Free Fatty Acids Research Articles

Loss of Cdkn1a protects against MASLD alone or with alcohol intake by preserving lipid homeostasis

Background & AimExpression of P21, encoded by the CDKN1A gene, has been associated with fibrosis progression in steatotic liver disease (SLD); however, the underlying mechanisms remain unknown. In the present study, we investigated the function of CDKN1A in SLD. MethodsCDKN1A expression levels were evaluated in different patients‘ cohorts with SLD, fibrosis, and advanced chronic liver disease (ACLD). Cdkn1a-/- and Cdkn1a+/+ mice were fed with either a Western diet (WD), a Lieber-DeCarli (LdC) diet plus multiple EtOH binges, or a DuAL diet. Primary hepatocytes were isolated and functional assays performed. ResultsA significant increase in CDKN1A expression was observed in patients with steatohepatitis and fibrosis (with a positive correlation with both NAS and fibrosis staging scores), cirrhosis and ACLD. Cdkn1a+/+ mice, fed a DuAL diet exhibited liver injury and cell death increased reactive oxygen species (ROS), and markers of senescence (γH2AX, β-GAL, Cdkn1a/p53) contributing to steatosis and inflammation. In contrast, Cdkn1a-/- mutant mice showed a significant decrease in senescence-associated markers as well as in markers of liver injury, hepatic steatosis and an increase in – fatty acid oxidation (FAO) and reduction in free fatty acid (FFA) uptake as well as de novo lipogenesis. Mechanistically, activation of the AMPK-SIRT3 was observed in Cdkn1a-deleted animals. ConclusionsCdkn1a deletion protected against preclinical SLD by promoting FAO and preventing FFA uptake and de novo lipogenesis via the AMPK-SIRT3 axis. CDKN1A expression was found to be directly correlated with increased severity of NAS and fibrosis in SLD patients. CDKN1A could be a potential theragnostic target for the treatment of metabolic dysregulation in SLD patients, with and without alcohol consumption.

Synergistic effects of gamma irradiation and butylated hydroxyanisole on the sensory, physicochemical, and microbiological quality of beef

The objective of this study was to investigate the impact of gamma irradiation, in combination with the synthetic antioxidant butylated hydroxyanisole (BHA), on the safety and quality characteristics of refrigerated beef. The samples were divided into four treatment groups, which were subjected to marinating with 0.01% BHA and gamma irradiation at different dosages. The treatment groups were labeled as follows: T0 (control, non-irradiated), T1 (3 kGy), T2 (5 kGy), and T3 (7 kGy). The specimens in each group were stored under refrigerated conditions at a temperature of 4°C for intervals of 0, 5, 10, or 15 days. Data analyses were conducted using a Completely Randomized Design (CRD) with a 4 × 4 factorial experiment. The experiment consisted of two factors, each with four treatments, and was reproduced three times with a 4-day gap. The instrumental color value CIE: lightness (L*), redness (a*) and yellowness (b*) and physicochemical properties, including pH, drip loss, cook loss, extract release volume, and water holding capacity, were analyzed. The proximate components, including dry matter (DM), crude protein (CP), ether extract (EE), ash, and moisture, were found to have a significant effect (p < 0.01)(p < 0.01) among treatment groups, time intervals, and their interaction. Free fatty acids (FFA), peroxide value (POV), and thiobarbituric acid reactive substances (TBARS) significantly increased (p < 0.01)(p < 0.01)(p < 0.01) among treatments and over the course of storage. Following the irradiation with BHA, there was a notable reduction in microbial populations and a delay in lipid oxidation. The sensory characteristics stipulated that both the control samples and the samples treated with BHA were more favored than the irradiated samples as the storage time progressed. Although treatment may cause some changes in the sensory characteristics of the meat, the samples were deemed suitable for refrigerated storage for a maximum duration of 10 days. In summary, the utilization of irradiation in conjunction with BHA presents a possible avenue for enhancing the quality and safety of refrigerated beef storage, hence offering promising applications within the meat sector.

