Robinetin Alleviates Metabolic Failure in Liver through Suppression of p300-CD38 Axis.

Metabolic abnormalities in the liver are closely associated with diverse metabolic diseases such as non-alcoholic fatty liver disease, type 2 diabetes, and obesity. The aim of this study was to evaluate the ameliorating effect of robinetin (RBN) on the significant pathogenic features of metabolic failure in the liver and to identify the underlying molecular mechanism. RBN significantly decreased triglyceride (TG) accumulation by downregulating lipogenesis-related transcription factors in AML-12 murine hepatocyte cell line. In addition, mice fed with Western diet (WD) containing 0.025% or 0.05% RBN showed reduced liver mass and lipid droplet size, as well as improved plasma insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) values. CD38 was identified as a target of RBN using the BioAssay database, and its expression was increased in OPA-treated AML-12 cells and liver tissues of WD-fed mice. Furthermore, RBN elicited these effects through its anti-histone acetyltransferase (HAT) activity. Computational simulation revealed that RBN can dock into the HAT domain pocket of p300, a histone acetyltransferase, which leads to the abrogation of its catalytic activity. Additionally, knock-down of p300 using siRNA reduced CD38 expression. The chromatin immunoprecipitation (ChIP) assay showed that p300 occupancy on the promoter region of CD38 was significantly decreased, and H3K9 acetylation levels were diminished in lipid-accumulated AML-12 cells treated with RBN. RBN improves the pathogenic features of metabolic failure by suppressing the p300-CD38 axis through its anti-HAT activity, which suggests that RBN can be used as a new phytoceutical candidate for preventing or improving this condition.

Immobilized Candida antarctica lipase B as an sn-1,3 regiospecific biocatalyst for the interesterification of triacylglycerols with fatty acid ethyl esters.

Candida antarctica lipase B (CALB) is regarded as non-regiospecific. This study aimed to investigate the regiospecificity of CALB in the solvent-free interesterification of high-oleic sunflower oil with stearic acid ethyl ester for 1,3-distearoyl-2-oleoylglycerol (SOS)-rich fat preparation using a packed bed reactor. The content ratio of 1,2-distearoyl-3-oleoylglycerol (SSO) to SOS (denoted by SSO/SOS content) obtained using Lipozyme 435 (a commercially immobilized CALB; 0-4.1%), at residence times (1-32 min) was similar to that obtained using Lipozyme RM IM (0-3.0%), but lower than that obtained using Lipozyme TL IM (6.0-39.4%). When immobilized on Lewatit VP OC 1600, Lipozyme CALB had an SSO/SOS content of 0-10.4%, which was greater than that of Palatase 20,000 L (0-1.1%) but was lower than that of Lipozyme TL 100 L (8.8-97.7%). Our findings suggest that immobilized CALB shows distinct sn-1,3 regiospecificity in the interesterification of triacylglycerol with fatty acid ethyl esters.

Schisandrin A in Schisandra chinensis Upregulates the LDL Receptor by Inhibiting PCSK9 Protein Stabilization in Steatotic Model.

Schisandra chinensis extract (SCE) protects against hypocholesterolemia by inhibiting proprotein convertase subtilisin/kexin 9 (PCSK9) protein stabilization. We hypothesized that the hypocholesterolemic activity of SCE can be attributable to upregulation of the PCSK9 inhibition-associated low-density lipoprotein receptor (LDLR). Male mice were fed a low-fat diet or a Western diet (WD) containing SCE at 1% for 12 weeks. WD increased final body weight and blood LDL cholesterol levels as well as alanine transaminase and aspartate aminotransferase expression. However, SCE supplementation significantly attenuated the increase in blood markers caused by WD. SCE also attenuated WD-mediated increases in hepatic LDLR protein expression in the obese mice. In addition, SCE increased LDLR protein expression and attenuated cellular PCSK9 levels in HepG2 cells supplemented with delipidated serum (DLPS). Non-toxic concentrations of schisandrin A (SA), one of the active components of SCE, significantly increased LDLR expression and tended to decrease PCSK9 protein levels in DLPS-treated HepG2 cells. High levels of SA-mediated PCSK9 attenuation was not attributable to reduced PCSK9 gene expression, but was associated with free PCSK9 protein degradation in this cell model. Our findings show that PCSK9 secretion can be significantly reduced by SA treatment, contributing to reductions in free cholesterol levels.

