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Background Adipocyte fatty acid–binding protein (FABP4) is an adipokine that plays an important role in development of cardiovascular and metabolic diseases. The aim of this study was to assess the 3-month prognostic value of serum levels of FABP4 in Chinese patients with aneurysmal subarachnoid hemorrhage (aSAH) on hospital admission. Methods This was a prospective observational study from a stroke treatment center in Zhengzhou, China. From October 2016 to May 2018, patients with aSAH who were hospitalized within 24 h were included. In addition, 202 age- and gender-matched healthy volunteers were assigned to the healthy control group. At admission, serum levels of FABP4 were measured, and patients’ characteristics, Hunt–Hess grade, and modified Fisher grade evaluated. At 3-month follow-up, functional outcome (Glasgow Outcome Scale score; dichotomized as poor [score 1–3] or good [score 4–5]) and all-cause mortality were recorded. Univariate and multivariate logistic regression models were used to investigate the association of FABP4 with the two endpoints. Results A total of 418 patients with aSAH were included in this study. The median age was 58 years (interquartile range, 49–66 years), and 57.9% were women. FABP4 serum levels were related to Hunt–Hess score ( r [Spearman] = 0.381; P  < 0.001). Patients with a poor outcome and non-survivors had significantly increased serum FABP4 levels on admission ( P  < 0.001 for all). In multivariate logistic regression analysis, FABP4 was an independent predictor of poor outcome and mortality, with increased risks of 7% (odds ratios 1.07, 95% confidence interval [CI] 1.02–1.13; P  = 0.001) and 5% (odds ratio 1.05, 95% CI, 1.01–1.12; P  = 0.003), respectively. Receiver operating characteristics to predict functional outcome and mortality were significantly different between conventional risk factors (difference area under the curve 0.024, 95% CI 0.018–0.032) and FABP4 plus conventional risk factors (area under the curve 0.015, 95%CI 0.011–0.020). After FABP4 was added to the existing risk factors, mortality was better reclassified and was associated with the net reclassification improvement statistic ( P  = 0.009), while poor outcome was better reclassified and associated with both the integrated discrimination improvement and net reclassification improvement statistics ( P  < 0.05 for all). Conclusions Elevated serum FABP4 levels were related to poor outcome and mortality in a cohort of patients with aSAH.

Aims Adipocyte fatty acid‐binding protein (AFABP) is associated with cardiovascular diseases in type 2 diabetes. Whether circulating AFABP levels are associated with the risk of heart failure (HF) in type 2 diabetes remains undefined. We investigated the prospective association of circulating AFABP levels with incident HF hospitalization in type 2 diabetes, and its relationship to the use of sodium glucose co‐transporter 2 inhibitors (SGLT2i) which reduce HF risk. Methods and results Baseline serum AFABP level was measured in 3322 Chinese participants without known history of cardiovascular diseases or hospitalization for HF, recruited from the Hong Kong West Diabetes Registry. Its association with incident HF hospitalization was evaluated using multivariable Cox regression analysis. Use of SGLT2i was included as a time‐dependent covariate. Among these 3322 participants (52.9% men; mean age 60.0 ± 12.6), 176 (5.3%) developed HF hospitalization over a median follow‐up of 8 years. Seven hundred and thirty‐one (22%) were started on SGLT2i during the study period (empagliflozin 55.1%, dapagliflozin 44.2%, canagliflozin 0.4%, and ertugliflozin 0.3%). Serum AFABP levels were significantly higher in participants who developed HF hospitalization than those who did not (men: 14.8 vs. 8.3 ng/mL; women: 21.5 vs. 14.6 ng/mL; all: 18.6 vs. 10.9 ng/mL, P < 0.001). In multivariable Cox regression analysis, baseline serum AFABP level was significantly associated with incident HF hospitalization [hazard ratio (HR) 1.38, 95% confidence interval (CI) 1.06–1.80, P = 0.019] independent of the use of SGLT2i, in a model also consisting of age; sex; body mass index; smoking status; duration of diabetes; hypertension, dyslipidaemia; atrial fibrillation; presence of chronic kidney disease and albuminuria; glycated haemoglobin and high‐sensitivity C‐reactive protein levels; and use of metformin, insulin, aspirin, furosemide, and beta‐blockers at baseline. High cumulative defined daily dose (cDDD) of SGLT2i was protective of incident HF hospitalization (HR 0.10, 95% CI 0.01–0.68, P = 0.019). The addition of circulating AFABP level to a clinical model of conventional HF risk factors provided significant improvement in the category‐free net reclassification index (11.5%, 95% CI 1.6–22.1, P = 0.02) and integrated discrimination improvement (0.3%, 95% CI 0.1–1.7, P = 0.04). A dose‐dependent reduction in cumulative incidence of HF hospitalization in response to SGLT2i, based on cDDD, was more clearly observed in participants with a higher baseline AFABP level above the sex‐specific median (P for trend <0.01). Conclusions Circulating AFABP level is independently associated with incident HF hospitalization in type 2 diabetes and is potentially helpful in risk stratification for the prevention of HF hospitalization.

