Background: Metabolic derangements are common in human immunodeficiency virus (HIV)-positive subjects undergoing antiretroviral therapy, but little is known about postprandial conditions. Methods: We investigated the relationship between leptin, adiponectin, nonesterified fatty acids (NEFA), and insulin in response to a day-long meal pattern and evaluated gender differences in HIV-positive men (n = 12) and women (n = 13) undergoing highly active antiretroviral therapy (HAART). Results: For both men and women, a significant decrease in postprandial NEFA levels was observed following breakfast (0.53 vs. 0.22 mmol/L, P < 0.001, baseline and at 3 hours, respectively), whereas day-long postprandial leptin and adiponectin levels showed small nonsignificant oscillations. In contrast to NEFA and adiponectin, postprandial leptin levels were significantly higher among women compared to men (P < 0.05). Postprandial NEFA levels correlated positively with fasting insulin levels (r2 = 0.25, P = 0.016), and the postbreakfast decrease in NEFA levels correlated significantly with the postbreakfast increase in insulin levels (r2 = 0.17, P = 0.038). No significant association between postprandial adipokines and insulin was observed. Conclusions: In HAART-treated, HIV-infected men and women, levels of NEFA, but not adipokines, showed significant postprandial variation. Furthermore, food intake resulted in significant NEFA suppression in proportion to the food-stimulated insulin increase.

The hypothesis was tested that plasma levels of adiponectin would be associated with coronary artery disease (CAD) across African-American and Caucasian ethnicity and gender. Adiponectin levels, cardiovascular risk factors, and extent of CAD were measured in 453 subjects (173 African-American and 280 Caucasian men and women). The distribution of adiponectin levels differed significantly between African-Americans and Caucasians (P<0.0001). Among African-Americans, the adiponectin distribution was skewed toward lower levels. For women, adiponectin levels were higher among Caucasians compared with African-Americans (P<0.001), whereas no interethnic difference was observed for men. Irrespective of ethnic group, subjects with CAD had lower levels of adiponectin than did subjects without CAD. Adiponectin was negatively and significantly associated with waist-hip ratio, body mass index, diastolic blood pressure, insulin level, and homeostasis model assessment-insulin resistance in both ethnic groups. Among lipid parameters, total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels were negatively correlated with adiponectin, whereas the high-density lipoprotein cholesterol level correlated positively for both African-Americans and Caucasians. In a multiple regression model, controlling for gender, ethnicity, and other CAD risk factors, adiponectin levels were negatively associated with CAD (P<0.05). The results indicate that, across gender and ethnicity, low adiponectin levels may be an independent risk factor for CAD.

BACKGROUND:Features of the dyslipidemic pattern reported with the use of antiretroviral therapy predict enhanced postprandial lipemia, which is an emerging cardiovascular disease risk factor.OBJECTIVE:We evaluated the postprandial response to a physiologic, meal-based challenge in HIV-positive subjects without hyperlipidemia.DESIGN:We measured hourly lipid, lipoprotein, glucose, and insulin concentrations during a 13-h period in 25 nonwhite patients (13 women, 12 men): 13 receiving a protease inhibitor (PI)-based regimen (6 nelfinavir and 7 indinavir) and 12 receiving a nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimen (6 efavirenz and 6 nevirapine).RESULTS:Mean fasting HDL-cholesterol concentrations were lower in HIV patients than in healthy subjects without HIV infection matched for age, sex, and ethnicity (z score: -0.81 +/- 0.9; P = 0.0001). Fasting triacylglycerol concentrations were not significantly different between HIV-infected patients and healthy subjects but were higher in PI-treated than in NNRTI-treated patients [median (interquartile range): 144 (110-191) and 89 (62-135) mg/dL; P = 0.007]. Average daylong triacylglycerol concentrations, but not incremental concentrations, were higher in the PI group than in the NNRTI group [205% (185-248%) and 125% (78-191%); P < 0.05]. For all HIV-positive patients, the fractional triacylglycerol increase was lower after breakfast than after lunch (20 +/- 18% and 42 +/- 40%, respectively; P < 0.04). Insulin concentrations were higher in PI-treated than in NNRTI-treated patients [22.6 (13.1-29.8) and 11.8 (7.1-19.1) microU/mL; P = 0.01] and increased in both groups in response to each meal, whereas glucose concentrations increased only after breakfast.CONCLUSIONS:Despite baseline differences, incremental triacylglycerol and insulin responses to a physiologic caloric load among HIV-positive patients were not significantly affected by differences in the type of antiretroviral therapy.

