Plasma and Mucosal Fatty Acid Pattern in Colectomized Ulcerative Colitis Patients

Patients with inflammatory bowel disease (IBD)have increased plasma n3 polyunsaturated fatty acids(PUFAs), which in ulcerative colitis (UC) patientspersists six months after colectomy, suggesting aprimary abnormality in fatty acid (FA) metabolism inIBD. This finding needed to be confirmed in a largerseries of UC long-term colectomized patients. We aimedto assess the plasma FA pattern in UC colectomized patients with either Brooke's ileostomy (UC-BI)or ileal pouch anal anastomosis (UC-IPAA) and themucosal FA pattern in the ileal reservoir of the UC-IPAApatients. Plasma FAs were assessed in 63 UC colectomized patients (31 with BI and 32 with IPAA) and 30controls. In 26 UC-IPAA (8 with pouchitis and 18 withoutpouchitis) and in 13 healthy controls gut mucosal FAswere also investigated. FAs were detected by capillary column gas-liquid chromatography.Increased levels of saturated fatty acids (SFAs) anddecreased percentages of monounsaturated fatty acids(MUFAs) were observed in both groups of patients. There were no changes in plasma n3 and n6 PUFAs. Themucosal FA pattern of the ileal reservoir consisted ofincreased long-chain PUFAs, specially n6 PUFA, and adecrease of their essential precursors. High percentages of SFAs and low percentages of MUFAs were alsoseen. The plasma FA profile previously described in IBDis not observed long-term after colectomy in UC,suggesting that it is related with the presence of inflamed intestine. High concentrations of SFAsand decreased percentages of MUFAs might represent earlyevents in disturbed FA metabolism in IBD. The changes inFAs of the ileal reservoir, which closely resemble those found in human and experimentalIBD, probably represent a common pattern of intestinalinflammation.     

Relationship of dietary fat and serum cholesterol ester and phospholipid fatty acids to markers of insulin resistance in men and women with a range of glucose tolerance

High-fat diets are associated with insulin resistance, however, this effect may vary depending on the type of fat consumed. The purpose of this study was to determine the relationship between intakes of specific dietary fatty acids (assessed by 3-day diet records and fatty acid composition of serum cholesterol esters [CEs] and phospholipids [PLs]) and glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Nineteen men and 19 women completed the study. Nine subjects had type 2 diabetes or impaired glucose tolerance. Fasting insulin correlated with reported intakes of total fat (r = .50, P < .01), monounsaturated fat (r = .44, P < .01), and saturated fat (r = .49, P < .01), but not with trans fatty acid intake (r = .11, not significant [NS]). Fasting glucose also correlated with total (r = .39, P < .05) and monounsaturated fat intakes (r = .37, P < .05). In multivariate analysis, both total and saturated fat intake were strong single predictors of fasting insulin (R2 approximately .25), and a model combining dietary and anthropometric measures accounted for 47% of the variance in fasting insulin. Significant relationships were observed between fasting insulin and the serum CE enrichments of myristic (C14:0), palmitoleic (C16:1), and dihomo-gamma-linolenic (C20:3n-6) acids. In multivariate analysis, a model containing CE 14:0 and percent body fat explained 45% of the variance in fasting insulin, and C14:0 and age explained 30% of the variance in fasting glucose. PL C20:3n-6 explained 30% of the variance in fasting insulin, and a model including PL C18:1n-11 cis, C20:3n-6, age and body fat had an R2 of .58. In conclusion, self-reported intake of saturated and monounsaturated fats, but not trans fatty acids, are associated with markers of insulin resistance. Furthermore, enhancement of dihomo-gamma-linolenic and myristic acids in serum CE and PL, presumably markers for dietary intake, predicted insulin resistance.     

Diet,fatty acids,and regulation of genes important for heart disease

Diets rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs), such as alpha-linoleic acid, eicosapentaenoic acid, and docosahexaenoic acid, are associated with decreased incidence and severity of coronary heart disease. Similarly, conjugated linoleic acids (CLAs), which are found in meat and dairy products, have beneficial effects against atherosclerosis, diabetes, and obesity. The effects of n3-PUFAs and CLAs are in contrast to fatty acids with virtually identical structures, such as linoleic acid and arachidonic acid (ie, n-6 PUFAs). This article discusses the possibility that cognate receptors exist for fatty acids or their metabolites that are able to regulate gene expression and coordinately affect metabolic or signaling pathways associated with coronary heart disease. Three nuclear receptors are emphasized as fatty acid receptors that respond to dietary and endogenous ligands: peroxisome proliferator activated receptors, retinoid X receptors, and liver X receptors.     