Antiobesity effects of onion (Allium cepa) in subjects with obesity: Systematic review and meta-analysis.

Onions are rich in bioactive compounds and have been found to prevent various chronic diseases, including obesity. We performed a systematic review and meta-analysis to investigate the antiobesity effect of onions. Studies were identified in PubMed/MEDLINE, Embase, Web of Science, and CENTRAL focusing on clinical trials evaluating the antiobesity effects of onion in obese subjects. The risk of bias in the studies was evaluated using Cochrane's Risk of Bias tool. The effect of onions was analyzed using data from the selected studies, and the results were indicated by weighted mean difference with 95% CI. The I 2 static test was used to examine heterogeneity between the studies. A total of 38 studies were reviewed, of which five clinical trials meeting the criteria were selected. As investigational products, onion peels were used in four studies and onions were used in one study. Following systematic review, it was determined that the risk of bias was generally low, and body weight, BMI, waist circumference, and triglyceride levels were significantly reduced in the onion groups compared to the placebo. In conclusion, onion intake had an antiobesity effect by reducing body weight and body fat, and this effect was particularly pronounced with onion peel.

Physiologic and epigenetic effects of nutrients on disease pathways.

BACKGROUND/OBJECTIVES: Epigenetic regulation by nutrients can influence the development of specific diseases. This study sought to examine the effect of individual nutrients and nutrient families in the context of preventing chronic metabolic diseases via epigenetic regulation. The inhibition of lipid accumulation and inflammation by nutrients including proteins, lipids, vitamins, and minerals were observed, and histone acetylation by histone acetyltransferase (HAT) was measured. Correlative analyses were also performed. MATERIALS/METHODS: Nutrients were selected according to information from the Korean Ministry of Food and Drug Safety. Selected nutrient functionalities, including the attenuation of fatty acid-induced lipid accumulation and lipopolysaccharide-mediated acute inflammation were evaluated in mouse macrophage Raw264.7 and mouse hepatocyte AML-12 cells. Effects of the selected nutrients on in vitro HAT inhibition were also evaluated. RESULTS: Nitric oxide (NO) production correlated with HAT activity, which was regulated by the amino acids group, suggesting that amino acids potentially contribute to the attenuation of NO production via the inhibition of HAT activity. Unsaturated fatty acids tended to attenuate inflammation by inhibiting NO production, which may be attributable to the inhibition of in vitro HAT activity. In contrast to water-soluble vitamins, the lipid-soluble vitamins significantly decreased NO production. Water- and lipid-soluble vitamins both exhibited significant inhibitory activities against HAT. In addition, calcium and manganese significantly inhibited lipid accumulation, NO production, and HAT activity. CONCLUSIONS: Several candidate nutrients and their family members may have roles in the prevention of diseases, including hepatic steatosis and inflammation-related diseases (i.e., nonalcoholic steatohepatitis) via epigenetic regulation. Further studies are warranted to determine which specific amino acids, unsaturated fatty acids and lipid-soluble vitamins or specific minerals influence the development of steatosis and inflammatory-related diseases.

Dnmt1/Tet2-mediated changes in Cmip methylation regulate the development of nonalcoholic fatty liver disease by controlling the Gbp2-Pparγ-CD36 axis.

Dynamic alteration of DNA methylation leads to various human diseases, including nonalcoholic fatty liver disease (NAFLD). Although C-Maf-inducing protein (Cmip) has been reported to be associated with NAFLD, its exact underlying mechanism remains unclear. Here, we aimed to elucidate this mechanism in NAFLD in vitro and in vivo. We first identified alterations in the methylation status of the Cmip intron 1 region in mouse liver tissues with high-fat high-sucrose diet-induced NAFLD. Knockdown of DNA methyltransferase (Dnmt) 1 significantly increased Cmip expression. Chromatin immunoprecipitation assays of AML12 cells treated with oleic and palmitic acid (OPA) revealed that Dnmt1 was dissociated and that methylation of H3K27me3 was significantly decreased in the Cmip intron 1 region. Conversely, the knockdown of Tet methylcytosine dioxygenase 2 (Tet2) decreased Cmip expression. Following OPA treatment, the CCCTC-binding factor (Ctcf) was recruited, and H3K4me3 was significantly hypermethylated. Intravenous Cmip siRNA injection ameliorated NAFLD pathogenic features in ob/ob mice. Additionally, Pparγ and Cd36 expression levels were dramatically decreased in the livers of ob/ob mice administered siCmip, and RNA sequencing revealed that Gbp2 was involved. Gbp2 knockdown also induced a decrease in Pparγ and Cd36 expression, resulting in the abrogation of fatty acid uptake into cells. Our data demonstrate that Cmip and Gbp2 expression levels are enhanced in human liver tissues bearing NAFLD features. We also show that Dnmt1-Trt2/Ctcf-mediated reversible modulation of Cmip methylation regulates the Gbp2-Pparγ-Cd36 signaling pathway, indicating the potential of Cmip as a novel therapeutic target for NAFLD.

