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Background. Chronic human immunodeficiency virus (HIV) infection is associated with intestinal permeability and microbial translocation that contributes to systemic immune activation, which is an independent predictor of HIV disease progression. The association of microbial translocation with clinical outcome remains unknown. Methods. This nested case-control study included 74 subjects who died, 120 of whom developed cardiovascular disease and 81 of whom developed AIDS during the Strategies for Management of Anti-Retroviral Therapy (SMART) study with matched control subjects. Intestinal fatty acid binding protein (I-FABP), lipopolysaccharide (LPS), soluble CD14 (sCD14), endotoxin core antibody (EndoCAb), and 16S ribosomal DNA (rDNA) were measured in baseline plasma samples. Results. Subjects with the highest quartile of sCD14 levels had a 6-fold higher risk of death than did those in the lowest quartile (95% confidence interval, 2.2-16.1; P<. 001), with minimal change after adjustment for inflammatory markers, CD4⁺ T cell count, and HIV RNA level. No other marker was significantly associated with clinical outcomes. I-FABP, LPS, and sCD14 were increased and EndoCAb was decreased in study subjects, compared with healthy volunteers. sCD14 level correlated with levels of IL-6, C-reactive protein, serum amyloid A and D-dimer. Conclusions. sCD14, a marker of monocyte response to LPS, is an independent predictor of mortality in HIV infection. Therapeutic attenuation of innate immune activation may improve survival in patients with HIV infection.

PurposeExercise-induced changes in intestinal permeability are exacerbated in the heat. The aim of this study was to determine the effect of 14 days of bovine colostrum (Col) supplementation on intestinal cell damage (plasma intestinal fatty acid-binding protein, I-FABP) and bacterial translocation (plasma bacterial DNA) following exercise in the heat.MethodsIn a double-blind, placebo-controlled, crossover design, 12 males completed two experimental arms (14 days of 20 g/day supplementation with Col or placebo, Plac) consisting of 60 min treadmill running at 70% maximal aerobic capacity (30 °C, 60% relative humidity). Blood samples were collected pre-exercise (Pre-Ex), post-exercise (Post-Ex) and 1 h post-exercise (1 h Post-Ex) to determine plasma I-FABP concentration, and bacterial DNA (for an abundant gut species, Bacteroides).ResultsTwo-way repeated measures ANOVA revealed an arm × time interaction for I-FABP (P = 0.005, with greater Post-Ex increase in Plac than Col, P = 0.01: Plac 407 ± 194% of Pre-Ex vs Col, 311 ± 134%) and 1 h Post-Ex (P = 0.036: Plac 265 ± 80% of Pre-Ex vs Col, 229 ± 56%). There was no interaction (P = 0.904) but there was a main effect of arm (P = 0.046) for plasma Bacteroides/total bacterial DNA, with lower overall levels evident in Col.ConclusionThis is the first investigation to demonstrate that Col can be effective at reducing intestinal injury following exercise in the heat, but exercise responses (temporal pattern) of bacterial DNA were not influenced by Col (although overall levels may be lower).

Multiple sclerosis (MS) involves dysregulation of innate immune cells including monocytes, especially in progressive MS. Fatty acid binding proteins (FABP) are essential for fatty acid transport and metabolism in multiple cell types. FABP7, a brain-FABP, maintains metabolic function in astrocytes and neural stem cells, but the effect of FABP7 on monocytes is unknown. Here we find elevated levels of FABP7 in the serum and cerebrospinal fluid of patients with secondary progressive MS. Elevated serum FABP7 levels positively correlate with higher disability scores, brain lesion volumes, and lower brain volumes. FABP7 levels are increased in astrocytes from MS postmortem brain lesion. Mechanistically, in vitro treatment of FABP7 induces CD16, CD80 and IL-1β expression in monocytes via increased glycolysis. FABP7-induced gene expression reflects enhanced inflammation, chemotaxis and glucose metabolism in monocytes. In conclusion, we find that FABP7 induces pro-inflammatory profiles in monocytes, correlates with disability and represents a potential biomarker and therapeutic target for progressive MS. While immune dysregulation is acknowledged as causal for multiple sclerosis (MS), how monocytes contribute to MS etiology is still unclear. Here the authors analyze peripheral blood and cerebrospinal fluid samples as well as brain MRI image data from MS patients to implicate FABP7 in alteration of monocyte glycolysis, and as a potential marker for MS progression.