Ubiquitin-specific peptidase 25 ameliorates hepatic steatosis by stabilizing peroxisome proliferator-activated receptor alpha

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. USP25 in adipocytes has been proven to be involved in insulin resistance, a noteworthy characteristic of NAFLD. However, the roles of USP25 in NAFLD remain unclear. In this study, we aimed to elucidate the role of USP25 in NAFLD. Hepatic USP25 protein levels were measured in NAFLD patients and models. USP25 expression was manipulated in both mice and cells to evaluate its role in NAFLD. A downstream target of USP25 in NAFLD progression was identified through proteomic profiling analyses and confirmed. Additionally, a USP25 inhibitor was used to determine whether USP25 could be a viable treatment target for NAFLD. We found that USP25 protein levels were significantly decreased in the livers of NAFLD patients and NAFLD model mice. USP25 protein levels were also decreased in both mouse primary hepatocytes and Huh7 cells treated with free fatty acids (FFAs). We also found that Usp25 knockout mice presented much more severe hepatic steatosis when they were fed a high-fat diet. Similarly, knocking down USP25 in Huh7 cell lines aggravated FFA-induced steatosis, whereas USP25 overexpression ameliorated FFA-induced steatosis in Huh7 cell lines. Further proteomic profiling revealed that the PPARα signaling pathway was a downstream target of USP25, which was confirmed in both mice and cell lines. Moreover, USP25 could stabilize PPARα by promoting its deubiquitination. Finally, a USP25 inhibitor exacerbated diet-induced steatosis in mice. In conclusion, USP25 may play a role in NAFLD through the PPARα signaling pathway and could be a potential therapeutic target for NAFLD.

Lipids: A Major Culprit in Diabetic Nephropathy.

The pathophysiology of diabetic nephropathy (DN) is too complex and involves a variety of pathways and mediators. Hyperglycaemia and dyslipidemia are identified as major risk factors for diabetic nephropathy. Various studies revealed the fact that dyslipidemia is a major contributor to the process of diabetic nephropathy. Dyslipidemia refers to abnormal lipid levels. Lipids like LDL, free fatty acids, abnormal lipoproteins, ceramides, etc., are unsafe for kidneys. They target proximal tubular epithelial cells, podocytes, and tubulointerstitial tissues through biochemical changes, especially by enhancing the release of reactive oxygen species (ROS) and lipid peroxidation, endorsing tissue inflammation and mitochondrial damage, which give rise to nephropathy. Major lipid targets identified are SREBP1, LXR, FXR PPAR, CD-36, PKc, AGE/RAGE pathway, and ferroptosis. The drug acting on these targets has shown improvement in DN patients. Various preclinical and clinical studies support the fact that hyperlipidemic agents are promising targets for DN. Therefore, in conjunction with other standard therapies, drugs acting on dyslipidemia can be added as a part of the regimen in order to prevent the incidence of ESRD and CVD.

Review on the role of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway in diabetes: mechanistic insights and therapeutic implications.

This review explores the pivotal role of the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome in the pathogenesis of diabetes and its complications, highlighting the therapeutic potential of various oral hypoglycemic drugs targeting this pathway. NLRP3 inflammasome activation, triggered by metabolic stressors like hyperglycemia, hyperlipidemia, and free fatty acids (FFAs), leads to the release of pro-inflammatory cytokines interleukin-1β and interleukin-18, driving insulin resistance, pancreatic β-cell dysfunction, and systemic inflammation. These processes contribute to diabetic complications such as nephropathy, neuropathy, retinopathy, and cardiovascular diseases (CVD). Here we discuss the various transcriptional, epigenetic, and gut microbiome mediated regulation of NLRP3 activation in diabetes. Different classes of oral hypoglycemic drugs modulate NLRP3 inflammasome activity through various mechanisms: sulfonylureas inhibit NLRP3 activation and reduce inflammatory cytokine levels; sodium-glucose co-transporter 2 inhibitors (SGLT2i) suppress inflammasome activity by reducing oxidative stress and modulating intracellular signaling pathways; dipeptidyl peptidase-4 inhibitors mitigate inflammasome activation, protecting against renal and vascular complications; glucagon-like peptide-1 receptor agonists attenuate NLRP3 activity, reducing inflammation and improving metabolic outcomes; alpha-glucosidase inhibitors and thiazolidinediones exhibit anti-inflammatory properties by directly inhibiting NLRP3 activation. Agents that specifically target NLRP3 and inhibit their activation have been identified recently such as MCC950, Anakinra, CY-09, and many more. Targeting the NLRP3 inflammasome, thus, presents a promising strategy for managing diabetes and its complications, with oral hypoglycemic drugs offering dual benefits of glycemic control and inflammation reduction. Further research into the specific mechanisms and long-term effects of these drugs on NLRP3 inflammasome activity is warranted.