Composition of platelet fatty acids and their modulation by plasma fatty acids in humans: effect of age and sex

This study evaluates the influence of sex on platelet fatty acid (FA) composition, and whether sex differences are conditioned by age. Since plasma FA have a specific relationship with platelet FA their variations with age and sex are also considered. Forty-nine male-female human couples (16-75 years), where within each couple the partners were on qualitatively similar diets and of similar age, were studied. Few differences were found between the whole groups of men and women in platelet FA. A comparison of data on FA in platelet phospholipids (PL) from 3 age groups (16-40, 40-60 and over 60) showed an increase in saturated FA of middle-aged subjects, an age-dependent decrease in 20: 5 in both sexes and of 18: 2 mainly in women. The percentage of plasma phosphatidylserine plus phosphatidylinositol decreased in middle-aged subjects. With regard to the influence of FA of plasma PL on FA of platelet PL, we found a higher correlation coefficient (r) for 16:0 and 18:0 and 20:4 and a lower one for 20:5 in middle-aged men and post-menopausal women. Considering that an increase in saturated FA and 20:4 and a decrease in 20:5 in platelet PL may increase platelet function, the plasma FA influence on platelets may help to explain the higher incidence of CHD in those groups of subjects.     

Cardiovascular disease-related genes and regulation by diet

Diets rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs) such as α-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid are associated with decreased incidence and severity of cardiovascular disease (CVD). At least some of the beneficial effects of these dietary fatty acids are mediated by metabolites such as prostaglandins, leukotrienes, thromboxanes, and resolvins. The effects of n-3 PUFAs often differ from those of other fatty acids with very similar structures, such as linoleic acid and arachidonic acid (n-6 PUFAs) and their corresponding metabolites. This article reviews the evidence that specific receptors exist for fatty acids or their metabolites that are able to regulate gene expression and coordinately affect metabolic or signaling pathways associated with CVD. Four nuclear receptor subfamilies that respond to dietary and endogenous ligands and have implications for CVD are emphasized in this article: peroxisome proliferator-activated receptors, retinoid X receptors, liver X receptors, and the farnesoid X receptor.     

Polyunsaturated fatty acids effect on serum triglycerides concentration in the presence of metabolic syndrome components. The Alaska-Siberia Project

Serum fatty acids (FAs) have wide effects on metabolism: Serum saturated fatty acids (SFAs) increase triglyceride (TG) levels in plasma, whereas polyunsaturated fatty acids (PUFAs) reduce them. Traditionally, Eskimos have a high consumption of omega-3 fatty acids (ω3 FAs); but the Westernization of their food habits has increased their dietary SFAs, partly reflected in their serum concentrations. We studied the joint effect of serum SFAs and PUFAs on circulating levels of TGs in the presence of metabolic syndrome components. We included 212 men and 240 women (age, 47.9 ± 15.7 years; body mass index [BMI], 26.9 ± 5.3) from 4 villages located in Alaska for a cross-sectional study. Generalized linear models were used to build surface responses of TG as functions of SFAs and PUFAs measured in blood samples adjusting by sex, BMI, and village. The effects of individual FAs were assessed by multiple linear regression analysis, and partial correlations (r) were calculated. The most important predictors for TG levels were glucose tolerance (r = 0.116, P = .018) and BMI (r = 0.42, P < .001). Triglyceride concentration showed negative associations with 20:3ω6 (r = −0.16, P = .001), 20:4ω6 (r = −0.14, P = .005), 20:5ω3 (r = −0.17, P < .001), and 22:5ω3 (r = −0.26, P < .001), and positive associations with palmitic acid (r = 0.16, P < .001) and 18:3ω3 (r = 0.15, P < .001). The surface response analysis suggested that the effect of palmitic acid on TG is blunted in different degrees according to the PUFA chemical structure. The long-chain ω3, even in the presence of high levels of saturated fat, was associated with lower TG levels. Eicosapentaenoic acid (20:5ω3) had the strongest effect against palmitic acid on TG. The total FA showed moderate association with levels of TG, whereas SFA was positively associated and large-chain PUFA was negatively associated. The Westernized dietary habits among Eskimos are likely to change their metabolic profile and increase comorbidities related to metabolic disease.     

