Fatty Acid Binding Protein Research Articles

Effect of FABP4 Gene Polymorphisms on Fatty Acid Composition, Chemical Composition, and Carcass Traits in Sonid Sheep

Fatty acids (FAs) are a group of organic compounds that are regulated by polygenic and environmental factors and affect the taste, nutritional value, and quality of meat. Lamb meat is rich in FAs required by the human body, which has directed more attention to sheep research and meat production. The fatty acid-binding protein 4 (FABP4) gene is considered a candidate gene that can affect FA composition in livestock. Therefore, the aim of this study was to screen for genetic polymorphisms of FABP4 and confirm the association between these polymorphisms and FAs, chemical composition, and carcass traits in Sonid lambs. The results of the association study showed that g.57764667T>C, g.57764436T>G, g.57764242G>A, and g.57757988A>G were associated with the composition of certain long-chain FAs, and g.57764242G>A, g.57764436T>G, and g.57758026G>A were associated with free amino acid levels. In addition, g.57764667T>C and g.57757988A>G were associated with carcass weight and live weight in Sonid lambs. Therefore, the polymorphisms of the FABP4 gene are expected to be a genetic selection marker for superior traits in Sonid sheep breeding, which also provides new insights into how the ovine FABP4 gene affects traits of lamb quality.

Lupeol Attenuates Palmitate-Induced Hypertrophy in 3T3-L1 Adipocytes

Obesity is characterized by the enlargement of adipose tissue due to an increased calorie intake exceeding the body’s energy expenditure. Changes in the size of adipose tissue can lead to harmful consequences, with excessive fat accumulation resulting in adipocyte hypertrophy and promoting metabolic dysfunction. These adiposity-associated pathologies can be influenced by dietary components and their potential health benefits. Lupeol, a pharmacologically active pentacyclic triterpenoid found in medicinal plants, vegetables, and fruits, has been shown to exhibit antioxidant and anti-inflammatory properties. This study investigated the role of lupeol on adipocyte hypertrophy by evaluating key adipogenic regulators in vitro. First, 3T3-L1 MBX mouse embryonic cells were differentiated into adipocytes and hypertrophy was induced using 500 µM palmitic acid. The treated adipocytes showed a significantly increased lipid droplet size, confirming adipocyte hypertrophy. Both adipocytes and hypertrophied adipocytes were then treated with or without 60 µM lupeol, following a dose-dependent study. Lipid droplet size was assessed and validated by Oil Red O staining. Western blot analysis was performed to measure the expression of adipogenic and inflammatory markers. Differentiated adipocytes showed increased fatty acid-binding protein 4 (FABP4) expression and Oil Red O staining, indicating an increased lipid content. Western blot analysis revealed that lupeol treatment reduced the expression of FABP4, peroxisome proliferator-activated receptor-γ (PPARγ), and adipokines. In conclusion, the results suggest that lupeol reverts the inflammatory and adipogenic markers that are enhanced in adipocyte hypertrophy. Through its anti-inflammatory effects, lupeol offers protective effects against adipocyte hypertrophy and contributes to reducing hypertrophic adiposity.

FABP5 regulates ROS-NLRP3 inflammasome in glutamate-induced retinal excitotoxic glaucomatous model.

Fatty acid binding proteins (FABPs) are a class of small molecular mass intracellular lipid chaperone proteins that bind to hydrophobic ligands, such as long-chain fatty acids. FABP5 expression was significantly upregulated in the N-methyl-d-aspartic acid (NMDA) model, the microbead-induced chronic glaucoma model, and the DBA/2J mice. Previous studies have demonstrated that FABP5 can mediate mitochondrial dysfunction and oxidative stress in ischemic neurons, but the role of FABP5 in oxidative stress and cell death in retina NMDA injury models is unclear. In this study, we found that FABP5 is significantly altered in a model of glutamate excitotoxicity and is regulated by Stat3. Inhibition of FABP5 alleviated oxidative stress imbalance and activation of NLRP3 inflammasome, reduced the release of inflammatory factors, and ultimately attenuated glutamate excitotoxicity-induced retinal ganglion cell loss. Meanwhile, caspase1 inhibitors could alleviate the retinal ganglion cell loss induced by glutamate excitotoxicity. In conclusion, FABP5 inhibition protects retina ganglion cells from excitotoxic damage by suppressing the ROS-NLRP3 inflammasome pathway. FABP5 maybe a promising new target for glaucoma diagnosis and treatment.

