• Journal of Ginseng Research
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• 제16권3호
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• pp.222-227
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• 1992

Unlike carbohydrats and fats, alcohol is essentially foreign to the body and it is known that the body get rid of it by oxidizing alcohol maily in the liver. Acetaldehyde is produced during ethanol metabolism and is known to be oxidized mainly by aldehyde dehydrogenase (ALDH). ALDH activity was found mainly in the mitochondrial fraction but a significant ALDH activity was also present in microsomal and cytosol fraction. Wistar rats (150~200 g, male) were given freely with 12% ethanol (Control) and/or 12% ethanol containing 0.1% ginseng saponins (Test) instead of water for 6 days and the liver was analyzed. ALDH activities of both control and test group were lower than that of normal group but test AkDH was less inhibited than control. ADH activies of both control and test were slightly higher than that of normal group but our previous data showed that it became gradually steady after prolonged ethanol feeding. MEOS activities of both control and test group were much higher than that of normal group. MEOS enzymes are inducible but the activity of test group was greatly higher than that of control. Ethanol containing [1-i4C] ethanol (5 $\mu$Ci) was injected to the above three groups and 30 min later, the distribution of radioactivity of hepatic lipids was investigated. Radioactivities of hepatic lipids of both control and test group were higher than that of normal group, however, that of test group was much lower than that of control. Analysis of individual lipids showed that phospholipid biosynthesis was significantly impaired and fatty acid and triglycerides biosynthesis were greatly stimulated. However, it was realized that the saponin prevented phospholipid biosynthesis depression and the increase of triglyceride biosynthesis considerably. It seemed that the saponin might stimulate ADH, ALDH and MEOS and the acetaldehyde formed would be removed faster. The excess hydrogen can be shunt more quickly into lipid biosynthesis. Electron microscopic observation showed that the hepatic cell of control group was si gnificantly damaged. Mitochondria were swollen and rough endoplasmic reticulum were dilated, however, hepatocytes of test group were not damaged.

• 식품과학과 산업
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• 제55권3호
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• pp.264-275
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• 2022

The regulation of macrophages is a major target for dietary immune modulation for their involvement in both innate and adoptive immune responses. Studies revealed that macrophages are unique in their plasticity to polarize into either inflammatory M1 subset or anti-inflammatory M2 cells. Recently, cellular energy metabolism including both glycolysis and oxidative phosphorylation is demonstrated to control macrophage dichotomy. In this review, the differential utilization of glucose, lipids, amino acids, and irons by M1 and M2 cells are discussed in detail. In addition, several dietary approaches for the alteration of inflammatory M1 cells to M2 phenotypes are reviewed for development of functional foods for immune regulation.

• Biomolecules & Therapeutics
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• 제27권6호
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• pp.562-569
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• 2019

Niacinamide (NIA) is a water-soluble vitamin that is widely used in the treatment of skin diseases. Moreover, NIA displays antioxidant effects and helps repair damaged DNA. Recent studies showed that particulate matter 2.5 ($PM_{2.5}$) induced reactive oxygen species (ROS), causing disruption of DNA, lipids, and protein, mitochondrial depolarization, and apoptosis of skin keratinocytes. Here, we investigated the protective effects of NIA on $PM_{2.5}$-induced oxidative stress in human HaCaT keratinocytes. We found that NIA could inhibit the ROS generation induced by $PM_{2.5}$, as well block the $PM_{2.5}$-induced oxidation of molecules, such as lipids, proteins, and DNA. Furthermore, NIA alleviated $PM_{2.5}$-induced accumulation of cellular $Ca^{2+}$, which caused cell membrane depolarization and apoptosis, and reduced the number of apoptotic cells. Collectively, the findings show that NIA can protect keratinocytes from $PM_{2.5}$-induced oxidative stress and cell damage.

• 한국식품영양과학회지
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• 제24권6호
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• pp.867-873
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• 1995