Intake of total omega-3 fatty acids,eicosapentaenoic acid and docosahexaenoic acid and risk of coronary heart disease in the Spanish EPIC cohort study

Background and aimsThe evidence about the benefits of omega-3 fatty acid intake on coronary heart disease (CHD) is not consistent. We thus aimed to assess the relation between dietary intake of total omega-3 fatty acids (from plant and marine foods) and marine polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on the risk of CHD in the Spanish cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC).Methods and resultsThe analysis included 41,091 men and women aged 20–69 years, recruited from 1992 to1996 and followed-up until December 2004. Omega-3 fatty acid intake was estimated from a validated dietary questionnaire. Only participants with definite incident CHD event were considered as cases. Cox regression models were used to assess the association between the intake of total omega-3 fatty acids, EPA or DHA and CHD. A total of 609 participants (79% men) had a definite CHD event. Mean intakes of total omega-3 fatty acids, EPA and DHA were very similar in the cases and in the cohort, both in men and women. In the multivariate adjusted model, omega-3 fatty acids, EPA and DHA were not related to incident CHD in either men or women. The hazard ratios (HR) for omega-3 were 1.23 in men (95% CI 0.94–15.9, p = 0.20); and 0.77 in women (95% CI 0.46–1.30, p = 0.76).ConclusionIn the Spanish EPIC cohort, with a relatively high intake of fish, no association was found between EPA, DHA and total omega-3 fatty acid intake and risk of CHD.     

Plasma fatty acid profile in advanced cirrhosis: unsaturation deficit of lipid fractions

Fatty acid (FA) profile of plasma total lipids, phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG) were measured in 101 patients with advanced liver cirrhosis and in 44 age- and sex-matched healthy controls. Plasma levels of lipidic phosphorus, esterified cholesterol, and TG also were measured, and the unsaturation index (UI) was calculated for each fraction. Total plasma concentrations of saturated FA, linoleate, and polyunsaturated FA (PUFA) were lower in cirrhotics than in controls. This profile was also found in plasma levels of PL- and CE-associated FA. No detectable amounts of C20:3n9 were found in cirrhotic patients. Percent FA distribution of lipid fractions showed a lower percentage of linoleate and PUFA and a higher relative amount of saturated and monoenoic FA in cirrhotics than in controls. As a consequence, the UI of PL and CE was diminished in liver cirrhosis. Linoleate and PUFA deficiency was more marked in CE than in PL, as shown by the number of patients with values below the 5th percentile of the control group, suggesting an attempt to maintain the unsaturation of PL as the most important component of cell membranes. Hepatic failure, poor essential FA intake, and malnutrition are some of the possible etiologic factors for PUFA deficiency in cirrhosis. Their relative contribution to plasma FA abnormalities, as well as the clinical and pathophysiological consequences of PUFA deficit in cirrhotic patients, requires further investigation.     

Plasma fatty acids and lipid hydroperoxides increase after antibiotic therapy in cystic fibrosis.

The present authors investigated whether cystic fibrosis is linked to a defect in fatty acids and assessed the impact of the main patients' characteristics on the levels of several fatty acids, mostly during respiratory exacerbation and after antibiotic therapy. Fatty acid phospholipid and cholesteryl ester levels were measured in stable-state patients and controls. No differences were found concerning either the fractions of palmitic and oleic acids or the cholesteryl esters of alpha-linolenic and arachidonic acids. However, phospholipids of alpha-linolenic and arachidonic acids, as well as cholesteryl esters and phospholipids of stearic and linoleic acids, were lower in patients than in controls, but fractions of dihomo-gamma-linolenic, docosatetraenoic, docosapentaenoic, palmitoleic and eicosatrienoic acids were higher. Fatty acid levels, oxidative stress markers, nutrients, body mass index and forced expiratory volume in one second (FEV(1)) were measured in patients before and after antibiotic courses for bronchial exacerbation. After adjustments, palmitic, stearic, alpha-linolenic, linoleic, arachidonic, palmitoleic and oleic acids generally decreased during exacerbation but almost all increased after antibiotic courses. Nearly all fractions increased along with FEV(1) and a positive relationship linked fatty acids to lipid hydroperoxides. There was no general drop in fatty acids. Patients' fatty acid profiles depended on the pulmonary function and the inflammation state.     