Limited Diagnostic Value of miRNAs in Early Trauma-Induced Liver Injury: Only miRNA-122 Emerges as a Late-Phase Marker

Background/Objectives: Liver injury is common after abdominal trauma. However, the established biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), lack accuracy. This study investigates whether specific liver-related microRNAs (miRNAs) are released into the circulation in trauma patients with liver injury and whether they can indicate liver damage in the early phase after major trauma. Methods: A retrospective analysis of prospectively collected data and blood samples from 26 trauma patients was conducted. The levels of miRNA-21-5p, -122-5p, -191-5p, -192-3p, and -212-3p were measured in patients with computed tomography-confirmed liver trauma (LT group, n = 12) and polytrauma patients without liver trauma (PT group, n = 14) upon emergency room (ER) admission, and 24 and 48 h after trauma. Additionally, liver-type fatty acid binding protein (L-FABP) was measured, as it has recently been discussed in the context of abdominal trauma. Results: Only miRNA-122-5p showed a significant increase in the LT group compared to the PT group, but only at the 48 h time point (p = 0.032). Conversely, L-FABP (p = 0.018) and ALT (p = 0.05) were significantly elevated in the LT group compared to the PT group at the time of ER admission. There was a moderate correlation between miRNA-122-5p and AISAbdomen (p = 0.056) and transfused red blood cell concentrates (p = 0.055). L-FABP correlated strongly with the ALT levels (p = 0.0009) and the length of stay in the ICU (p = 0.0086). Conclusions: In this study, the liver-specific miRNA-122-5p did not effectively indicate liver injury in the early acute post-traumatic phase. Future research with a large sample size should investigate whether other miRNAs can more accurately predict liver injury and the extent of hepatocellular injury, particularly in the acute post-traumatic phase.

Feeding Preferences and Salivary Protein Profiles of Spodoptera frugiperda on Saccharum Species.

The invasion of the fall armyworm poses substantial threats to local agricultural safety, including the sugarcane industry. Exploring the insect-resistance mechanism is crucial for breeding resistant varieties. This study selected three representative materials from the Saccharum genus─Saccharum officinarum L. (Badila), S. spp. hybrid (GT58), and Saccharum spontaneum (SES208), to investigate feeding preferences and developmental fitness of Spodoptera frugiperda. Larvae exhibited a strong preference and highest fitness parameters in Badila leaves compared to SES208. Additionally, proteomic analyses of larval saliva from insects feeding on Badila and SES208 were carried out to test the types and abundance of proteins on different hosts. Furthermore, we identified fatty acid-binding protein 1-like activates plant defense responses, while aldehyde dehydrogenase negatively suppressed plant defense response. Our findings suggest that the plasticity of salivary proteins induced by different host plants, and also offer new insights into the molecular interactions between S. frugiperda and plants.

Evaluation of Intestinal Permeability Using Serum Biomarkers in Learning Early About Peanut Allergy Trial.

Intestinal barrier dysfunction may lead to a break in tolerance and development of food allergy (FA). There is contradictory evidence on whether intestinal permeability (IP) is altered in IgE-mediated FA. Thus, we sought to determine whether IP differed between children with eczema who did (FA group) or did not (atopic controls, ACs) develop FA and whether peanut sensitization, allergy, and early introduction impacted IP using serum biomarkers zonulin, soluble CD14, and Intestinal Fatty Acid Binding Protein among randomly selected participants enrolled in the Learning Early About Peanut allergy trial. FA group was defined as having at least one FA at either baseline (4-11 months) or 60 months of age (V60). ACs had eczema at baseline and no FA at either visit. Serum IP markers (sIPMs) were measured by ELISA at baseline and V60, and their relationship with the clinical characteristics of participants was analyzed using parametric tests and linear regression models. We evaluated 237 FA subjects and 76 ACs. sIPM levels were similar in FA subjects and ACs at baseline and V60. Age when the child first developed any FA (< 1 year vs. > 1 year), eczema severity, peanut sensitization, peanut allergy, and early peanut introduction were not statistically significantly associated with sIPM levels. Total IgE and eosinophil levels, peanut-specific IgE, IgG4, and IgG4/IgE ratio were not correlated with sIPM levels. No differences in sIPMs were detected to support altered IP in infants with FA compared to ACs or following early peanut introduction among peanut-sensitized children.