Abstract Context Several cross-sectional studies have reported the association between serum adipocyte fatty acid–binding protein (A-FABP) level and presarcopenia. However, data on the effects of serum A-FABP level and its changes over time on the development and improvement of presarcopenia are scarce. Objective This study aimed to explore the association of serum A-FABP level with the incidence and improvement of presarcopenia in a community-based cohort, and further investigated the association of changes in serum A-FABP level with the incidence and improvement of presarcopenia. Methods This longitudinal cohort study included 1496 adults (41.2% men; median age, 58 [53-63] years) in 2013 to 2014 and was followed up to 2015 to 2016. Participants underwent serum A-FABP level measurements at baseline and a follow-up visit. Visceral fat area (VFA) was measured using magnetic resonance imaging. Skeletal muscle mass (SMM) was estimated by bioelectrical impedance analysis and converted to a skeletal muscle index (SMI). Presarcopenia was defined as SMI less than 1 SD of the sex-specific mean for the young reference group. Results During an average follow-up period of 2.1 years, baseline serum A-FABP level was positively associated with the incidence of presarcopenia (standardized by weight: risk ratio [RR] 3.22; 95% CI, 1.96-5.38; standardized by VFA: RR 2.11, 95% CI, 1.29-3.51) and negatively associated with the improvement of presarcopenia (standardized by weight: RR 0.66; 95% CI, 0.45-0.97; standardized by VFA: RR 0.71; 95% CI, 0.54-0.94), regardless of whether SMM was standardized by weight or VFA. Moreover, changes in serum A-FABP level provided additional information on the incidence and improvement of presarcopenia, independent of baseline serum A-FABP level (all P < .05). Conclusion Baseline serum A-FABP level and its changes were positively associated with the incidence and negatively associated with the improvement of presarcopenia.

Purpose Intestinal cell damage due to physiological stressors (e.g. heat, oxidative, hypoperfusion/ischaemic) may contribute to increased intestinal permeability. The aim of this study was to assess changes in plasma intestinal fatty acid-binding protein (I-FABP) in response to exercise (with bovine colostrum supplementation, Col, positive control) and compare this to intestinal barrier integrity/permeability (5 h urinary lactulose/rhamnose ratio, L/R ). Methods In a double-blind, placebo-controlled, crossover design, 18 males completed two experimental arms (14 days of 20 g/day supplementation with Col or placebo, Plac). For each arm participants performed two baseline (resting) intestinal permeability assessments ( L/R ) pre-supplementation and one post-exercise following supplementation. Blood samples were collected pre- and post-exercise to determine I-FABP concentration. Results Two-way repeated measures ANOVA revealed an arm × time interaction for L/R and I-FABP ( P  < 0.001). Post hoc analyses showed urinary L/R increased post-exercise in Plac (273% of pre, P  < 0.001) and Col (148% of pre, P  < 0.001) with post-exercise values significantly lower with Col ( P  < 0.001). Plasma I-FABP increased post-exercise in Plac (191% of pre-exercise, P  = 0.002) but not in the Col arm (107%, P  = 0.862) with post-exercise values significantly lower with Col ( P  = 0.013). Correlations between the increase in I-FABP and L/R were evident for visit one ( P  = 0.044) but not visit two ( P  = 0.200) although overall plots/patterns do appear similar for each. Conclusion These findings suggest that exercise-induced intestinal cellular damage/injury is partly implicated in changes in permeability but other factors must also contribute.