Influence of dietary cod liver oil on fatty acid composition of plasma lipids in human male subjects after myocardial infarction

A randomized crossover study was carried out to investigate the fatty acid profile and concentrations of plasma lipids in male patients with myocardial infarction (MI) who supplemented their diet with 20 ml cod liver oil daily for 6 weeks. Subjects were divided into two groups, A and B. Group A received cod liver oil daily for 6 weeks after hospital discharge, but none for the subsequent 6 weeks. Group B did not start taking cod liver oil until 6 weeks after hospital discharge, and they then took cod liver oil for 6 weeks. Diet, medication or smoking habits were kept as constant as possible during the study. During the period of cod liver oil intake, eicosapentaenoic acid (20:5 (n-3), EPA) and docosahexaenoic acid (22:6 (n-3), DHA) increased significantly in phospholipids (PL), triglycerides (TG) and cholesterol esters (CE), whereas linoleic acid (18:2 (n-6), LA), dihomo-gamma-linolenic acid (20:3 (n-6), DHGLA) and arachidonic acid (20:4 (n-6), AA) were significantly decreased in phospholipids. The plasma level of TG was significantly decreased during the cod liver oil intake. Total cholesterol, high density lipoprotein (HDL) cholesterol, and levels of apolipoproteins A1 and B were not affected by cod liver oil in these MI patients.     

Changes in phosphatidylcholine fatty acid composition are associated with altered skeletal muscle insulin responsiveness in normal man

The fatty acid composition of skeletal muscle cell membrane phospholipids (PLs) is known to influence insulin responsiveness in man. We have recently shown that the fatty acid composition of phosphatidylcholine (PC), and not phosphatidylethanolamine (PE), from skeletal muscle membranes is of particular importance in this relationship. Efforts to alter the PL fatty acid composition in animal models have demonstrated induction of insulin resistance. However, it has been more difficult to determine if changes in insulin sensitivity are associated with changes in the skeletal muscle membrane fatty acid composition of PL in man. Using nicotinic acid (NA), an agent known to induce insulin resistance in man, 9 normal subjects were studied before and after treatment for 1 month. Skeletal muscle membrane fatty acid composition of PC and PE from biopsies of vastus lateralis was correlated with insulin responsiveness using a 3-step hyperinsulinemic-euglycemic clamp. Treatment with NA was associated with a 25% increase in the half-maximal insulin concentration ([ED50] 52.0 +/- 7.5 to 64.6 +/- 9.0 microU/mL, P < .05), consistent with decreased peripheral insulin sensitivity. Significant changes in the fatty acid composition of PC, but not PE, were also observed after NA administration. An increase in the percentage of 16:0 (21% +/- 0.3% to 21.7% +/- 0.4%, P < .05) and decreases in 18:0 (6.2% +/- 0.5% to 5.1% +/- 0.4%, P = .01), long-chain n-3 fatty acids (1.7% +/- 0.2% to 1.4% +/- 0.1%, P < .01), and total polyunsaturated fatty acids ([PUFAs] 8.7% +/- 0.8% to 8.0% +/- 0.8%, P < .05) are consistent with a decrease in fatty acid length and unsaturation in PC following NA administration. The change in ED50 was significantly correlated with the change in PUFAs (r = -.65, P < .05). These studies suggest that the induction of insulin resistance with NA is associated with changes in the fatty acid composition of PC in man.     

Vitamin E intake affects serum thromboxane and tissue essential fatty acid composition in the rat

The influence of dietary vitamin E on the composition of essential fatty acids in rat tissue and plasma lipids as well as serum thromboxane B2 was studied. Diets containing deficient (0 mg/kg diet), adequate (100 mg/kg) or supplemental (1,000 mg/kg) vitamin E were fed to young male rats for 10 weeks. The ratio of dihomo-gamma-linolenic acid to arachidonic acid in phospholipids of plasma, liver, and testes was increased in vitamin-E-supplemented rats. Serum thromboxane B2 was increased in vitamin-E-deficient rats. The data support a role for vitamin E in affecting both metabolism of long chain fatty acids, i.e. dihomo-gamma-linolenic acid, and conversion of arachidonic acid to thromboxane A2.     

