• Biomedical Science Letters
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• v.22 no.4
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• pp.220-226
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• 2016

Hypertriglyceridemia induces atherosclerosis and accordingly is a major causative factor in cardiovascular diseases. Macrophages that develop into foam cells are a crucial component in the development of atherosclerosis. Monocytes can be differentiated into M1 or M2 macrophages. M1 macrophages promote inflammatory responses, whereas M2 macrophages exhibit anti-inflammatory activity. Recently, we found that triglyceride (TG)-treated THP-1 monocytes express a variety of macrophage-specific surface markers, indicating that TG treatment could trigger the differentiation of monocytes into macrophages. In this study, we investigated whether TG-induced macrophages express the M1 or the M2 macrophage phenotype. THP-1 cells were treated with various concentrations of TG for different times and the expression of M1- and M2-specific markers was evaluated by RT-PCR. We found increased expression of M1 markers (CD40, CD80, and CD86) in TG-treated THP-1 cells in a TG dose- and time-dependent manner. The expression of M2 markers (CD163, CD200R, and CD206) showed variable responses to TG treatment. Taken together, our results indicate that TG treatment triggers the differentiation of monocytes into M1 macrophages, rather than into M2 macrophages, suggesting that TG contributes to pro-inflammatory responses.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.23 no.1
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• pp.98-104
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• 2020

Purpose: To investigate the impact of omega-3-enriched lipid emulsion (LE) on liver enzyme (aspartate transaminase [AST] and alanine aminotransferase [ALT]) and triglyceride (TG) levels of children undergoing gastrointestinal surgery. Methods: This experimental randomized controlled group pretest-posttest design study included 14 children who underwent gastrointestinal surgery due to duodenal atresia, jejunal atresia, esophageal atresia, and need for parenteral nutrition for a minimum of 3 days at RSUD Dr. Soetomo Surabaya between August 2018 and January 2019. These children were divided into two groups, those who received standard intravenous LE (medium-chain triglyceride [MCT]/long-chain triglyceride [LCT]) and those who received intravenous omega-3-enriched LE. Differences in AST, ALT, and TG levels were measured before surgery and 3 days after the administration of parenteral nutrition. Results: Liver enzyme and TG levels in each group did not differ significantly before versus 3 days after surgery. However, TG levels were significantly lower in the omega-3-enriched intravenous LE group (p=0.041) at 3 days after surgery, and statistically significant difference in changes in TG levels was noted at 3 days after surgery between MCT/LCT intravenous LE group and the omega-3-enriched intravenous LE group (p=0.008). Conclusion: The intravenous omega-3-enriched LE had a better TG-lowering effect than the MCT/LCT intravenous LE in children undergoing gastrointestinal surgery.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.17 no.4
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• pp.291-298
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• 1984

The extracted hagfish (Eptatretus burgeri) flesh lipid was separated into following fractions by column chromatography on Bio-beads SX-2 and Sephadex LH-20 prior to gab chromatographic analysis of their fatty acid compositions: polar lipid, triglyceride and free fatty acid. The major fatty acids of total lipid and triglyceride in hagfish were $C_{16:0},\;C_{16:1},\;and\;C_{18:1}$. The ratio of $C_{18:0}/C_{18:1}$ in the total lipid and triglyceride of hagfish was 0.1. The polar lipid of the hagfish muscle was mainly composed of phosphatidyl choline ($65.5\%$) and phosphatidyl ethanolamine ($28.0\%$). The triglyceride obtained was fractionated into four fractions by HPLC on the basis of partition numbers. Both the fatty acid composition and triglyceride composition on the basis of the total carbon number in the acyl chains of the triglyceride were analysed by the GLC. From the information obtained on triglyceride compositions based on the total carbon number by GLC and the partition number by HPLC and fatty acid composition by GLC, the combination of fatty acid in each triglycerides was estimated. A computer was used for estimation of the fatty acid combination in the triglyceride because hagfish lipid triglyceride was composed of various kinds of fatty acids. Fortyfour kinds of triglyceride were estimated. The major triglycerides in hagfish flesh lipid were found to those of ($1{\times}C_{16:0},\;2{\times}C_{18:1};\;13.5\%$), ($1{\times}C_{16:0},\;1{\times}C_{18:0},\;1{\times}C_{18:1};\;7.2\%$), ($1{\times}C_{16:1},\;2{\times}C_{18:1};\;5.4\%$), ($2{\times}C_{16:0},\;1{\times}C_{22:5};\;5.2\%$), ($1{\times}C_{14:0},\;2{\times}C_{18:1};\;4.5\%$), ($2{\times}C_{18:1},\;1{\times}C_{22:5};\;3.6\%$), ($1{\times}C_{14:0},\;1{\times}C_{18:0},\;1{\times}C_{18:1};\;2.7\%$) and ($1{\times}C_{14:0},\;1{\times}C_{16:0},\;1{\times}C_{18:2};\;2.2\%$).