The synergistic potential of polyethylene glycol 400 for the control of Hyphantria cunea larvae by Beauveria bassiana

The efficacy of entomopathogenic fungi as pest control agents is constrained by both their physiological state and external environmental factors. This study identified synergists capable of enhancing the insecticidal activity of Beauveria bassiana (Bb) and investigated the underlying synergistic mechanisms. Our results found that among 6 potential synergists, polyethylene glycol 400 (PEG) and trehalose significantly improved Bb's lethality against Hyphantria cunea larvae, with PEG demonstrating the most pronounced effect. PEG treatment markedly increased Bb spore adhesion and germination rates, while spore hydrophobicity and growth rates remained unaffected. Moreover, PEG-treated spores exhibited higher thermal tolerance compared to untreated ones. In the Bb + PEG treatment group, the hemocyte count, encapsulation and melanization activities, and the expression of related regulatory genes were significantly lower than those in the Bb treatment group. Additionally, pathogen recognition, signal transduction, and humoral immunity effector genes expression were markedly suppressed in the Bb + PEG group. A significant reduction in the content of total amino acids, free fatty acids, glucose, and trehalose, alongside decreased expression of key regulatory genes in the tricarboxylic acid cycle and glycolysis pathways, was observed in the Bb + PEG treatment group. Furthermore, PEG enhanced Bb-induced apoptosis in H. cunea larvae, as evidenced by the upregulation of apoptosis-related genes. Notably, PEG alone did not significantly impact the innate immunity, energy metabolism, or apoptosis in H. cunea larvae. Overall, PEG exhibits considerable potential in amplifying Bb's insecticidal activity by directly optimizing spore performance and indirectly modulating the larvae's innate immunity, energy metabolism, and apoptosis.

Pde3a and Pde3b regulation of murine pulmonary artery smooth muscle cell growth and metabolism.

A role for metabolically active adipose tissue in pulmonary hypertension (PH) pathogenesis is emerging. Alterations in cellular metabolism in metabolic syndrome are triggers of PH-related vascular dysfunction. Metabolic reprogramming in proliferative pulmonary vascular cells causes a metabolic switch from oxidative phosphorylation to glycolysis. PDE3A and PDE3B subtypes in the regulation of metabolism in pulmonary artery smooth muscle cells (PASMC) are poorly understood. We previously found that PDE3A modulates the cellular energy sensor, AMPK, in human PASMC. We demonstrate that global Pde3a knockout mice have right ventricular (RV) hypertrophy, elevated RV systolic pressures, and metabolic dysfunction with elevated serum free fatty acids (FFA). Therefore, we sought to delineate Pde3a/Pde3b regulation of metabolic pathways in PASMC. We found that PASMC Pde3a deficiency, and to a lesser extent Pde3b deficiency, downregulates AMPK, CREB and PPARγ, and upregulates pyruvate kinase dehydrogenase expression, suggesting decreased oxidative phosphorylation. Interestingly, siRNA Pde3a knockdown in adipocytes led to elevated FFA secretion. Furthermore, PASMC exposed to siPDE3A-transfected adipocyte media led to decreased α-SMA, AMPK and CREB phosphorylation, and greater viable cell numbers compared to controls under the same conditions. These data demonstrate that deficiencies of Pde3a and Pde3b alter pathways that affect cell growth and metabolism in PASMC.

Biopolymeric emulsions with added silicon as pork fat substitutes in the reformulation of healthy pâtés: Effect on technological, nutritional and sensory properties and on lipid digestibility after in vitro gastrointestinal digestion

Four different pork lard emulsions were elaborated in order to be used as pork backfat replacers in the reformulation of healthy pâtés: an emulsion stabilized with soy protein concentrate (SPC, E1), E1 with added silicon (Si) (E2), E1 with a mixture of methylcellulose (MC) and carboxymethylcellulose (CMC) (E3), and E3 with added Si (E4). These four emulsions were characterized in terms of texture, color and in vitro gastrointestinal digestion (GID) and were then used in the reformulation of four pork liver pâtés (PE1-PE4). These pâtés were compared to a control pâté elaborated with 100% pork backfat (PC). The technological, nutritional and sensory properties of the pâtés were assessed, along with lipid digestibility based on the content of free fatty acids (FFAs) released after in vitro GID. The reformulated pâtés had highly adequate physicochemical and sensory properties, comparable to those of the PC control. The addition of a mixture of MC/CMC and Si in the SPC-stabilized emulsion caused a slow down of in vitro GID and, consequently, lower lipid bioaccessibility (BA) of the main fatty acids when E3 and E4 were incorporated into the reformulated pâtés PE3 and PE4. Si BA was higher in the absence of cellulose ethers (14.6%) that in their presence (8.84%).