Short-term Blood Pressure Variability and Incident CKD in Patients With Hypertension: Findings From the Cardiovascular and Metabolic Disease Etiology Research Center-High Risk (CMERC-HI) Study.

RATIONALE & OBJECTIVE: The association between short-term blood pressure variability (BPV) and kidney outcomes is poorly understood. This study evaluated the association between short-term BPV and kidney disease outcomes in people with hypertension. STUDY DESIGN: Prospective observational cohort study. SETTING & PARTICIPANTS: 1,173 hypertensive participants in the Cardiovascular and Metabolic Disease Etiology Research Center-High Risk (2013-2018) Study with estimated glomerular filtration rate (eGFR) ≥60mL/min/1.73m2. EXPOSURE: Short-term BPV assessed by average real variability (ARV). OUTCOME: Composite kidney disease outcome (30% decline in eGFR from baseline, new occurrence of eGFR <60mL/min/1.73m2, or onset of UACR >300mg/g). ANALYTICAL APPROACH: Multivariable Cox regression analyses to evaluate the association between systolic and diastolic BP ARV (SBP-ARV and DBP-ARV) and outcomes. RESULTS: During a median follow-up of 5.4 [4.1-6.5] years, 271 events of the composite kidney disease outcome occurred (46.5 per 1,000 person-years). Multivariable Cox analysis revealed that the highest SBP-ARV and DBP-ARV tertiles were associated with a higher risk of the composite kidney disease outcome than the lowest tertiles, independent of the 24-hour SBP or DBP levels (HR, 1.64 [95% CI, 1.16-2.33], and 1.60 [95% CI, 1.15-2.24] for SBP-ARV and DBP-ARV, respectively). These associations were consistent when SBP-ARV and DBP-ARV were treated as continuous variables (HR per 1.0-unit greater SBP-ARV, 1.03 [95% CI, 1.01-1.06]; HR per 1.0-unit greater DBP-ARV, 1.04 [95% CI, 1.01-1.08]). These associations were consistent, irrespective of subgroups (age, sex, 24-hour SBP or DBP, and moderate albuminuria). However, other measures of short-term BPV including SD, coefficient of variation, and dipping patterns were not associated with the composite kidney disease outcome. LIMITATIONS: Observational study design, the use of single measurement of 24-hour BP, lack of information on changes in antihypertensive medication during the follow-up. CONCLUSIONS: Short-term BPV is associated with the development of a composite kidney disease outcome in hypertensive patients.

Porphyra tenera Protects against PM2.5-Induced Cognitive Dysfunction with the Regulation of Gut Function.

To evaluate the biological effects of Porphyra tenera (P. tenera), we tried to confirm the possibility that the intake of P. tenera could modulate cognitive and intestinal functions in PM2.5-induced cognitive decline mice. P. tenera attenuated PM2.5-induced learning and memory impairment through antioxidant and anti-inflammatory effects by regulating the mitochondrial function and TLR-initiated NF-κB signaling. In addition, P. tenera effectively alleviated Aß production/tau phosphorylation by inhibiting the JNK phosphorylation. Also, the bioactive constituents of P. tenera determined the sulfated galactan, mycosporine-like amino acids (MAAs), and chlorophyll derivatives. Moreover, the bioactive compounds of P. tenera by gut fermentation protected against gut dysbiosis and intestinal tight junction damage with a decrease in inflammatory response and short-chain fatty acid production. Based on these results, our findings suggest that P. tenera with sulfated galactan and MAAs is a potential material for cognitive function improvement.