Purpose To examine the dose–response effects of acute glutamine supplementation on markers of gastrointestinal (GI) permeability, damage and, secondary, subjective symptoms of GI discomfort in response to running in the heat. Methods Ten recreationally active males completed a total of four exercise trials; a placebo trial and three glutamine trials at 0.25, 0.5 and 0.9 g kg −1 of fat-free mass (FFM) consumed 2 h before exercise. Each exercise trial consisted of a 60-min treadmill run at 70% of V ˙ O 2max in an environmental chamber set at 30 °C. GI permeability was measured using ratio of lactulose to rhamnose (L:R) in serum. Plasma glutamine and intestinal fatty acid binding protein (I-FABP) concentrations were determined pre and post exercise. Subjective GI symptoms were assessed 45 min and 24 h post-exercise. Results Relative to placebo, L:R was likely lower following 0.25 g kg −1 (mean difference: − 0.023; ± 0.021) and 0.5 g kg −1 (− 0.019; ± 0.019) and very likely following 0.9 g kg − 1 (− 0.034; ± 0.024). GI symptoms were typically low and there was no effect of supplementation. Discussion Acute oral glutamine consumption attenuates GI permeability relative to placebo even at lower doses of 0.25 g kg −1 , although larger doses may be more effective. It remains unclear if this will lead to reductions in GI symptoms. Athletes competing in the heat may, therefore, benefit from acute glutamine supplementation prior to exercise in order to maintain gastrointestinal integrity.

Adipocyte fatty acid-binding protein (FABP4) is expressed in adipose tissue and may impair glucose homeostasis and promote atherosclerotic processes. We examined the association between serum FABP4 and risk of type 2 diabetes (T2D), myocardial infarction (MI), and stroke. Case-cohort study embedded within a sample of 27,548 participants of the EPIC-Potsdam cohort. A randomly selected subcohort (n = 2194) of participants who were free of cardiovascular disease and T2D at study baseline and 728 incident T2D cases, 206 incident stroke cases, and 185 incident MI cases with an average 8.2 (±1.7) years of follow-up. Incident T2D, MI, and stroke. In a multivariable-adjusted model, the hazard ratios (HRs) in the highest vs lowest quartile of FABP4 were 1.81 (95% CI, 1.21 to 2.70; Ptrend = 0.01) for T2D, 0.93 (95% CI, 0.55 to 1.55; Ptrend = 0.68) for MI, and 1.41 (95% CI, 0.80 to 2.49; Ptrend = 0.24) for stroke, respectively. In analyses stratified by sex, no statistically significant differences could be seen for associations between FABP4 and T2D and MI (Pinteraction by sex = 0.27 and 0.84, respectively), whereas a higher risk of stroke was observed in men (HR: 2.70, 95% CI 1.20 to 6.00; P = 0.04), but not in women (HR: 0.70, 95% CI 0.31 to 1.60; P = 0.53; Pinteraction = 0.02). These data support the hypothesis that elevated FABP4 levels may contribute to T2D risk. In contrast, our data did not support the hypothesis that circulating FABP4 may be relevant for MI, whereas the observed association with stroke in men may need further evaluation.

Background Circulating fatty acid-binding protein 4 (FABP4) influences cardiovascular disease and glucose metabolism. Acute aerobic exercise increases circulating FABP4 concentrations, but the factors underlying this effect in humans are unclear. We investigated the effect of exercise duration on circulating FABP4 concentrations in healthy men. Methods This randomized crossover study enrolled healthy young men randomly assigned to two trials, short-duration (SE) and long-duration (LE) aerobic exercises trials. Both involved acute aerobic exercise followed by 60 min of bed rest. The exercise intensity was the same (40% peak oxygen uptake); however, the duration was 40 and 70 min for the SE and LE trials, respectively. Venous blood samples were collected to measure hormones, metabolites, and FABP4 concentrations. Results Twelve healthy young men completed both trials. Changes in hormone levels did not differ significantly between the SE and LE trials ( p  > 0.05). However, the circulating FABP4 concentration increased significantly only in the LE trial immediately after exercise ( p  = 0.018). It increased significantly 30–60 min post-exercise in both the SE and LE trials ( p  < 0.018), with the extent of the increase being significantly higher in the LE trial than in the SE trial ( p  < 0.001). In each trial, the total incremental area under the curve of circulating FABP4 concentration was significantly positively correlated with body fat percentage (SE trial: r s  = 0.699, p  = 0.019; LE trial: r s  = 0.643, p  = 0.024). Conclusion Our findings suggest that exercise duration is associated with the magnitude of increased FABP4 secretion into the blood circulation. Body fat accumulation may also be involved in the magnitude of FABP4 secretion induced by acute aerobic exercise. Trial registration The study was pre-registered with the University Hospital Medical Information Network Center (UMIN), a clinical trial registration system (ID: UMIN000051068).