Porous polymeric materials prepared via pickering emulsion templating targeted as a bronsted acid catalyst in room-temperature biodiesel production

The present work is about preparing a set of magnetic macroporous polymers using the Pickering high internal phase w/o emulsions (HIPEs) templating method. The octyl-modified core-shell magnetic nanoparticles (Fe3O4@SiO2-Octyl) were used as a solid stabilizer and Span 80 surfactant to stabilize the HIPEs. The effect of Fe3O4@SiO2-Octyl content, Span 80 content, and molar ratio of styrene/divinylbenzene (St/DVB) on physical properties, morphology, pore size, and void size of the macroporous polyHIPEs was precisely evaluated. The optimized polyHIPE prepared by 2 wt% of Fe3O4@SiO2-Octyl nanoparticles, 9 wt% of Span 80, and St/DVB molar ratio of 8 with the porosity of 86±1.1 % and an average pore size of 4.1 µm was selected as catalyst support to functionalize with sulfonic acid groups. The resulting catalyst (polyHIPE–SO3H) showed excellent performance in reacting long-chain free fatty acids (FFA) with methanol to give fatty acid monoalkyl esters (FAMEs) at room temperature. In this way, the polyHIPE–SO3H was found to be very active and reusable in the mentioned process, giving high yields (∼92–98 %) of various biodiesel compounds under very mild reaction conditions and recycling in the next subsequent runs without significant loss of activity.

Effect of inoculation with different Eurotium cristatum strains on the microbial communities and volatile organic compounds of Fu brick tea

Eurotium cristatum is the primary fungus in Fu brick tea (FBT) and plays a crucial role in its special flavor. This study investigated the effect of inoculation with different E. cristatum strains (i.e., ZJ, GX, GZ, HN, and SX) on the microbial communities and volatile organic compounds (VOCs) of FBT. A total of 113 VOCs were identified in all samples, with the concentration of VOCs (alcohols, aldehydes, and ketones) significantly higher in GXE FBT than in other samples. The core VOCs of GXE (19), GZE (16), HNE (19), SXE (15), and ZJE (13) FBT were identified using orthogonal partial least squares discriminant analysis and relative odor activity value (ROAV) analysis. Methional (a27), butanal (a41), 1-octen-3-one (a69), and ethyl acetate (a77) were key markers for inoculated FBTs, and 1-octen-3-ol, dimethyl disulfide, and acetoin-M were the specific markers of HNE. Linalool and (E)-2-octenal were particularly prominent in GXE, and isoamyl acetate-D was an important aroma component of GZE. Differences in microbial diversity were observed among the different inoculated fermented FBTs, and E. cristatum inoculation remarkably influenced the richness and diversity of bacterial communities. The VOCs were closely associated with fungi and bacteria, and 19 potentially dominant microorganisms (10 fungal and 9 bacterial genera) correlated with VOCs were identified. Among them, Aspergillus (fungi) and Pseudomonas (bacteria) exerted the greatest role. The FBT inoculated with E. cristatum from ZJ had the highest content of theaflavins and theabrownins, which intensified the red and yellow colors of the tea. E. cristatum greatly decreased the free amino acids and fatty acids, contributing to the aroma formation of FBT. Therefore, inoculating FBT with E. cristatum remarkably influenced the microbial communities and improved its flavor profile. This work provides a theoretical foundation on the role of E. cristatum in the formation and regulation of FBT flavor.

Sensing steroid hormone 17α-hydroxypregnenolone by GPR56 enables protection from ferroptosis-induced liver injury.