Effects of Panax ginseng on hyperglycemia, hypertension, and hyperlipidemia: A systematic review and meta-analysis.

Panax ginseng is a medicinal plant is a material with various pharmacological activities and research suggests that it is particularly effective in representative metabolic diseases such as hyperglycemia, hypertension, and hyperlipidemia. Therefore, in this study, systematic review and meta-analysis were performed to investigate the comprehensive effect of P. ginseng on metabolic parameters representing these metabolic diseases. A total of 23 papers were collected for inclusion in the study, from which 27 datasets were collected. The investigational products included P. ginseng and Korean Red ginseng. Across the included studies, the dose ranged from 200 mg to 8 g and the supplementation period lasted from four to 24 weeks. The study subjects varied from healthy adults to those with diabetes, hypertension, obesity, and/or hyperlipidemia. As a result of the analysis, the levels of glucose and insulin area under the curves, % body fat, systolic and diastolic blood pressures, total cholesterol, triglycerides, and low-density lipoprotein cholesterol were significantly reduced in the P. ginseng group as compared with in the placebo group. In conclusion, P. ginseng supplementation may act as an adjuvant to prevent the development of metabolic diseases by improving markers related to blood glucose, blood pressure, and blood lipids.

Tamarixetin Abrogates Adipogenesis Through Inhibiting p300/CBP-Associated Factor Acetyltransferase Activity in 3T3-L1 Preadipocyte Cells.

Tamarixetin (TX) is an O-methylated flavonoid naturally derived from quercetin. TX has bioactive properties; however, whether it shows antilipogenic activity remains unknown. Therefore, in the present study, we aimed to determine the antilipogenic effects of TX using 3T3-L1 adipocytes. The 3T3-L1 adipocytes were cultured in a differentiation medium with or without TX. Lipid accumulation was diminished and the mRNA expression of lipogenesis-related genes was decreased following TX treatment. We found that TX exhibited antilipogenic effects by inhibiting the expression of p300/CBP-associated factor (pCAF), a histone acetyltransferase, as confirmed by pCAF knockdown. Furthermore, TX inhibited both pCAF expression and its activity, thereby reducing the total acetylation level of nonhistone and histone proteins. Finally, TX decreased the expression of CCAAT/enhancer-binding protein alpha and beta (CEBPα and CEBPß), and peroxisome proliferator-activated receptor γ along with pCAF expression during adipogenesis of 3T3-L1 cells in a time-dependent manner. Collectively, our findings suggest that TX is a potent antilipogenic agent derived from natural products and may be used as a pCAF inhibitor.

Barley Sprout Water Extract and Saponarin Mitigate Triacylglycerol Accumulation in 3T3-L1 Adipocytes.

The mechanisms of action responsible for the reported hypolipidemic activity of barley sprouts have yet to be elucidated. The objective of this study was to compare the content of saponarin (the sole flavonoid present in barley sprout leaves), hypolipidemic activity between barley sprout water extract (BSW) and barley sprout ethanol extract (BSE), and the associated relevance to hypolipidemic activity in 3T3-L1 preadipocytes. BSW elicited superior antiadipogenic effects when compared with BSE in MDI mixture [IBMX 0.5 mM + dexamethasone 1 µM + insulin 1 µg/mL]-treated 3T3-L1 preadipocytes. BSW attenuated MDI-mediated triacylglycerol (TAG) accumulation by inhibiting fatty acid synthase (FAS). FAS protein expression was markedly and dose dependently attenuated by BSW, with higher doses suppressing expression to a level equivalent to the controls. BSW also significantly attenuated MDI-mediated increases in the expression of genes involved in TAG synthesis as well as FAS in 3T3-L1 preadipocytes. High-performance liquid chromatography analysis indicated that BSW contains more than four times more saponarin than BSE. Further investigation of saponarin-mediated hypotriacylglycerolemic activity and related gene expression revealed that saponarin significantly inhibited TAG accumulation, which was attributed to reductions in TAG synthesis-related gene expression. Taken together, these findings provide a basis for further development of barley sprout extract for functional health food purposes.

AMPK Activity: A Primary Target for Diabetes Prevention with Therapeutic Phytochemicals.