• Journal of Life Science
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• v.16 no.6
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• pp.960-963
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• 2006

The purpose of this study is to evaluate the different type of exercise training on the changes of blood variables and leptin in SD rats. For this study, SD rats were divided into three groups: control group (CG: n=10), swim trained group (SG: n=10), and treadmill trained group (TG: n=10). The animals were housed in a pathogen-free animal facility ($22-24^{\circ}C$, 50-60% relative humidity, 08:00-20:00 lighting hours) at D university animal center, Pusan, Korea). Food and water were available ad libitum. The trained rats underwent a 8-wk endurance swim training (5 times/wk) in water at $26-29^{\circ}C$ (SG) and treadmill training (5 times/wk) in DAEJONG treadmill for 60 min. All data were expressed as mean and standard deviation by using SPSS package program (ver 10.0). The result through the statistical analysis of this data were summarized as follows: 1. In the weight changes, there were significant differences among CG, SG and TG(p<.05) after regular swim and treadmill training. TG showed the lowest weight than the other groups. 2. In the epididymal & perirenal adipose tissue levels, there were significant differences among CG, SG and TG(p<.05) after regular swim and treadmill training. TG showed the lowest adipose tissue levels than the other groups. 3. In the triglyceride changes, For the SG and TG, there were significantly decreased after regular swim and treadmill training. TG showed the lowest triglyceride levels than the other groups. 4. In the insulin hormone, For the SG and TG, there were significantly decreased after regular swim and treadmill training. TG showed the lowest insulin levels than the other groups. 5. In the leptin changes, For the SG and TG, there were significantly decreased after regular swim and treadmill training. TG was the lowest than the other groups. Based on the results, Regular swim and treadmill training decrease body weight, epididymal & perirenal adipose tissue levels significantly, this is caused but by decreased triglycerides, insulin, and leptin hormone levels not by the other factors. Regular treadmill training decreased insulin hormone levels compare to swim training, however there was no direct insulin effect on the weight changes. and it might be the direct effect of leptin hormones.

• BMB Reports
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• v.53 no.11
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• pp.588-593
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• 2020

The accumulation of triglycerides (TGs) in macrophages induces cell death, a risk factor in the pathogenesis of atherosclerosis. We had previously reported that TG-induced macrophage death is triggered by caspase-1 and -2, therefore we investigated the mechanism underlying this phenomenon. We found that potassium efflux is increased in TG-treated THP-1 macrophages and that the inhibition of potassium efflux blocks TG-induced cell death as well as caspase-1 and -2 activation. Furthermore, reducing ATP concentration (known to induce potassium efflux), restored cell viability and caspase-1 and -2 activity. The activation of pannexin-1 (a channel that releases ATP), was increased after TG treatment in THP-1 macrophages. Inhibition of pannexin-1 activity using its inhibitor, probenecid, recovered cell viability and blocked the activation of caspase-1 and -2 in TG-treated macrophages. These results suggest that TG-induced THP-1 macrophage cell death is induced via pannexin-1 activation, which increases extracellular ATP, leading to an increase in potassium efflux.

• BMB Reports
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• v.56 no.3
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• pp.166-171
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• 2023

Monocytes are peripheral leukocytes that function in innate immunity. Excessive triglyceride (TG) accumulation causes monocyte death and thus can compromise innate immunity. However, the mechanisms by which TG mediates monocyte death remain unclear to date. Thus, this study aimed to elucidate the mechanisms by which TG induces monocyte death. Results showed that TG induced monocyte death by activating caspase-3/7 and promoting poly (ADP-ribose) polymerase (PARP) cleavage. In addition, TG induced DNA damage and activated the ataxia telangiectasia mutated (ATM)/checkpoint kinase 2 and ATM-and Rad3-related (ATR)/checkpoint kinase 1 pathways, leading to the cell death. Furthermore, TG-induced DNA damage and monocyte death were mediated by caspase-2 and -8, and caspase-8 acted as an upstream molecule of caspase-2. Taken together, these results suggest that TG-induced monocyte death is mediated via the caspase-8/caspase-2/DNA damage/executioner caspase/PARP pathways.

• Biomedical Science Letters
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• v.19 no.1
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• pp.9-16
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• 2013

Elevated blood triglyceride (TG) levels correlate with development of atherosclerosis suggesting that TG may promote the development of this disease. During atherosclerosis, TG is taken up by tissue macrophages which result in dramatic changes in various secreted factors. One such factor is the family of matrix metalloproteases (MMP) which are involved in tissue remodeling during both physiological and pathological processes. In this study, we examined the MMP expression profile in PMA-differentiated THP-1 macrophages treated with TG. We found that TG-treated THP-1 macrophages showed decreased expression of MMP-3, MMP-7, MMP-8 and MMP-9 in a time- and dose-dependent manner. In contrast, expression of MMP-1, MMP-2, and MMP-10 remained relatively unchanged after TG treatment. In addition, we found that expression of select MMPs was affected by various inhibitors of signaling pathways. In particular, expression of MMP-3 was slightly recovered by cRAF and PLC signaling pathway inhibitors. These data suggests a possible role of MMPs in macrophages during TG-induced atherosclerosis.