An electrochemiluminescence (ECL) immunosensor was developed for the highly sensitive and specific detection of heart-type fatty acid binding protein (H-FABP) and the rapid diagnosis of acute myocardial infarction (AMI). H-FABP is a biomarker that is highly specific to cardiac tissue and is associated with a range of cardiac diseases. Following myocardial injury, the rate of increase in H-FABP levels is greater than that observed for myoglobin and troponin. Therefore, the measurement of H-FABP is crucial for the early exclusion of AMI. Silver-cysteine nanorod (AgCysNR), which served as the ECL emitter, was produced with a one-step, green, simple, template-free aqueous phase method. The surfaces of AgCysNR displayed many amino and carboxyl groups that were connected to a large number of a secondary H-FABP-specific antibody. Ferrum-doped molybdenum oxide (FeMoO ν ), with a large specific surface area, was richly decorated with silver nanoparticle (AgNP), which increased the interfacial electron transfer rate of FeMoO ν . The AgNP was used as a co-reaction accelerator to promote persulfate to produce more sulfate anion radical and then enhance the ECL intensity of AgCysNR. The linear range of the ECL immunosensor was 10 fg/mL to 100 ng/mL, and the detection limit was 2.3 fg/mL (signal/noise = 3). The sensor was determined to be stable, repeatable, and reproducible, and the method achieved recoveries of 101.0 to 102.6% with relative standard deviations of 1.4 to 2.0%. This immunosensor represents a promising tool for the early diagnosis of AMI. Graphical abstract

Purpose To quantify the impact of a 14-day bovine colostrum (BC) supplementation on intestinal cell damage following exercise in a hot and humid environment. Methods Ten male participants (20 ± 2 years, VO 2max 55.80 ± 3.79 mL kg −1  min −1 , 11.81 ± 2.71% body fat) ran for 46 ± 7.75 min at 95% of ventiliatory threshold in 40 °C and 50% RH following a 14-day double-blinded supplementation with either BC or placebo (Plac). Core temperature, skin temperature, heart rate, and rating of perceived exertion were recorded every 5 min during exercise. Blood was taken pre, post, 1 h, and 4 h post exercise. Intestinal cell damage was assessed via intestinal fatty acid binding protein (I-FABP). Results I-FABP concentrations were similar between conditions at all time points [pre 989.39 ± 490.88 pg ml −1 (BC) 851.35 ± 450.71 pg ml −1 (Plac) post 1505.10 ± 788.63 pg ml −1 (BC) 1267.12 ± 521.51 pg ml −1 (Plac) 1-h, 1087.77 ± 397.06 pg ml −1 (BC) 997.25 ± 524.74 pg ml −1 (Plac) 4-h, 511.35 ± 243.10 pg ml −1 (BC) 501.46 ± 222.54 pg ml −1 (Plac)]. I-FABP was elevated pre to post exercise for both BC (162 ± 50%) and Plac (162 ± 56%) ( p  < 0.05). BC had no effect on mean body temperature [beginning 36.11 ± 0.30 °C, ending: 39.52 ± 0.28 °C (BC); beginning:35.96 ± 0.43 °C, ending:39.42 ± 0.38 °C (Plac)]. Conclusions While BC supplementation may protect against enterocyte damage during exercise in thermonuetral environments, our data suggest that BC supplementation may not be an effective technique for preventing enterocyte damage during exercise when core temperature exceeds 39 °C.