Diabetes is a metabolic syndrome characterized by inadequate blood glucose control and is associated with reduced quality of life and various complications, significantly shortening life expectancy. Natural phytochemicals found in plants have been traditionally used as medicines for the prevention of chronic diseases including diabetes in East Asia since ancient times. Many of these phytochemicals have been characterized as having few side effects, and scientific research into the mechanisms of action responsible has accumulated mounting evidence for their efficacy. These compounds, which may help to prevent metabolic syndrome disorders including diabetes, act through relevant intracellular signaling pathways. In this review, we examine the anti-diabetic efficacy of several compounds and extracts derived from medicinal plants, with a focus on AMP-activated protein kinase (AMPK) activity.

Black Mulberry Extract Elicits Hepatoprotective Effects in Nonalcoholic Fatty Liver Disease Models by Inhibition of Histone Acetylation.

Epigenetic regulation by histone acetyltransferase (HAT) is associated with various biological processes and the progression of diseases, including nonalcoholic fatty liver disease (NAFLD). The objective of this study was to investigate whether the hypolipidemic properties of black mulberry (Morus atropurpurea Roxb.) fruit extract (BME) contribute toward protection against NAFLD by HAT inhibition. HepG2 cells were treated with oleic and palmitic acids to induce lipid accumulation, which was significantly attenuated by the treatment with BME at 50 and 100 µg/mL. BME also markedly reduced the expression of proteins associated with lipogenesis, which was attributed to the BME-mediated downregulation of lipogenic genes in HepG2 cells. BME significantly inhibited in vitro total HAT and p300 activities. In addition, BME suppressed total acetylated lysine as well as specific histone acetylation of proteins H3K14 and H3K27 in HepG2 cells. Mice were then fed with either a chow diet or western diet (WD), with or without BME (1%, w/w) supplementation, for 12 weeks to confirm hypolipidemic activity of BME. BME attenuated serum nonesterified fatty acids and low-density lipoprotein (LDL) cholesterol levels, which was likely associated with the downregulation of hepatic lipogenic gene expression in WD-fed obese mice. Taken together, the hypolipidemic activity of BME was observed in HepG2 cells treated with fatty acids as well as in livers of obese mice, and the hepatoprotection of BME is likely associated with the inhibition of acetylation. Further investigation is warranted to determine whether BME can be developed into an efficacious dietary intervention to attenuate the progression of NAFLD by epigenetic regulation in clinical settings.

Preparation of Low-Diacylglycerol Cocoa Butter Equivalents by Hexane Fractionation of Palm Stearin and Shea Butter.

Herein, we prepared 1,3-dipalmitoyl-2-oleoyl glycerol (POP)-rich fats with reduced levels of diacylglycerols (DAGs), adversely affecting the tempering of chocolate, via two-step hexane fractionation of palm stearin. DAG content in the as-prepared fats was lower than that in POP-rich fats obtained by previously reported conventional two-step acetone fractionation. Cocoa butter equivalents (CBEs) were fabricated by blending the as-prepared fats with 1,3-distearoyl-2-oleoyl glycerol (SOS)-rich fats obtained by hexane fractionation of degummed shea butter. POP-rich fats achieved under the best conditions for the fractionation of palm stearin had a significantly lower DAG content (1.6 w/w%) than that in the counterpart (4.6 w/w%) prepared by the previously reported method. The CBEs fabricated by blending the POP- and SOS-rich fats in a weight ratio of 40:60 contained 63.7 w/w% total symmetric monounsaturated triacylglycerols, including 22.0 w/w% POP, 8.6 w/w% palmitoyl-2-oleoyl-3-stearoyl-rac-glycerol, 33.1 w/w% SOS, and 1.3 w/w% DAGs, which was not substantially different from the DAG content in cocoa butter (1.1 w/w%). Based on the solid-fat content results, it was concluded that, when these CBEs were used for chocolate manufacture, they blended with cocoa butter at levels up to 40 w/w%, without distinctively altering the hardness and melting behavior of cocoa butter.

Anacardic Acid Suppresses Adipogenesis Through Inhibition of the Hsp90/Akt Signaling Pathway in 3T3-L1 Preadipocytes.