Background: Eicosapentaenoic acid is a fish oil fatty acid that has been shown to decrease blood pressure (BP) in humans. The mechanism by which this fatty acid produces this effect is unknown. Angiotensin II increases BP by inducing vasoconstriction of vascular smooth muscle cells, an event that is mediated by an increase of intracellular calcium and an increase of protein kinase C activity.Methods: We determined the effects of eicosapentaenoic acid on angiotensin II-induced calcium signaling, and protein kinase C activity in cultured rat aortic smooth muscle cells. Incorporation of eicosapentaenoic acid into cell phospholipids was determined by gas chromatography/mass spectrometry. Intracellular calcium concentration was determined using fura-2, and protein kinase C activity was assessed by an ELISA assay using a phosphospecific antiserum for protein kinase C substrates.Results: We found that eicosapentaenoic acid was incorporated into cell phospholipids within 20 min. Eicosapentaenoic acid (10 or 25 mumol/L) did not alter basal intracellular calcium concentration, but decreased the peak response to 100 nmol/L angiotensin II. Eicosapentaenoic acid also decreased the amount of calcium released by thapsigargin, a drug that releases calcium from the sarcoplasmic reticulum, and decreased cation influx after angiotensin II stimulation. Angiotensin II stimulated phosphorylation of protein kinase C substrates. Preincubation of cells with 10 or 25 mumol/L eicosapentaenoic acid significantly inhibited this phosphorylation.Conclusions: Our results demonstrate that acute incorporation of eicosapentaenoic acid into vascular smooth muscle cell phospholipids inhibits intracellular calcium mobilization and protein kinase C activation. These are potential mechanisms by which eicosapentaenoic acid reduces vasoconstriction.

This study was conducted to investigate whether altered vascular responsiveness to vasoactive compounds contributes to the development of hypertension in diet-induced hyperinsulinemic rats. Male Sprague-Dawley rats were randomly assigned to receive high fructose, high sucrose, or standard rat chow for 13-18 wk. Blood pressure was monitored by indirect (tail-cuff) measurements at regular intervals during the diet treatment. Vascular responses to various vasoactive agents were studied both in vivo and in vitro. Blood pressure response, as assessed by direct (intra-arterial) measurement, to graded dose infusions of norepinephrine or angiotensin II or bolus infusion of acetylcholine were determined. In vitro vascular responses of the tail arteries to exogenous norepinephrine were also studied. The fructose- and the sucrose-fed rats had significantly higher blood pressure than controls. Serum insulin levels were also significantly higher in fructose- and sucrose-fed rats than in controls. The blood pressure responses to graded infusions of norepinephrine were significantly less in the fructose-fed rats than in controls. The blood pressure responses to angiotensin II and acetylcholine infusion were not significantly different among the three groups of rats. In vitro studies of vascular reactivity in the tail arteries revealed than the concentration of norepinephrine that produced half-maximal contraction (NE EC50) was significantly higher in the fructose group than control. Thus, impaired vascular responses to exogenous norepinephrine were observed in fructose-fed rats both in vivo and in vitro. This may be due to an adaptation to increased sympathetic nervous activity, or may be a compensatory response to other structural or functional changes that produce hypertension in this model.

The purpose of this study was to optimize the counting and measuring of marine fouling organisms on experimental panels using automated computer techniques. A script was developed that reduced the time required for the counting and measuring of marine fouling tubeworms by at least one order of magnitude over manual counts, with an error of five percent or less. Small, distinct tubeworms can be successfully counted by computer using a correction factor. Measurements of percentage cover or area should be made with larger tubeworms that have overlapping tubes.