics of 4 very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL) types containing: (1) otherAposϪCIIIϪ: none of apoCIII, apoAII, apoCI, apoCII, or apoE; (2) otherAposϩCIIIϪ: no apoCIII but at least one of the others; (3) otherAposϪCIIIϩ: apoCIII, but not any others; and (4) otherAposϩCIIIϩ: apoCIII and at least one other. VLDL and IDL otherAposϪCIIIϩ and otherAposϪCIIIϪ had similar rates of lipolytic conversion to smaller particles. However, light LDL otherAposϪCIIIϩ compared with otherAposϪCIIIϪ had much faster conversion to dense LDL as did light LDL otherAposϩCIIIϩ compared with otherAposϩCIIIϪ. VLDL and IDL otherAposϪCIIIϩ had minimal direct removal from circulation, whereas VLDL and IDL otherAposϩCIIIϪ, rich in apoE, showed fast clearance. Lipoproteins in fraction otherAposϩCIIIϩ also rich in apoE had very low clearance. Conclusions-The results suggest that apoCIII strongly inhibits hepatic uptake of VLDL and IDL overriding the opposite influence of apoE when both are present. The presence of apoCIII on dense VLDL is not associated with slow conversion to IDL, a lipoprotein lipase-dependent process; but when on light LDL, apoCIII is associated with enhanced conversion to dense LDL, a process involving hepatic lipase. Key Words: Apolipoprotein B100 Ⅲ apolipoprotein CIII Ⅲ kinetics Ⅲ low-density lipoproteins Ⅲ metabolism A poCIII is a small apolipoprotein, synthesized mainly in the liver, which circulates in plasma associated with apoB containing lipoproteins and high-density lipoprotein. 1 In case-control studies with angiographic or clinical end points and prospective observational studies, plasma concentrations of lipoproteins with apoCIII are strong independent risk factors for cardiovascular disease. 1 Humans with genetic deficiency of apoCIII have lower triglyceride (TG) and low-density lipoprotein (LDL) cholesterol levels and reduced atherosclerosis. 2 The prevailing idea about the function of apoCIII is that it is an antagonist to apoCII and apoE, impairing intravascular lipolysis by lipoprotein lipase and liver clearance of apoB lipoproteins. This concept is supported by in vitro evidence showing that apoCIII noncompetitively inhibits lipoprotein lipase (LPL) 3,4 and by the markedly accelerated catabolism of triglyceride-rich lipoproteins (TRL) in human subjects with a genetic deficiency of apoCIII. 5 Also, apoCIII strongly inhibits the in vitro binding of apoB lipoproteins to the hepatic LDL receptor. 6 Nevertheless, kinetic studies in humans do not support the idea of apoCIII as a LPL inhibitor in vivo, because very-lowdensity lipoprotein (VLDL) with apoCIII show faster, not slower, lipolytic conversion rates to smaller lipoproteins than particles without it. 7 A great part of the complexity in elucidating the true effect of apoCIII in vivo stems from the fact that apoB lipoproteins with apo...

Background--High-density lipoproteins (HDL) are structurally and metabolically heterogeneous and subclasses with differential effects on coronary heart disease (CHD) might exist. Apolipoprotein (apo) C-III, a small proinflammatory protein that resides on the surface of lipoproteins, enhances the atherogenicity of VLDL and LDL particles, but little is known about the role apoC-III on HDL. We investigated whether the presence or absence of apoC-III differentiates HDL into subtypes with nonprotective or protective associations with risk of future CHD.

Background LDL that contains apolipoprotein C-III (apoC-III) comprises only 10 to 20% of plasma LDL, but has a markedly altered metabolism and proatherogenic effects on vascular cells. Methods and results We examined the association between plasma LDL with apoC-III and coronary heart disease (CHD) in 320 women and 419 men initially free of cardiovascular disease who developed a fatal or non-fatal myocardial infarction during 10 to 14 years of follow-up, and matched controls who remained free of CHD. Concentrations of LDL with apoC-III (measured as apoB in this fraction) were associated with risk of CHD in multivariable analysis that included the total cholesterol to HDL cholesterol ratio, LDL cholesterol, apolipoprotein B, triglycerides, or HDL cholesterol; and other risk factors. In all models, the relative risks for the top versus bottom quintile of LDL with apoC-III were greater than those for LDL without apoC-III. When included in the same multivariable adjusted model, the risk associated with LDL with apoC-III (relative risk for top versus bottom quintile 2.38, 95 percent confidence interval, 1.54 to 3.68; P for trend <0.001) was significantly greater than that associated with LDL without apoC-III (relative risk for top versus bottom quintile 1.25, 95 percent confidence interval, 0.76 to 2.05; P for trend=0.97), P for interaction <0.001. This divergence in association with CHD persisted even after adjustment for plasma triglycerides. Conclusions The risk of CHD contributed by LDL appeared to result to a large extent from LDL that contains apoC-III.