G protein-coupled receptors (GPCRs) mediate most cellular responses to hormones, neurotransmitters, and environmental stimulants. However, whether GPCRs participate in tissue homeostasis through ferroptosis remains unclear. Here we identify that GPR56/ADGRG1 renders cells resistant to ferroptosis and deficiency of GPR56 exacerbates ferroptosis-mediated liver injury induced by doxorubicin (DOX) or ischemia-reperfusion (IR). Mechanistically, GPR56 decreases the abundance of phospholipids containing free polyunsaturated fatty acids (PUFAs) by promoting endocytosis-lysosomal degradation of CD36. By screening a panel of steroid hormones, we identified that 17α-hydroxypregnenolone (17-OH PREG) acts as an agonist of GPR56 to antagonize ferroptosis and efficiently attenuates liver injury before or after insult. Moreover, disease-associated GPR56 mutants were unresponsive to 17-OH PREG activation and insufficient to defend against ferroptosis. Together, our findings uncover that 17-OH PREG-GPR56 axis-mediated signal transduction works as a new anti-ferroptotic pathway to maintain liver homeostasis, providing novel insights into the potential therapy for liver injury.

Caveolin-1 ameliorates hepatic injury in non-alcoholic fatty liver disease by inhibiting ferroptosis via the NOX4/ROS/GPX4 pathway

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease globally, with a complex and contentious pathogenesis. Caveolin-1 (CAV1) is an important regulator of liver function and can mitigate liver injury by scavenging reactive oxygen species (ROS). Evidence suggests that NOX4 is a source of ROS production, that oxidative stress and ferroptosis are closely related, and that both are involved in the onset and progression of NAFLD. However, whether CAV1 attenuates liver injury in NAFLD caused by high-fat diet via the NOX4/ROS/GPX4 pathway remains unclear. An in vivo fatty liver model was established by feeding mice with a high-fat diet for 16 weeks. In addition, an in vitro fatty liver model was established by incubating AML-12 cells with free fatty acids for 24 h using an in vitro culture method. In our study, it was observed that a high-fat diet induces mitochondrial damage and worsens oxidative stress in NAFLD. This diet also hinders GPX4 expression, leading to an escalation of ferroptosis and lipid accumulation. To counteract these effects, intraperitoneal administration of CSD peptide in mice attenuated the high-fat diet-induced liver mitochondrial damage and ferroptosis. Likewise, overexpression of CAV1 resulted in an increase in GPX4 expression and a reduction in levels of ROS-mediated iron metamorphosis, thus mitigating the progression of the disease. However, the effects of CAV1 on GPX4-mediated ferroptosis and lipid deposition could be reversed by CAV1 small interfering RNA (SiRNA). Finally, NOX4 inhibitor (GLX351322) treatment increased CAV1 siRNA-mediated GPX4 expression and decreased the level of ROS-mediated ferroptosis. These findings suggest a potential mechanism underlying the protective role of CAV1 against high-fat diet-induced hepatotoxicity in NAFLD, shedding new light on the interplay between CAV1, GPX4, and ferroptosis in liver pathology

Constructing stable emulsion gel from gelatin and sodium alginate as pork fat substitute: Emphasis on lipid digestion in vitro

This study aimed to develop a gelatin-sodium alginate (G-SA) emulsion gel that can efficiently hold corn oil, as a substitute for pork fat while controlling the digestive behaviors of lipids in vitro. UV, fluorescence, and circular dichroism spectra and surface hydrophobicity measurements of the G-SA mixtures indicated that gelatin and sodium alginate primarily form aggregates through hydrogen bonds and hydrophobic interactions, and the optimum gelatin-to-sodium alginate w/w ratio was identified as 1.9. The final emulsion gel contained 3.15% gelatin and 1.65% sodium alginate (w/w) with a corn oil content of 40% (w/w). G-SA emulsion gel had a higher proportion of polyunsaturated fatty acids (PUFAs, 53.95 g/100 g) than pork fat (15.17 g/100 g). In addition, the G-SA emulsion gel exhibited stable viscoelastic properties without storage and loss moduli changes at increasing shear rates. The G-SA emulsion gel had a higher melting temperature (42.63 °C) than pork fat (35.07 °C). In vitro digestion studies showed that corn oil had a higher free fatty acid release (40.32%) compared to the G-SA emulsion gel (12.66%) and pork fat (8.53%) (P<0.05), indicating that the digestibility of corn oil was reduced in the G-SA emulsion gel. Calcein release experiments revealed that G-SA emulsion gel released the least amount of calcein (P<0.05) during digestion at a slow rate. The G-SA emulsion gel, similar to pork fat, contained evenly distributed digestive particles encapsulating corn oil after in vitro gastric digestion, with the smallest particle size among the treatments. After the in vitro small intestinal digestion phase, the G-SA emulsion gel maintained small droplet sizes with bridging flocculation. The in vitro digesta of the G-SA emulsion gel contained a significantly higher proportion of PUFAs compared to pork fat (P<0.05). Consequently, the G-SA emulsion gel can be a potential substitute for pork fat, offering higher proportions of PUFAs, lower fat content, and controlled lipid digestion with reduced lipid digestibility.