Effects of long-term volleyball training on multimodal responses in adolescent female athletes: a follow-up study.

The aim of this study was to examine the effects of long-term (10 months) volleyball training on biochemical responses in adolescent female athletes since the cumulative effects of chronic training on this population are not yet clear. Twenty-one adolescent female volleyball players competing at the national level served as the participants. All athletes carried out volleyball training, which consisted of ball handling, specialized drills, and practical game-style exercises, including physical training in the school gymnasium. The average training cycle consisted of 6 days per week, with a total of about 2 to 2.5 hours of volleyball training per day. In order to determine the cumulative effects on autonomic, immune, renal function and bone resorption, salivary and urinary samples were collected before volleyball training on 3 consecutive days (days 1, 3 and 5) at months 0 and 10, respectively. No significant changes in body mass, salivary secretion rate, urinary albumin, L-type fatty acid binding protein and type I collagen cross-linked N-telopeptide concentration were found. In contrast, significant decreases were noted in salivary α-amylase activity (% change: -22.9), total protein (%change: -21.4), and immunoglobulin A concentration (% change: -20.1). The results of this study imply that the autonomic function after chronic volleyball training in adolescent female athletes may be enhanced due to training adaptation, although the immune function may be attenuated as a result of cumulative overtraining. Moreover, long-term volleyball training in adolescent female athletes appears to suppress bone resorption and not to induce cumulative damage to renal function.

Advanced Dual-Mode Microfluidic Sensing Platform Based on Amphiphilic Polymer-Capped Perovskite Nanozymes Induced Photoelectrochemical Signal Amplification and Fluorescence Emission.

A novel dual-mode microfluidic sensing platform integrating photoelectrochemical (PEC) and fluorescence (FL) sensors was developed for the sensitive monitoring of heart fatty acid binding protein (h-FABP). First, BiVO4/AgInS2 (BVAIS) composites with excellent photoelectric activity were synthesized as sensing matrices. The BVAIS heterojunction with a well-matched internal energy level structure provided a stable photocurrent. Second, an innovative signal amplification strategy based on octylamine-modified poly(acrylic acid) (OPA)-capped CsPbBr3 (OPCB) nanocrystals (NCs) with excellent catalytic activity and fluorescence property was proposed. On the OPCB nanozyme possessing ascorbate oxidase-like catalytic activity could catalyze the oxidation of ascorbic acid, which achieved quenching of the photocurrent signals by competitively consuming the electron donor. On the other hand, the OPCB NCs that overcame the water stability defect processed good luminescence performance and were able to produce obvious FL signals. Mutually verified dual-response signals effectively enhance the precision of test outcomes and avoid false-positive or false-negative results. Finally, the constructed microfluidic sensing platform realized sensitive detection of h-FABP in the linear range of 0.0001-150 ng/mL (PEC mode) and 0.001-150 ng/mL (FL mode), with detection limits of 36 fg/mL and 0.32 pg/mL, respectively. The present work provided a new perspective for designing an efficient dual-mode sensing strategy to achieve sensitive detection of disease markers.

Intestinal TM6SF2 protects against metabolic dysfunction-associated steatohepatitis through the gut-liver axis.