Objective A prevailing concept is that HDL is secreted into the systemic circulation as a small mainly discoidal particle; which expands progressively and becomes spherical by uptake and esterification of cellular cholesterol; and then contracts by cholesterol ester delivery to the liver, a process known as reverse cholesterol transport, thought to be impaired in people with low HDL cholesterol (HDLc). This metabolic framework has not been established in humans. Approach and results We studied the metabolism of apolipoproteinA-I in four standard HDL sizes by endogenous isotopic labeling in six overweight adults with low HDLc and in six adults with normal body weight with high plasma HDLc. Contrary to expectation, HDL was secreted into the circulation in its entire size distribution from very small to very large, similarly in both groups. Very small (prebeta) HDL comprised only 8% of total apoA-I secretion. Each HDL subfraction circulated mostly within its secreted size range for 1–4 days, and then was cleared. Enlargement of very small and medium to large and very large HDL, and generation of very small from medium HDL were minor metabolic pathways. Prebeta HDL was cleared slower whereas medium, large and very large HDL were cleared faster in the low HDLc group. Conclusions A new model is proposed from these results in which HDL is metabolized in plasma mainly within several discrete, stable sizes, across the common range of HDLc concentrations.

MUFA intake activates synthetic and rapid catabolic pathways for TRL metabolism that involve apo E and apo C-III and suppresses the metabolism of more slowly metabolized VLDLs and IDLs, which do not contain these apolipoproteins.

We measured the sperm fatty acid composition using gas chromatography in anonymized semen samples of 33 men undergoing infertility evaluation at an academic medical center. Trans fatty acids were present in human sperm and were inversely related to sperm concentration (r = − 0.44). Keywords fatty acids; diet; sperm; semen analysis; infertilityTrans fatty acids are unsaturated fatty acids with at least one double bond in the trans, instead of the physiologic cis, configuration. There are two sources of trans fats in the diet. Most are found in foods containing partially hydrogenated vegetable oils used in margarines and commercially prepared foods (1). Smaller amounts are found in meats and dairy products from ruminants (e.g. cattle, goats and sheep), as a result of bacterial action in the animal's rumen (1-2). Little is known about the reproductive health effects of trans fats. Their intake has been related to a higher risk of fetal loss (3) and infertility due to anovulation (4). In addition, rodent models have shown that trans fatty acid intake impairs spermatogenesis (5-7) but it is unknown whether the same relation exists in humans.We collected semen samples as part of a pilot study to determine the feasibility of measuring sperm fatty acid composition in large scale studies. Between September 2008 and February 2009 we collected 33 de-identified semen samples from the same number of men presenting for evaluation of infertility at the Massachusetts General Hospital (MGH) Fertility Center. Samples from men presenting for post-vasectomy semen analysis were not included. SemenCorresponding Author: Jorge E. Chavarro, MD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115, Phone: 617-432-4584, Fax: 617-432-2435, jchavarr@hsph.harvard.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. samples were produced on-site by masturbation into a sterile plastic specimen cup. Men were instructed to abstain from ejaculation for 48 hours before producing the semen sample. After collection, the sample was liquefied at 37ºC for 20 minutes before analysis. All semen samples were analyzed using Computer-Assisted Semen Analysis (CASA; Hamilton-Thorn Version 10HTM-IVOS) as previously described (8-9). Following the CASA assessment, study samples were chosen based on their sperm concentration value by over-selecting samples with concentrations below 20×10 6 sperm/mL in order to address the goals of the pilot study. Samples from azoospermic men were not included in the study. For each man we collected up to four 250μL aliquots in cryotubes f...