만성적인 알코올 섭취가 미토콘드리아의 지질조성 및 ATPase 활성도에 미치는 영향을 조사하고 아울러 간의 발암물질인 2-AAF를 토여하여 간 미토콘드리아의 기능에 미치는 상호 효과를 조사하기 위하여 120~125g 숫쥐에게 열량의 35%를 알코올로 공급하여 6주간 사육하였으며 알코올 섭취 4주 후에 2-AAF를 3일 간격으로 2회 복강투여하여 실험한 결과를 요약하면 다음과 같다. 1. 체중 증가, 식이 섭취량 및 식이효율에 대한 알코올의 효과는 유의적인 차이를 보였으나, 2-AAF에 의한 유의적인 효과는 관찰할 수 없었다. 알코올 섭취군이 대조군 보다 체중은 유의적으로 감소하였다. 2. 미토콘드리아 ATPase 활성도는 알코올 섭취에 의해 유의적으로 감소되었고, 2-AAF 투여에 의해서는 유의적이지 않으나 감소되는 경향을 보였다. 따라서 대조군(C)에 비하여 알코올 섭취와 2-AAF투여군(EA)에서 ATPase 활성도가 29.3%의 감소를 나타냈다. 3. 간 미토콘드리아 콜레스테롤 함량은 알코올 섭취에 의해 유의적으로 증가하였으며 미토콘드리아 총 인지질량은 알코올과 2-AAF에 의한 상호작용에 의해 알코올 투여군에서만 2-AAF 투여시 유의적인 증가 효과를 보여주었다. C/PL 비율은 알코올 섭취와 2-AAF 투여 보두에서 유의적인 효과는 보이지 않았으나 군간 비교시 알코올군(E)이 대조군(C) 보다 유의적으로 증가하였다. 4. 간 미토콘드리아의 CL량은 알코올군에서 감소하는 경향을 보였고 PS와 PI량은 차이가 없었다. 알코올 섭취로 PC량은 유의적으로 증가하였으나 PE량은 차이가 없엇으며, 2-AAF 투여시 PC량은 유의적인 감소를 보였고 PE량은 유의적으로 증가하였다. PE/PC 비율은 알코올 투여에 의해 유의성은 없었으나 감소경향을 나타냈으며, 2-AAF 투여에 의해서는 유의적인 증가 효과가 나타났다. 5. 알코올 섭취시 미토콘드리아의 지방산 조성은 palmitic acid가 유의적으로 감소하였고, stearic acid는 유의적으로 증가함을 보였다. UFA/SFA와 UI는 알코올군에서 유의적이지는 않으나 증가되는 경향을 보였다. 2-AAF 투여에 의해서도 linoleic acid는 감소되고 arachidonic acid는 증가되는 경향을 보여 UI값이 증가되는 경향이 있었다. 따라서 본 실험에서 나타난 ATPase 호라성도 변화는 비토콘드리아의 콜레스테롤변화, C/PL 비율, 인지질 조성이나 지방산 조성의 변화 등 막지질 조성의 변화에 기인하는 것으로 생각된다.

• Asian Pacific Journal of Cancer Prevention
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• 제13권11호
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• pp.5333-5338
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• 2012

Vitamin B6 functions as a coenzyme in >140 enzymatic reactions involved in the metabolism of amino acids, carbohydrates, neurotransmitters, and lipids. It comprises a group of three related 3-hydroxy-2-methyl-pyrimidine derivatives: pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM) and their phosphorylated derivatives [pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP)], In the folate metabolism pathway, PLP is a cofactor for the mitochondrial and cytoplasmic isozymes of serine hydroxymethyltransferase (SHMT2 and SHMT1), the P-protein of the glycine cleavage system, cystathionine ${\beta}$-synthase (CBS) and ${\gamma}$-cystathionase, and betaine hydroxymethyltransferase (BHMT), all of which contribute to homocysteine metabolism either through folate-mediated one-carbon metabolism or the transsulfuration pathway. Folate cofactors carry and chemically activate single carbons for the synthesis of purines, thymidylate and methionine. So the evidence indicates that vitamin B6 plays an important role in maintenance of the genome, epigenetic stability and homocysteine metabolism. This article focuses on studies of strand breaks, micronuclei, or chromosomal aberrations regarding protective effects of vitamin B6, and probes whether it is folate-mediated one-carbon metabolism or the transsulfuration pathway for vitamin B6 which plays critical roles in prevention of cancer and cardiovascular disease.

• Biomolecules & Therapeutics
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• 제23권2호
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• pp.165-173
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• 2015

Most skin damage caused by ultraviolet B (UVB) radiation is owing to the generation of reactive oxygen species. Phytochemicals can act as antioxidants against UVB-induced oxidative stress. This study investigated the protective effects of the flavone galangin against UVB-induced oxidative damage in human keratinocytes. Galangin efficiently scavenged free radicals and reduced UVB-induced damage to cellular macromolecules, such as DNA, lipids, and proteins. Furthermore, galangin rescued cells undergoing apoptosis induced by UVB radiation via recovering mitochondrial polarization and down-regulating apoptotic proteins. These results showed that galangin protects human keratinocytes against UVB radiation-induced cellular damage and apoptosis via its antioxidant effects.