Transmembrane-6 superfamily member 2 (TM6SF2) regulates hepatic fat metabolism and is associated with metabolic dysfunction-associated steatohepatitis (MASH). TM6SF2 genetic variants are associated with steatotic liver disease. The pathogenesis of MASH involves genetic factors and gut microbiota alteration, yet the role of host-microbe interactions in MASH development remains unclear. Here, we discover that mice with intestinal epithelial cell-specific knockout of Tm6sf2 (Tm6sf2ΔIEC) develop MASH, accompanied by impaired intestinal barrier and microbial dysbiosis. Transplanting stools from Tm6sf2ΔIEC mice induces steatohepatitis in germ-free recipient mice, whereas MASH is alleviated in Tm6sf2ΔIEC mice co-housed with wild-type mice. Mechanistically, Tm6sf2-deficient intestinal cells secrete more free fatty acids by interacting with fatty acid-binding protein 5 to induce intestinal barrier dysfunction, enrichment of pathobionts, and elevation of lysophosphatidic acid (LPA) levels. LPA is translocated from the gut to the liver, contributing to lipid accumulation and inflammation. Pharmacological inhibition of the LPA receptor suppresses MASH in both Tm6sf2ΔIEC and wild-type mice. Hence, modulating microbiota or blocking the LPA receptor is a potential therapeutic strategy in TM6SF2 deficiency-induced MASH.

Liver fatty acid binding protein FABP1 transfers substrates to cytochrome P450 4A11 for catalysis.

Cytochrome P450 (P450) 4A11 is a human P450 family 4 ω-oxidase that selectively catalyzes the hydroxylation of the terminal methyl group of fatty acids. Cytosolic lipids are the substrates for the enzyme but are considered to be primarily bound in cells by liver fatty acid binding protein (FABP1). Lipid binding to recombinant FABP1 with a fluorophore displacement assay showed substantial preference of FABP1 for ≥16-carbon fatty acids (Kd < 70 nM). Comparison of palmitate binding studies revealed that FABP1 bound the lipid >100-fold more tightly than P450 4A11. Tight binding of P450 4A11 to Alexa-488 dye-labeled FABP1 was observed in fluorescence assays, and the interaction was dependent on ionic strength (Kd 3-124 nM). Kinetic studies with Alexa-FABP1 indicated that the rate of protein-protein association is fast (∼2 s-1), and a palmitate delivery experiment suggested that substrate transfer (from FABP1 to P450) is not rate-limiting. From these results we constructed a kinetic model of the FABP1-P450 interaction and applied it to a catalytic study of FABP1 on P450 4A11 palmitate ω-hydroxylation, the results of which conclusively rejected the free ligand hypothesis. Our results are explained by a direct transfer model in which lipid-bound FABP1 interacts with P450 4A11, transfers the substrate, and a slower P450 conformational change follows to position the molecule in a mode for oxidation. Given the limited free lipid pool in vivo, interaction with FABP1 may be a dominant mechanism by which P450 4A11 accesses its substrates and may offer a novel means to target P450 4A11 activity.

Tissue-Specific Ablation of Liver Fatty Acid-Binding Protein Induces a Metabolically Healthy Obese Phenotype in Female Mice.

Obesity is associated with numerous metabolic complications including insulin resistance, dyslipidemia, and a reduced capacity for physical activity. Whole-body ablation of liver fatty acid-binding protein (LFABP) in mice was shown to alleviate several of these metabolic complications; high fat (HF) fed LFABP knockout (LFABP -/- ) mice developed higher fat mass than their wild-type (WT) counterparts but displayed a metabolically healthy obese (MHO) phenotype with normoglycemia, normoinsulinemia, and reduced hepatic steatosis compared with WT. LFABP is expressed in both liver and intestine, thus in the present study, LFABP conditional knockout (cKO) mice were generated to determine the contributions of LFABP specifically within the liver or the intestine to the whole body phenotype of the global knockout. Female liver-specific LFABP knockout (LFABP liv-/- ), intestine-specific LFABP knockout (LFABP int-/- ), and floxed LFABP (LFABP fl/fl ) control mice were fed a 45% Kcal fat semipurified HF diet for 12 weeks. While not as dramatic as found for whole-body LFABP -/- mice, both LFABP liv-/- and LFABP int-/- mice had significantly higher body weights and fat mass compared with LFABP fl/fl control mice. As with the global LFABP nulls, both LFABP liv-/- and LFABP int-/- mice remained normoglycemic and normoinsulinemic. Despite their greater fat mass, the LFABP liv-/- mice did not develop hepatic steatosis. Additionally, LFABP liv-/- and LFABP int-/- mice had higher endurance exercise capacity when compared with LFABP fl/fl control mice. The results suggest, therefore, that either liver-specific or intestine-specific ablation of LFABP in female mice is sufficient to induce, at least in part, the MHO phenotype observed following whole-body ablation of LFABP.