Anacardic acid (AA), a major component of cashew nut shell liquid, has extensive bioactivities. However, little is known about its antiadipogenic properties or the mechanism that underpins them. The aim of this study was to investigate the effect of AA on 3T3-L1 preadipocyte differentiation and its mechanisms of action. AA inhibits lipid accumulation during adipogenesis in 3T3-L1 preadipocyte (IC50 = 25.45 µM). AA abrogates mRNA expressions of the genes implicated in lipogenesis and their transcription factors, especially Pparg and Cebpa. Furthermore, antibody microarray and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis results showed that the proteins implicated in the Akt signaling pathway were most likely altered by AA. Notably, upon AA treatment, heat shock protein 90 (Hsp90), a positive regulator of Akt, was decreased, resulting in Akt degradation. These findings indicate that AA, a natural product that acts as a Hsp90/Akt signaling inhibitor, may be a possible antiadipogenic agent.

The Cholesterol-Lowering Effect of Capsella Bursa-Pastoris Is Mediated via SREBP2 and HNF-1α-Regulated PCSK9 Inhibition in Obese Mice and HepG2 Cells.

The objective of the present study was to investigate the mechanism by which capsella bursa-pastoris ethanol extract (CBE), containing 17.5 milligrams of icaritin per kilogram of the extract, and icaritin, mediate hypocholesterolemic activity via the low-density lipoprotein receptor (LDLR) and pro-protein convertase subtilisin/kexin type 9 (PCSK9) in obese mice and HepG2 cells. CBE significantly attenuated serum total and LDL cholesterol levels in obese mice, which was associated with significantly decreased PCSK9 gene expression. HepG2 cells were cultured using delipidated serum (DLPS), and CBE significantly reduced PCSK9 and maintained the LDLR level. CBE co-treatment with rosuvastatin attenuated statin-mediated PCSK9 expression, and further increased LDLR. The icaritin contained in CBE decreased intracellular PCSK9 and LDLR levels by suppressing transcription factors SREBP2 and HNF-1α. Icaritin also significantly suppressed the extracellular PCSK9 level, which likely contributed to post-translational stabilization of LDLR in the HepG2 cells. PCSK9 inhibition by CBE is actively attributed to icaritin, and the use of CBE and icaritin could be an alternative therapeutic approach in the treatment of hypercholesterolemia.

3,4-dihydroxytoluene, a metabolite of rutin, suppresses the progression of nonalcoholic fatty liver disease in mice by inhibiting p300 histone acetyltransferase activity.

3,3',4',5,7-Pentahydroxyflavone-3-rhamnoglucoside (rutin) is a flavonoid with a wide range of pharmacological activities. Dietary rutin is hardly absorbed because the microflora in the large intestine metabolize rutin into a variety of compounds including quercetin and phenol derivatives such as 3,4-dihydroxyphenolacetic acid (DHPAA), 3,4-dihydroxytoluene (DHT), 3,4-hydroxyphenylacetic acid (HPAA) and homovanillic acid (HVA). We examined the potential of rutin and its metabolites as novel histone acetyltransferase (HAT) inhibitors. DHPAA, HPAA and DHT at the concentration of 25 µM significantly inhibited in vitro HAT activity with DHT having the strongest inhibitory activity. Furthermore, DHT was shown to be a highly efficient inhibitor of p300 HAT activity, which corresponded with its high degree of inhibition on intracellular lipid accumulation in HepG2 cells. Docking simulation revealed that DHT was bound to the p300 catalytic pocket, bromodomain. Drug affinity responsive target stability (DARTS) analysis further supported the possibility of direct binding between DHT and p300. In HepG2 cells, DHT concentration-dependently abrogated p300-histone binding and induced hypoacetylation of histone subunits H3K9, H3K36, H4K8 and H4K16, eventually leading to the downregulation of lipogenesis-related genes and attenuating lipid accumulation. In ob/ob mice, administration of DHT (10, 20 mg/kg, iv, every other day for 6 weeks) dose-dependently improved the NAFLD pathogenic features including body weight, liver mass, fat mass, lipid accumulation in the liver, and biochemical blood parameters, accompanied by the decreased mRNA expression of lipogenic genes in the liver. Our results demonstrate that DHT, a novel p300 histone acetyltransferase inhibitor, may be a potential preventive or therapeutic agent for NAFLD.