Aims/Introduction Individuals with type 2 diabetes mellitus are vulnerable to micro‐ and macrovascular complications in the presence of microalbuminuria. Adipocyte fatty acid‐binding protein (A‐FABP) was proposed as an indicator for albuminuria in patients with diabetes. The present study aimed to explore the associations between serum A‐FABP levels and microalbuminuria in the hyperglycemic population. Materials and Methods Serum A‐FABP levels were detected using sandwich enzyme‐linked immunosorbent assay. Microalbuminuria was identified by urinary albumin‐to‐creatinine ratio (UACR), when the value was between 30–300 mg/g. The participants were divided into the subgroups based on sex and the status of impaired glucose regulation or newly diagnosed type 2 diabetes mellitus. Results A total of 939 participants, consisting of 436 men and 503 women, were enrolled. Serum levels of A‐FABP were much higher in participants with microalbuminuria than those without microalbuminuria. This result held true for all subgroups (all P < 0.05). For Spearman's correlation analyses, serum A‐FABP levels showed a positive relationship with the UACR in men and women (both P < 0.01). Multiple stepwise regression analysis showed that serum A‐FABP levels were independently and positively correlated with UACR in both sexes (men: standardized β = 0.256, P < 0.001; women: standardized β = 0.155, P = 0.001). This relationship remained significant in every subgroup (all P < 0.01). Conclusions For hyperglycemic individuals, serum A‐FABP levels increased in the presence of microalbuminuria. Serum A‐FABP levels were identified as an independent factor positively associated with the UACR. Increased serum A‐FABP levels contributed to the presence of microalbuminuria. The serum A‐FABP levels were independently and positively associated with the UACR. Serum A‐FABP levels can be used as an indicator of microalbuminuria.

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.

Abstract Context There is little evidence regarding the joint effect of serum adipocyte fatty acid binding protein (A-FABP) levels and obesity phenotype on the risk of cardiovascular events. Objective To explore the association between serum A-FABP levels and obesity phenotype defined by fat percentage (fat%) and visceral fat area (VFA), and their joint impact on incident cardiovascular events. Methods A total of 1345 residents (579 men and 766 women) without previous cardiovascular diseases at baseline, with body composition and serum A-FABP data available, were included. A bioelectrical impedance analyzer and magnetic resonance imaging were used to assess fat% and VFA, respectively. Results During a mean follow-up of 7.6 years, 136 cases of cardiovascular events (13.9 per 1000 person-years) occurred. Per 1-unit increase in loge-transformed A-FABP levels was associated with an increase in cardiovascular events risk (hazard ratio [HR] 1.87, 95% CI 1.33-2.63). The highest tertiles of fat% and VFA levels were related to higher risks of cardiovascular events (fat%: HR 2.38, 95% CI 1.49-3.81; VFA: HR 1.79, 95% CI 1.09-2.93). The association between A-FABP levels and cardiovascular events was more pronounced in participants with low fat%, regardless of VFA levels. The joint effect of high A-FABP levels and obesity resulted in a greater risk of cardiovascular events. Conclusion Serum A-FABP levels were significantly associated with the risk of cardiovascular events, and this pattern of association was more prominent among the population with low fat%, which was independent of VFA.

Abstract Context Adipocyte fatty acid-binding protein (AFABP), fibroblast growth factor 21 (FGF21), and pigment epithelium–derived factor (PEDF) are 3 diabetes-related biomarkers whose circulating levels had been shown to associate with nephropathy progression in Chinese patients with type 2 diabetes. Objective Here, we evaluated and compared their prospective associations with the development of sight-threatening DR (STDR), another important diabetic microvascular complication. Methods Baseline serum AFABP, PEDF, and FGF21 levels were measured in 4760 Chinese individuals with type 2 diabetes and without STDR at baseline. The associations of these biomarkers with incident STDR were analyzed using Cox regression analysis. Results Among these 4760 participants (mean diabetes duration of 11 years and ≥ 50% with nonproliferative DR at baseline), 172 participants developed STDR over a median follow-up of 8.8 years. Participants with incident STDR had comparable baseline serum FGF21 levels but significantly higher baseline serum AFABP and PEDF levels (both P < .001) than those without. However, in multivariable Cox regression analysis, only serum AFABP remained independently associated with incident STDR (hazard ratio 1.28; 95% CI, 1.05-1.55; P = .013). The addition of serum AFABP to a clinical model of conventional STDR risk factors including diabetes duration, glycemic control, albuminuria, and baseline DR status significantly improved the c statistics (P < .001), net reclassification index (P = .0027), and integrated discrimination index (P = .033) in predicting incident STDR among participants without DR or with mild DR at baseline. Conclusion Among the 3 diabetes-related biomarkers, serum AFABP level appeared to be a more clinically useful biomarker for predicting incident STDR in type 2 diabetes.