Nb-FAR-1: A key developmental protein affects lipid droplet accumulation and cuticle formation in Nippostrongylus brasiliensis.

Fatty acid and retinol binding proteins (FARs) are lipid-binding protein that may be associated with modulating nematode pathogenicity to their hosts. However, the functional mechanism of FARs remains elusive. We attempt to study the function of a certain FAR that may be important in the development of Nippostrongylus brasiliensis. Nb-FAR-1 was highly expressed throughout developmental stages by RNA-seq data and qPCR analyses, and Nb-FAR-1 was a secretory protein and abundant in the excretory-secretory products. Nb-FAR-1 could bind fatty acids and retinol. Fatty acid pattern of parasitic adults was more similar to rat intestine than to free-living L3s, indicating that N. brasiliensis may be dependent on the host to obtain fatty acids. Lentivirus-mediated RNAi was performed on L3s, resulting in a reduction in the expression of Nb-far-1 gene. Furthermore, these RNAi effects could be maintained in several generations. The offspring L3s in Nb-far-1 RNAi group had a reduction in lipid droplets within the subcuticle and the swelling of the perioral epidermis, accompanied with down-regulated expression of enzymes in amino acid and glycerolipid metabolism and glycometabolism for growth by RNA-seq data. Adults in Nb-far-1 RNAi group had the crumpled epidermis loosely attached to the basal membrane of body surface and the breakage of mouth epidermis, accompanied with a decrease in adult egg-shedding and an appearance of abnormal eggs. In vitro culture of eggs showed decreased efficiency of egg hatchability and larval development in the Nb-far-1 RNAi group. Transcriptomic analysis showed that interference with Nb-far-1 expression induced downregulated expression of major sperm protein and serpin for reproduction, and collagen for epidermis formation in adults, most of which were relatively high expression in adults but low expression in L3s in the WT group. Thus, Nb-FAR-1 may affect the reproduction, growth, and development of N. brasiliensis by regulating the level of lipids.

Uncovering the potential of Fatty Acid Binding Proteins for predicting radiation-induced gastrointestinal injury

Uncovering the potential of Fatty Acid Binding Proteins for predicting radiation-induced gastrointestinal injury

Assessing the impact of conformational perturbants on folding and aggregation pathways of a β-barrel fold.

Here we explore the interplay between physical and chemical perturbants to unravel links among native folding, amorphous and ordered aggregation scenarios in IFABP (rat intestinal fatty acid binding protein). This small beta-barrel protein undergoes amyloid-like aggregation above 15% v/v trifluoroethanol. Our aim was to address the influence of sub-aggregating TFE concentrations on the unfolding transitions of IFABP. The urea-induced unfolding process can bona fide be considered a two-state transition where no aggregation takes place. On the other hand, with GdmCl, the appearance of amyloid-like aggregation becomes evident upon TFE challenge. Temperature-induced denaturation profiles show that both additives, TFE and GdmCl decrease protein stability. Whereas amorphous aggregation occurs upon heating in the presence of TFE, no aggregation takes place with GdmCl. Conversely, when both additives are present, amyloid-like aggregation prevails. The explanation for the choice of amorphous or amyloid-like pathways must reconcile the effects of perturbants on both the protein and solvent structures. Key points include the TFE-promoted desolvation of the polypeptide, a process further enhanced by heat. Although GdmCl might prevent amorphous thermal aggregation by solubilizing non-native states, this effect could also favor amyloid aggregation. In addition, the electrolyte-induced segregation of TFE at high enough GdmCl concentration might contribute to the development and/or stabilization of TFE clusters that could act as nucleation-inducing interfaces, thus leading to the observed amyloid aggregation outcome.