• Biomedical Science Letters
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• v.20 no.4
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• pp.237-243
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• 2014

Triglyceride (TG) can cause death of macrophages and formation of foam cells thereby increasing inflammation in atherosclerotic plaques. Accumulation of cholesterol in macrophages is another critical event that promotes development of inflammatory cardiovascular diseases. Several proteins are known to transport intracellular cholesterol outside of the cell and these proteins are thought to be protective against atherosclerosis pathogenesis. It is unknown whether TG can affect cholesterol efflux in macrophages. In the current study, we examined mRNA expression levels of genes that promote efflux of cholesterol (ABCA1, ABCG1 and SR-B1). We found that TG treated THP-1 macrophages exhibited an increase in ABCG1 expression in a dose- and time-dependent manner. In contrast, the expression of ABCA1 and SR-B1 remained unchanged. To identify cell signaling pathways that participate in up-regulation of ABCG1, THP-1 macrophages were treated with various cell signaling inhibitors. We found that inhibition of the JNK and p38 MAPK pathway completely abrogated up-regulation of ABCG1 whereas inhibition of MEK1 further enhanced ABCG1 expression in TG treated THP-1 macrophages. Also, TG induced phosphorylation of JNK and p38 MAPK in THP-1 macrophages. These results suggest that TG may potentially influence cholesterol efflux in macrophages.

• Korean Journal of Clinical Laboratory Science
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• v.44 no.3
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• pp.103-111
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• 2012

Low-Density Lipoprotein cholesterol (LDLC) is the most important marker for the treatment of hyperlipidemia in NCEP-ATP III(National Cholesterol Education Program-Adult Treatment Panel III) guideline. Therefore, LDL cholesterol is pathologically meaningful, accurate measurement should be a top priority. Currently, LDLC is directly measured in most cases, but, the estimate is still used in mass health examination or screening test. This study is about the comparison of LDL-Cholesterol direct measurement with the estimate using various formula (Friedewald: [LDL-F=TC-HDL-TG/5], Nakajima: [LDL-N=TC-HDL-TG/4], Hattori: [LDL-H =0.94TC-0.94HDL-0.19TG], Puavilai: [LDL-P=TC-HDL-TG/6], Carvalho: [LDL-C=3(TC-HDL)/4]) for calculating more accurate value. We analyzed total cholesterol (TC), try-glyceride (TG), high-density lipoprotein cholesterol (HDLC), and LDLC levels of 210 subjects between June and November in 2011. Until now, the Friedewald formula is the most commonly used estimate for the LDLC. When Friedewald formula was applied, the correlation coefficient (r) was 0.940, showing high correlation. But, the result of the direct method was significantly different, compared with those of the Friedewald formula in triglyceride levels ${\geq}400mg/dL$(p<0.05). There was the highest correlation when we used LDL-P formula(r=0.947) in triglyceride levels <400 mg/dl. Also there was the lowest mean difference regardless of triglyceride level. Therefore, the study showed that TG/6 is more precise means of calculation than TG/5. On the other hand, the calculation of LDL-Cholesterol was underestimated, compared with direct measurement. It is necessary to have more data and modified Friedewald formula should be used for the accurate calculation.

• Journal of Nutrition and Health
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• v.52 no.3
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• pp.268-276
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• 2019

Purpose: Metabolic syndrome causes diabetes and increases the risk of cardiovascular disease. This study examined the correlation between metabolic syndrome, nutrition intake, and triglyceride (TG)/high-density lipoprotein (HDL) cholesterol ratio. Methods: Using the data from the $7^{th}$ KNHANES (2016), this study was conducted on healthy adults aged 19 and older. The components and existence of metabolic syndrome and nutrition intake were independent variables and the TG/HDLcholesterol ratio was a dependent variable. A complex sample logistic progress test was used with age, sex, smoking, and drinking frequency corrected. Results: The TG/HDLcholesterol ratio of people with metabolic syndrome was as high as 1.314 on average, compared to people without metabolic syndrome (p < 0.0001). Among each component of metabolic syndrome, the TG/HDL cholesterol ratio had a significant association with fasting blood glucose, TG, HDL cholesterol, and waist circumference (p < 0.05). Only energy and carbohydrate intake were significantly related to the TG/HDLcholesterol ratio (p < 0.05). Conclusion: The TG/HDLcholesterol ratio is associated with each component of metabolic syndrome, but in particular, it is positively correlated with the presence of metabolic syndrome. Lower energy intakehad a positive correlation with the TG/HDLcholesterol ratio. These results show that metabolic syndrome can be predicted using the TG/HDLcholesterol ratio, and a diet strategy through nutrition and health education is necessary to prevent metabolic syndrome.