Animal Protein Intake Is Positively Associated with Metabolic Syndrome Risk Factors in Middle-Aged Korean Men.

Few studies have examined the relationship of protein intake by food source with metabolic syndrome in Korean adults, even though animal food intake has increased. This study examined the association between plant and animal protein intake and metabolic syndrome among middle-aged Korean adults. A total of 13,485 subjects aged 30-64 years were selected from the 2013-2018 Korea National Health and Nutrition Examination Survey. Protein intake was assessed using 24-h dietary recall data and divided into quintiles. Men had a higher percentage of energy intake from animal protein (7.4%) than plant protein (6.9%). Men in the highest quintile group of animal protein intake had a higher prevalence of abdominal obesity (OR: 1.30, 95% CI: 1.00-1.70), reduced high-density lipoprotein cholesterol (HDL-C) (OR: 1.43, 95% CI: 1.07-1.90), and elevated fasting glucose (OR: 1.32, 95% CI: 1.01-1.74), after adjusting for covariates. Furthermore, stronger associations of animal protein intake with abdominal obesity were shown in men who consumed less than estimated energy requirements (OR: 1.60, 95% CI: 1.11-2.31). Plant protein intake was negatively associated with increased blood pressure in men. Neither animal nor plant protein intakes were significantly associated with any of the metabolic syndrome risk factors in women. The results imply that lower animal protein intake may be a beneficial factor for metabolic syndrome management in middle-aged Korean men.

Isolation and compositional analysis of galactoglycerolipids from perilla [Perilla frutescens (L.) Britton] leaves and comparison to the galactoglycerolipids from spinach and parsley.

The aim of this study was to isolate monogalactosyldiacylglycerols (MGDGs) and digalactosyldiacylglycerols (DGDGs) from perilla [Perilla frutescens (L.) Britton] and to investigate their fatty acid profiles. Perilla displayed the greatest total MGDG and DGDG content among the three types of leaf vegetables tested, that is, spinach, parsley, and perilla, containing 0.16 g/100 g MGDG and 0.04 g/100 g DGDG (on wet weight basis). High purity MGDG (approximately 97 g/100 g) and DGDG (approximately 86 g/100 g) were isolated from perilla chloroform/methanol (2:1, v/v) extracts by two-step silica gel column chromatography. MGDGs were primarily composed of 18:3n-3 and 16:3n-3, predominantly located at the sn-1 and sn-2 positions, respectively. In DGDG, 18:3n-3 and 16:0 were the most abundant fatty acids and were primarily found at the sn-1 and sn-2 positions, respectively. PRACTICAL APPLICATION: MGDGs and DGDGs are the most prevalent forms of galactoglycerolipids found in leaf vegetables including perilla and have been shown to exert health-beneficial effects, such as antitumor, anti-inflammatory, anticancer, and appetite-suppressing activities. Both MGDGs and DGDGs possess emulsifying properties. The present study may help better understand the health-beneficial effects of MGDG and DGDG from perilla, by providing total composition and positional distribution of the fatty acids. The present study also successfully established a protocol to isolate high purity MGDG and DGDG from perilla, thereby increasing their possible use as an ingredient in foods and nutraceuticals.

Immobilized Phospholipase A1-Catalyzed Preparation of l-α-Glycerylphosphorylcholine from Phosphatidylcholine.

This study sought to prepare a cognitive enhancer l-α-glycerylphosphorylcholine (l-α-GPC) using an immobilized Lecitase Ultra (LU, phospholipase A1) to catalyze the hydrolysis of soy phosphatidylcholine (PC). Immobilization of LU on Lewatit VP OC 1600 provided the highest fixation level (83.1 g/100 g) and greatest catalytic activity achieving 100 g/100 g l-α-GPC within 20 h and was therefore selected as the optimal system for biocatalysis. Immobilization of LU increased its positional specificity compared to free LU, as shown by a decrease in the production of the phosphocholine byproduct. Under the optimal conditions determined by response surface methodology, PC was completely hydrolyzed to l-α-GPC and required a simple purification via phase separation of the biphasic media to obtain a yield of ∼26.4 g l-α-GPC from 100 g PC, with a purity of 98.5 g/100 g. Our findings suggest a possibility of using the immobilized LU as a new biocatalyst for the l-α-GPC production.