Fulvic acid inhibits the differentiation of 3T3-L1 adipocytes by activating the Ca2+/CaMKⅡ/AMPK pathway.

Type 2 diabetes increases the risk of developing obesity. Although fulvic acid alleviates back fat thickness in pigs, the mechanism underlying its anti-obesity effect remains unclear. Therefore, we investigated the anti-obesity mechanism of fulvic acid using 3T3-L1 adipocytes. We examined the effects of fulvic acid on adipocyte differentiation, cell viability, and lipid accumulation using molecular techniques. Fulvic acid treatment significantly decreased intracellular lipid accumulation in 3T3-L1 cells during the differentiation compared with that in the control group. Western blotting revealed fulvic acid-induced downregulated expression of the adipocyte differentiation-related markers peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding protein alpha, and sterol regulatory element-binding protein 1. The fulvic acid treatment decreased the expression of the lipid uptake-related markers fatty acid-binding protein 4 and the cluster of differentiation 36 in 3T3-L1 cells. Moreover, fulvic acid significantly increased cytosolic Ca2+ concentration via Ca2+ sequestration from the endoplasmic reticulum, enhanced Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity, and upregulated AMP-activated protein kinase (AMPK), thereby reducing adipocyte differentiation. Conclusively, fulvic acid attenuates adipocyte differentiation by activating the Ca2+/CaMKⅡ/AMPK pathway, suggesting its anti-obesity potential.

Alzheimer's disease and proteins involved in the transport of fatty acids into the brain. Literature review

Annotation. Alzheimer's disease is a primary cortical degenerative dementia characterized by the formation of extracellular amyloid plaques, intracellular neurofibrillary tangles, and the death of nerve cells. Impaired lipid metabolism plays an important role in the pathogenesis of various neurodegenerative diseases, such as Alzheimer's disease. The goal is to investigate the role of proteins in the transport of fatty acids, particularly long-chain polyunsaturated fatty acids, into the brain and the relationship with the development of neurodegenerative diseases such as Alzheimer's disease. For the scientific review, data from the scientometric databases PubMed, Web of Science, Google Scholar, Crossref, and WorldCat were used, referring mainly to publications from 2005-2023. Many studies have shown that a diet rich in omega-3 polyunsaturated fatty acids can improve cognitive function during normal aging and prevent the development of neurocognitive diseases. However, it is still unclear how polyunsaturated fatty acids are transported from the blood to the brain, or how they are related to cognitive performance. The transport of fatty acids into and out of the central nervous system depends on two major sets of barriers: the blood-brain barrier between the peripheral blood and brain tissue and the blood-CSF barrier. required components are delivered across the blood-brain barrier by several pathways, such as passive diffusion, transcytosis, and transport of fatty acids by transport proteins. There are a number of fatty acid transport proteins: fatty acid translocase/cluster of differentiation 36, caveolin-1, fatty acid-binding proteins, long-chain fatty acid acyl-CoA synthetase, and fatty acid transport proteins. In the course of the review, the importance of various mechanisms and possible pathways of fatty acid transport across the blood-brain barrier and between brain cells in the development of various neurodegenerative diseases was determined. Also, certain types of fatty acid transporter proteins can serve as marker substances for the diagnosis of neurodegenerative diseases.

An electrochemiluminescence biosensor based on silver-cysteine nanorod as an emitter and AgNP-decorated FeMoOν as a signal amplifier for sensitive detection of heart-type fatty acid binding protein

An electrochemiluminescence biosensor based on silver-cysteine nanorod as an emitter and AgNP-decorated FeMoOν as a signal amplifier for sensitive detection of heart-type fatty acid binding protein

Differences in Blood and Cerebrospinal Fluid Between Parkinson’s Disease and Related Diseases