It has been increasingly recognized that inflammation plays an important role in the pathogenesis of cardiovascular disease (CVD). In obesity, adipose tissue inflammation, especially in the visceral fat depots, contributes to systemic inflammation and promotes the development of atherosclerosis. Adipocyte fatty acid-binding protein (AFABP), a lipid chaperone abundantly secreted from the adipocytes and macrophages, is one of the key players mediating this adipose-vascular cross-talk, in part via its interaction with c-Jun NH2-terminal kinase (JNK) and activator protein-1 (AP-1) to form a positive feedback loop, and perpetuate inflammatory responses. In mice, selective JNK inactivation in the adipose tissue significantly reduced the expression of AFABP in their adipose tissue, as well as circulating AFABP levels. Importantly, fat transplant experiments showed that adipose-specific JNK inactivation in the visceral fat was sufficient to protect mice with apoE deficiency from atherosclerosis, with the beneficial effects attenuated by the continuous infusion of recombinant AFABP, supporting the role of AFABP as the link between visceral fat inflammation and atherosclerosis. In humans, raised circulating AFABP levels are associated with incident metabolic syndrome, type 2 diabetes and CVD, as well as non-alcoholic steatohepatitis, diabetic nephropathy and adverse renal outcomes, all being conditions closely related to inflammation and enhanced CV mortality. Collectively, these clinical data have provided support to AFABP as an important adipokine linking obesity, inflammation and CVD. This review will discuss recent findings on the role of AFABP in CVD and mortality, the possible underlying mechanisms, and pharmacological inhibition of AFABP as a potential strategy to combat CVD.

A high level of circulating free fatty acids (FFAs) is known to be an important trigger for macrophage apoptosis during the development of atherosclerosis. However, the underlying mechanism by which FFAs result in macrophage apoptosis is not well understood. In cultured human macrophage Thp-1 cells, we showed that palmitate (PA), the most abundant FFA in circulation, induced excessive reactive oxidative substance production, increased malondialdehyde concentration, and decreased adenosine triphosphate levels. Furthermore, PA treatment also led to mitochondrial dysfunction, including the decrease of mitochondrial number, the impairment of respiratory complex IV and succinate dehydrogenase activity, and the reduction of mitochondrial membrane potential. Mitochondrial apoptosis was also detected after PA treatment, indicated by a decrease in cytochrome release, downregulation of Bcl-2, upregulation of Bax, and increased caspase-3 activity. PA treatment upregulated the expression of adipocyte fatty acid-binding protein (A-FABP), a critical regulator of fatty acid trafficking and lipid metabolism. Inhibition of A-FABP with BMS309403, a small-molecule A-FABP inhibitor, almost reversed all of these indexes. Thus, this study suggested that PA-mediated macrophage apoptosis through A-FABP upregulation, which subsequently resulted in mitochondrial dysfunction and reactive oxidative stress. Inhibition of A-FABP may be a potential therapeutic target for macrophage apoptosis and to delay the progress of atherosclerosis.

Psoriasis is one of the most common skin diseases in dermatological practice. It affects about 1–3% of the general population and is associated with different comorbidities, especially metabolic syndrome. Fatty-acid-binding proteins (FABPs) are a family of cytosolic proteins which are an important link in lipid metabolism and transport; moreover, they have different tissue specificity and properties. So far, ten FABPs have been discovered and seven have been investigated in psoriasis. In this review, we discuss the nature of all FABPs and their role in psoriasis. FABPs have different organ and tissue expression, and hence various functions, and may be markers of different disorders. Considering the concentration of a few of them tends to be elevated in psoriasis, it confirms the current perception of psoriasis as a multiorgan disorder associated with plenty of comorbidities. Some FABPs may be also further investigated as biomarkers of psoriasis organ complications. FABP-1 and FABP-5 may become potential markers of metabolic complications and inflammation in psoriasis. FABP-7 could perhaps be further investigated as an indicator of the neurodegenerative processes in psoriatic patients.

Background Adipose tissue is significantly involved in inflammatory bowel disease (IBD). Vitamin D can affect both adipogenesis and inflammation. The aim of this study was to compare the production of selected adipokines, potentially involved in the pathogenesis of IBD - adiponectin, resistin, retinol binding protein 4 (RBP-4), adipocyte fatty acid binding protein and nesfatin-1 in children with IBD according to the presence of 25-hydroxyvitamin D (25(OH)D) deficiency. Methods The study was conducted as a case-control study in pediatric patients with IBD and healthy children of the same sex and age. In addition to adipokines and 25(OH)D, anthropometric parameters, markers of inflammation and disease activity were assessed in all participants. Results Children with IBD had significantly higher resistin levels regardless of 25(OH)D levels. IBD patients with 25(OH)D deficiency only had significantly lower RBP-4 compared to healthy controls and also compared to IBD patients without 25(OH)D deficiency. No other significant differences in adipokines were found in children with IBD with or without 25(OH)D deficiency. 25(OH)D levels in IBD patients corelated with RBP-4 only, and did not correlate with other adipokines. Conclusions Whether the lower RBP-4 levels in the 25(OH)D-deficient group of IBD patients directly reflect vitamin D deficiency remains uncertain. The production of other adipokines does not appear to be directly related to vitamin D deficiency.