High vitamin intake by Wistar rats during pregnancy alters tissue fatty acid concentration in the offspring fed an obesogenic diet

Diet during pregnancy affects the long-term health of the offspring. Vitamins are known to modulate lipid metabolism, which may be reflected in tissue fatty acid (FA) concentrations. The objective of this study was to investigate the effect of high vitamin intake during pregnancy on tissue FA concentration of the offspring. Wistar rats were fed an AIN-93G diet with either the recommended vitamin or 10-fold higher amounts (HV) during pregnancy. Afterward, offspring were weaned onto an obesogenic diet. Liver, quadriceps, adipose, and brain were collected over 48 weeks. Fatty acid concentration of tissue total lipids was analyzed by gas chromatography. At birth, the liver from HV offspring was higher in monounsaturated, stearic, and arachidonic acids. At weaning, the liver from HV offspring was higher in stearic and oleic acids; and in adipose tissue, n-6 and n-3 FAs were lower only in the male HV offspring (P < .05). At 12 weeks, HV offspring had higher concentrations of total fat, saturates, monounsaturates, and n-6 FA in muscle (P < .05), but not in other tissues. At 48 weeks, gestational diet did not affect tissue total lipid FA concentrations; but differences remained in specific tissue phospholipids species. Liver phospholipids from HV offspring were lower in monounsaturates and n-6 FA. Brain phosphatidylethanolamine was higher in oleic, n-6 FA, and docosahexaenoic acid in the HV offspring. Phosphatidylinositol was lower in saturates, monounsaturates, arachidonic, and docosahexaenoic acids only in HV female offspring. These observations demonstrate that high vitamin intake during pregnancy has short- and long-term effects on tissue FA concentration in the offspring.     

Erythrocyte-derived measures of membrane lipid composition in healthy men: associations with arachidonic acid at low to moderate but not high insulin sensitivity

The lipid composition of erythrocyte membranes was explored as a surrogate for that of skeletal muscle in investigations into the influence of membrane fatty acid composition on insulin sensitivity. In a preliminary study (study 1), erythrocyte and monocyte/platelet membrane fatty acid percentages were compared with those of muscle membrane in 10 otherwise healthy men undergoing orthopedic surgery. In a further study (study 2), relationships between erythrocyte membrane fatty acid concentrations and insulin sensitivity, S(I), measured using the intravenous glucose tolerance test (IVGTT), were evaluated in 30 asymptomatic men. In study 1, significant positive correlations were found between muscle and erythrocyte membrane fatty acid percentages for 16:0 saturated fatty acid (r = 0.92, P <.001), and for the 18:2n-6, 20:4n-6, 20:5n-3, and 22:5n-3 polyunsaturated fatty acids (PUFAs) (r = 0.67 to 0.83, P <.05 to.01). There were fewer and weaker associations between muscle and monocyte/platelet membrane fatty acid compositions. In study 2, highly insulin-sensitive individuals (n = 8) had significantly lower erythrocyte membrane fatty acid concentrations than those with low/normal S(I). Among those with low/normal S(I) (n = 22), S(I) correlated positively with erythrocyte membrane arachidonic acid concentration (r = 0.57, P <.01) and with total PUFAs (r = 0.46, P <.05). Indices of delta 6 and delta 5 desaturase activities were significantly higher and lower, respectively, in high compared with low/normal S(I) individuals. For a range of fatty acids, erythrocyte membrane fatty acid composition shows close associations with that of muscle membranes. Measurements in erythrocyte membranes support a role for membrane arachidonic acid content in the modulation of insulin sensitivity, specifically at low/normal insulin sensitivities.     

Malnutrition-related polyunsaturated fatty acid changes in plasma lipid fractions of cirrhotic patients.

Cirrhotic patients have both impaired liver function and nutritional derangement. In fact, the prevalence of protein-energy malnutrition (PEM) is very high in these patients. The aim of the present study was to elucidate whether the nutritional status in cirrhosis could be an additional factor that would affect levels of plasma lipids. Plasma lipid phosphorus, cholesterol, and triglycerides (TG), and fatty acid profiles in plasma and plasma fractions were determined in 50 healthy subjects and 92 patients with liver cirrhosis. The cirrhotic patients were prospectively included in three groups according to the result of nutritional assessment: group 1 (n = 38), acceptable nutritional status (including well-nourished and mildly malnourished patients); group 2 (n = 29), moderate PEM; and group 3 (n = 25), severe PEM. The main findings of this study were that the decrease in plasma cholesterol and linoleic, dihomo-gamma-linolenic, and arachidonic acid levels of cirrhotic patients was related to the degree of PEM. Cholesteryl esters (CE) appeared to be the most sensitive indicator of lipid changes in cirrhosis. We consider that the role of malnutrition in the changes observed for polyunsaturated fatty acid (PUFA) profiles in plasma lipids of cirrhotic patients may be of major importance, since severe malnourished subjects exhibited the lowest levels of those compounds. Dietary supplementation of both essential fatty acids (EFA) and long-chain PUFA in adequate amounts to the cirrhotic patient might be of importance in the management of the disease.     