Palmitoleate protects against Lipopolysaccharide-induced Inflammation and Inflammasome Activity

Inflammation is part of natural immune defense mechanism against any form of infection or injury. However, prolonged inflammation could perturb cell homeostasis and contribute to the development of metabolic and inflammatory diseases including maternal obesity, diabetes, cardiovascular diseases, and metabolic dysfunction-associated steatotic liver diseases. Polyunsaturated fatty acids have been shown to mitigate inflammatory response by generating specialized pro-resolving lipid mediators which take part in resolution of inflammation. Here, we show that palmitoleate, an omega-7 monounsaturated fatty acid exerts anti-inflammatory properties in response to lipopolysaccharide (LPS)-mediated inflammation. Exposure of bone-marrow derived macrophages (BMDMs) to LPS or TNFα induces robust increase in the expression of pro-inflammatory cytokines and supplementation of palmitoleate inhibited LPS-mediated upregulation of pro-inflammatory cytokines. We also observed that palmitoleate was able to block LPS+ATP-induced inflammasome activation mediated cleavage of pro-caspase 1 and pro-interleukin (IL)-1β. Further, treatment of palmitoleate protects against LPS-induced inflammation in human THP-1 derived macrophages and trophoblasts. Co-exposure of LPS and palmitate (saturated free fatty acid) induces inflammasome and cell death in BMDMs, however, treatment of palmitoleate blocked LPS and palmitate-induced cell death in BMDMs. Further, LPS and palmitate together results in the activation of mitogen activated protein kinases (MAPK) and pretreatment of palmitoleate inhibited the activation of MAPKs and nuclear translocation of nuclear factor kappa B (NF-kB) in BMDMs. In conclusion, palmitoleate shows anti-inflammatory properties against LPS-induced inflammation and LPS+palmitate/ATP-induced inflammasome activity and cell death.

Impacts of Seasons and Regions on the Physicochemical, Microbiological and Sensory Characteristics of Kars Fresh Kashar Cheeses

This study aimed to investigate the physicochemical, microbiological, and sensorial characteristics of Kars Kashar cheeses produced in different regions and seasons, elucidating the impact of these two variables on cheese quality. Significant differences were determined among samples in various parameters, including pH value, dry matter, fat in dry matter, salt, ash, total free fatty acids, water soluble nitrogen, 12% trichloroacetic acid-soluble nitrogen (% of total nitrogen), 5% phosphotungstic acid-soluble nitrogen (% of total nitrogen) contents, L*, a*, b* values, total aerobic mesophilic bacteria and mold counts (p<0.05). Statistical results show that there were no considerable differences between cheeses in terms of sensory properties (p>0.05). In general, summer samples exhibited higher levels of dry matter, fat, ash, salt, and total free fatty acids compared to spring samples. However, the converse was observed regarding protein values, where spring samples demonstrated higher levels than those collected during summer.

Effects of imeglimin on fasting blood free fatty acids concentration

Effects of imeglimin on fasting blood free fatty acids concentration

Supercritical CO2 as a green technology for carotenoids-rich virgin palm oil production: Process optimization, kinetics and thermodynamics modeling

The experimental conditions of supercritical carbon dioxide (scCO2) extraction of virgin palm oil (VPO) from oil palm mesocarp fiber (OPMF) were optimized using the Response Surface Methodology (RSM). Results showed that a maximum of 28.68% of VPO extraction was obtained at the optimal experimental conditions of scCO2 extraction: pressure of 31MPa, temperature of 340K, and extraction time of 80min. The second-order rate equation, Arrhenius equation and Eyring theory were employed to assess the kinetics behaviour, activation energy and thermodynamics behaviour of scCO2 extraction of VPO from oil palm mesocarp fiber. The lower activation energy value (12.17kJ/mol) of scCO2 for the extraction of VPO from OPMF indicates that the scCO2 extraction technology is less dependent on temperature during the extraction of VPO from OPMF. The physicochemical properties and fatty acids compositions analyses reveal that the scCO2 extracted VPO contains high carotenoids content (982μg/g), low free fatty acids content (0.31wt.%), higher oxidative stability and higher unsaturated fatty acids content.