It is difficult to distinguish Parkinson’s disease (PD) in the early stage from those of various disorders including atypical Parkinson’s syndrome (APS), vascular parkinsonism (VP), and even essential tremor (ET), because of the overlap of symptoms. Other, more challenging problems will arise when Parkinson’s disease develops into Parkinson’s disease dementia (PDD) in the middle and late stages. At this time, the differential diagnosis of PDD and DLB becomes thorny. These complicate the diagnostic process for PD, which traditionally heavily relies on symptomatic assessment and treatment response. Recent advances have identified several biomarkers in the blood and cerebrospinal fluid (CSF), including α-synuclein, lysosomal enzymes, fatty acid-binding proteins, and neurofilament light chain, whose concentration differs in PD and the related diseases. However, not all these molecules can effectively discriminate PD from related disorders. This review advocates for a paradigm shift toward biomarker-based diagnosis to effectively distinguish between PD and similar conditions. These biomarkers may reflect the diversity that exist among different diseases and provide an effective way to accurately understand their mechanisms. This review focused on blood and CSF biomarkers of PD that may have differential diagnostic value and the related molecular measurement methods with high diagnostic performance due to emerging technologies.Graphical

Newly Initiated Statin Treatment Is Associated with Decreased Plasma Coenzyme Q10 Level After Acute ST-Elevation Myocardial Infarction.

Coenzyme Q10 (CoQ10) plays a crucial role in facilitating electron transport during oxidative phosphorylation, thus contributing to cellular energy production. Statin treatment causes a decrease in CoQ10 levels in muscle tissue as well as in serum, which may contribute to the musculoskeletal side effects. Therefore, we aimed to assess the effect of newly initiated statin treatment on serum CoQ10 levels after acute ST-elevation myocardial infarction (STEMI) and the correlation of CoQ10 levels with key biomarkers of subclinical or clinically overt myopathy. In this study, we enrolled 67 non-diabetic, statin-naïve early-onset STEMI patients with preserved renal function. Plasma CoQ10 level was determined by ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC/MS-MS), while the myopathy marker serum fatty acid-binding protein 3 (FABP3) level was measured with enzyme-linked immunosorbent assay (ELISA) at hospital admission and after 3 months of statin treatment. The treatment significantly decreased the plasma CoQ10 (by 43%) and FABP3 levels (by 79%) as well as total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B100 (ApoB100), and oxidized LDL (oxLDL) levels. The change in CoQ10 level showed significant positive correlations with the changes in total cholesterol, LDL-C, ApoB100, and oxLDL levels, while it did not correlate with the change in FABP3 level. Our results prove the CoQ10-reducing effect of statin treatment and demonstrate its lipid-lowering efficacy but contradict the role of CoQ10 reduction in statin-induced myopathy.

Urinary fatty acid-binding protein 4 is a promising biomarker for glomerular damage in patients with diabetes mellitus.

Fatty acid-binding protein (FABP) 4, which acts as an adipokine secreted by adipocytes, macrophages, and capillary endothelial cells, is expressed in injured glomerular cells. It has been reported that urinary (U-) FABP4 is associated with renal dysfunction and proteinuria in several glomerular kidney diseases. However, the clinical significance of U-FABP4 in diabetic kidney disease (DKD) remains undetermined. Immunohistological analyses of FABP4 and FABP1 (liver-type FABP), an established biomarker for impaired proximal tubules, were performed in the kidneys of patients with DKD and nonobese diabetic mice (KK-Ta/Akita mice). The associations between U-FABP4 and U-FABP1 with kidney function and metabolic indices were also investigated in patients with type 1 diabetes (n = 57, mean age: 61 years) and patients with type 2 diabetes (n = 608, mean age: 65 years). In both patients with diabetes and diabetic mice, FABP4 was expressed in injured glomeruli with increased markers of endoplasmic reticulum stress in addition to peritubular capillaries, whereas FABP1 was mainly expressed in proximal tubules. Levels of U-FABP4 and U-FABP1 were independently associated with each other, and both levels were independently associated with estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR) after adjustment of age, sex, type of diabetes, duration of diabetes, and systolic blood pressure in patients with diabetes. Urinary level of FABP4 derived from injured glomeruli with increased endoplasmic reticulum stress is independently associated with eGFR and UACR, suggesting a promising biomarker for glomerular damage in patients with diabetes.