Effect of dietary cholesterol on the release of prostacyclin from the mesenteric vascular bed in diabetic rat

Streptozotocin-induced diabetic female rats and age-matched control rats were fed a regular chow with or without the addition of 1% cholesterol in the diet. The release of 6-keto-PGF1 alpha, a prostacyclin metabolite, from the mesenteric vascular bed was significantly increased in diabetic rats. The production of PGI2 in diabetic rats was significantly reduced whereas that in the control was not affected by cholesterol feeding. The examination of the fatty acid composition of phospholipids from the mesenteric vascular bed indicated that proportions of stearic (18:0), linoleic (18:2n-6) and dihomo-gamma-linolenic (20:3n-6) acids were higher whereas those of oleic (18:1n-9) was lower in diabetic rats than those in the controls. Cholesterol feeding had no significant effect on the levels of arachidonic acid (20:4n-6) in the controls but it significantly decreased those in diabetic rats. It is suggested that cholesterol feeding lowers the release of PGI2 from the mesenteric vascular bed possibly because of a reduced level of arachidonic acid, the major precursor for prostaglandin synthesis. This could be due to an impairment of delta-5 desaturase.     

Hepatic Triacylglycerol Accumulation Induced by Ethanol and Carbon Tetrachloride: Interactions with Essential Fatty Acids and Prostaglandins

Triacylglycerol accumulation in the liver (fatty liver) caused by ethanol or carbon tetrachloride involves interactions with essential fatty acids and prostaglandins. The degree to which the fatty liver develops is dependent on total dietary fat intake. Both ethanol and carbon tetrachloride impair desaturation of linoleic acid and dihomo-gamma-linolenic acid and this appears to be relevant to the pathogenesis of fatty liver from two points of view. First, low arachidonic acid in liver phospholipids is associated with increased liver triacylglycerol content whether caused by ethanol, carbon tetrachloride, or essential fatty acid deficiency. Second, essential fatty acids including gamma-linolenic acid and arachidonic acid, as well as the prostaglandins, prevent ethanol- and carbon tetrachloride-induced fatty liver. Arachidonic acid and possibly the prostaglandins are therefore likely to be directly involved in lipoprotein and triacylglycerol secretion by the liver.     

Changes in lipid composition of human peripheral blood lymphocytes infected by HIV.

The possible differences in lipid composition between human immunodeficiency virus- (HIV) infected and uninfected PHA-activated human peripheral blood mononuclear cells (PBMC) have been studied. The total fatty acid composition was similar, except for the proportion of arachidonic acid, that was slightly higher in infected than in noninfected cells. No significant differences were obtained in the incorporation of radiolabeled stearic or oleic acids in the different lipid classes. The staining of cells with Nile Red showed similar amounts of intracytoplasmic lipid droplets. On the contrary, the CH/PL ratio, the major factor in determining cell membrane fluidity, was clearly higher in infected than in uninfected cells (0.60 and 0.36, respectively). This fact is discussed in relation with the known high CH/PL ratio (0.95) of the lipid envelope of HIV.     

Anthropometric predictors of coronary heart disease in Chinese women

OBJECTIVE: To evaluate the associations of body size and fat distribution with incidence of coronary heart disease (CHD) in Chinese women. DESIGN: Population-based, prospective cohort study. SUBJECTS: A total of 67 334 women aged 40-70 y, who had no prior history of CHD, stroke, and cancer at study recruitment. MEASUREMENTS: Weight, standing and sitting heights, circumferences of waist and hip, and ratios of the anthropometric measurements. Outcome: incidence of CHD (non-fatal myocardial infarction (MI) or fatal CHD). RESULTS: After a mean follow-up of 2.5 y (168 164 person-years), there were 70 incident cases of CHD (49 non-fatal MIs and 21 CHD deaths). Body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-standing height ratio (WHtR), waist-to-sitting height ratio (WsHtR), and conicity index were all positively associated with the risk of CHD. With the exception of WHR, all other anthropometric indexes only predicted the risk of CHD among women 相似文献