Analyses of the physicochemical and sensory characteristics of black goat triceps brachii muscle based on slaughter age

In this study, we aimed to analyze the effects of slaughter age on black goat meat's physicochemical and nutritional characteristics. Goats (age: 3, 6, 9, 12, 24, and 36 months) reared under identical conditions were used in this study. The key parameters were analyzed, including color, cooking yield, shear force, free amino acid (FAA) levels, free fatty acid levels, and sensory attributes. Hue values decreased, whereas redness increased with age. Umami and sweet FAA levels increased with age, and bitter FAA levels increased from 9 months. The flavor scores increased with age up to 9 months. Off-flavors were significantly higher in goats aged 24 and 36 months than in those aged 3 and 6 months. Goats aged 9 and 12 months had significantly higher texture scores than those aged 3, 6, and 36 months. Overall, our findings suggest that goats aged 9 and 12 months exhibit the best sensory qualities.

AKR7A5 knockout promote acute liver injury by inducing inflammatory response, oxidative stress and apoptosis in mice.

Alcohol liver disease has become a worldwide critical health problem. The ingested alcohol could be converted into acetaldehyde or combined with free fatty acids to induce the endoplasmic reticulum oxidative stress in the liver. Coincidentally, AKR7A5 has both aldehyde detoxification and antioxidant effects. Therefore, we discuss the possible role and mechanism of AKR7A5 in the acute alcohol injury of mice liver. There were four experiment groups, the C57BL/6 mice of wild-type mice (WT) or AKR7A5-/- mice (KO) were intragastrically administrated with saline or 50% ethanol at 14 mL/kg, respectively. Compared to the WT + alcohol group, abnormal liver function, disordered hepatic cord, severe congestion in the hepatic sinus and the space of the hepatic cord, occurrence of oxidative stress, DNA damage and different expressions of apoptosis-related proteins were detected in the KO + alcohol group. Meanwhile, the biological process enrichment analysis showed that the down-regulated proteins were related to the metabolism of fatty acid, the up-regulated proteins positive regulation of reactive oxygen species metabolic process, negative regulation of coagulation and haemostasis. In conclusion, single ethanol binge combined with the absence of AKR7A5 caused more severe inflammatory response, oxidative stress, apoptosis of endogenous pathways, abnormal lipids metabolism and disordered coagulation in mice liver.

Enteroendocrine cell-derived peptide YY signalling is stimulated by pinolenic acid or Intralipid and involves coactivation of fatty acid receptors FFA1, FFA4 and GPR119

Long chain fatty acids are sensed by enteroendocrine L cells that express free-fatty acid receptors, including FFA1, FFA4 and the acylethanolamine receptor GPR119. Here we investigated the acute effects of single or multiple agonism at these G protein-coupled receptors in intestinal mucosae where L cell-derived peptide YY (PYY) is anti-secretory and acts via epithelial Y1 receptors. Mouse ileal or colonic mucosae were mounted in Ussing chambers, voltage-clamped and the resultant short-circuit current (Isc) recorded continuously. The agonists used were; FFA1, TAK-875 or AM-1638; for FFA4, Merck A; or for GPR119, AR231453, PSN632408 or AR440006. Their responses were compared with those of pinolenic acid (PA, a presumed dual FFA1/FFA4 agonist) and the lipid emulsion, Intralipid. The FFA1 agonist AM-1638 (EC50 = 38.2 nM) was more potent than TAK-875 (EC50 = 203.1 nM) but exhibited similar efficacy. GPR119 agonism (AR231453) pretreatment enhanced subsequent FFA1 (AM-1638 or TAK-875) and FFA4 (Merck A) signalling. PA (EC50 = 298.2 nM) co-activated epithelial FFA1 and FFA4 and involved endogenous PYY Y1/Y2-receptor mechanisms but desensitisation was observed between PA and high GPR119 agonist concentrations. Apical Intralipid co-activated FFA1, FFA4 and GPR119 with a residual component not being attributable to PYY, or this trio of fatty acid receptors.