• Kidney Research and Clinical Practice
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• 제35권2호
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• pp.69-77
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• 2016

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and its pathogenesis is complex and has not yet been fully elucidated. Abnormal glucose and lipid metabolism is key to understanding the pathogenesis of DN, which can develop in both type 1 and type 2 diabetes. A hallmark of this disease is the accumulation of glucose and lipids in renal cells, resulting in oxidative and endoplasmic reticulum stress, intracellular hypoxia, and inflammation, eventually leading to glomerulosclerosis and interstitial fibrosis. There is a growing body of evidence demonstrating that dysregulation of 50 adenosine monophosphate-activated protein kinase (AMPK), an enzyme that plays a principal role in cell growth and cellular energy homeostasis, in relevant tissues is a key component of the development of metabolic syndrome and type 2 diabetes mellitus; thus, targeting this enzyme may ameliorate some pathologic features of this disease. AMPK regulates the coordination of anabolic processes, with its activation proven to improve glucose and lipid homeostasis in insulin-resistant animal models, as well as demonstrating mitochondrial biogenesis and antitumor activity. In this review, we discuss new findings regarding the role of AMPK in the pathogenesis of DN and offer suggestions for feasible clinical use and future studies of the role of AMPK activators in this disorder.

• The Korean Journal of Physiology and Pharmacology
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• 제7권4호
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• pp.207-210
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• 2003

Lipids play many structural and metabolic roles, and dietary fat has great impact on metabolism and health. Fatty acid oxidation rate is dependent on tissue types. However there has been no report on the relationship between the rate of fatty acid oxidation and carnitine transport system in outer mitochondrial membrane of many tissues. In this study, the rate of fatty acid oxidation and carnitine palmitoyltransferase (CPT) I activity in the carnitine transport system were measured to understand the metabolic characteristics of fatty acid in various tissues. Palmitic acid oxidation rate and CPT I activity in various tissues were measured. Tissues were obtained from the white and red skeletal muscles, heart, liver, kidney and brain of rats. The highest lipid oxidation rate was demonstrated in the cardiac muscle, and the lowest oxidation rate was in brain. Red gastrocnemius muscle followed to the cardiac muscle. Lipid oxidation rates of kidney, white gastrocnemius muscle and liver were similar, ranging from 101 to 126 DPM/mg/hr. CPT I activity in the cardiac muscle was the highest, red gastrocnemius muscle followed by liver. Brain tissue showed the lowest CPT I activity as well as lipid oxidation rate, although the values were not significantly different from those of kidney and white gastrocnemius muscle. Therefore, lipid oxidation rate was highly (p＜0.001) related to CPT I activity. Lipid oxidation rate is variable, depending on tissue types, and is highly (p＜0.001) related to CPT I activity. CPT I activity may be a good marker to indicate lipid oxidation capacity in various tissues.

• Journal of Nutrition and Health
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• 제35권9호
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• pp.903-911
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• 2002

The effects of dietary levan, high-molecular-weight $\beta$-2,6-linked fructose polymer, on adiposity, serum leptin and UCP expression in rats fed high fat diet were studied. The adipose tissue hormone, leptin has been proposed to be involved in the regulation of food intake and energy expenditure. Uncoupling protein (UCP), a mitochondrial protein that uncouples the respiratory chain from oxidative phosphorylation, generates heat instead of ATP, thereby increase energy expenditure. To determine whether the dietary levan may have the anti-obesity effect, 4 wk old Sprague Dawley male rats fed high fat diet for 6 wks to induce obesity, and subsequently fed one of three diets for further 6 wks: 1) high fat (40% of calories) diet without levan 2) with 3% (w/w) levan 3) with 5% levan. For the comparison, control group fed AIN-76A diet. Visceral and peritoneal fat masses were lower in high fat diet with levan groups compared to high fat diet group. The effect of levan was dose-dependent. Adipocyte size was significantly reduced in the levan diet groups compared to the no levan diet group. Serum cholesterol level was not affected by levan containing diet, while the serum HDL cholesterol level was higher in leven diet groups. In addition, serum triglyceride level was markedly reduced by levan containing diet, thus lower than that of control group. Serum leptin was reduced by levan containing diet and lower in 5% levan group compared to 3% levan group (p < 0.001), as a result, serum leptin and insulin levels of 5% levan group were reduced to level of control group. Futhermore, the serum leptin level reflected the adiposity. The expression of UCP 1, and UCP 2 in brown adipose tissue was up-regulated by levan containing diet. In conclusions, levan containing diet reduced adiposity and serum triglyceride but increased UCP expression in the obese rats fed high fat diet. (Korean J Nutrition 35(9) : 903~911, 2002)

• Asian-Australasian Journal of Animal Sciences
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• 제28권1호
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• pp.127-134
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• 2015

Castration induces the accumulation of body fat and deposition of intramuscular fat in Korean cattle, resulting in improved beef quality. However, little is known about the metabolic adaptations in the liver following castration. To understand changes in lipid metabolism following castration, hepatic expression levels of lipid metabolism genes were compared between Korean bulls and steers. Steers had higher (p<0.001) hepatic lipids contents and higher (p<0.01) mRNA levels of lipogenic acetyl-CoA carboxylase. This differential gene expression may, in part, contribute to increased hepatic lipid content following the castration of bulls. However, we found no differences in the hepatic expression levels of genes related to triglyceride synthesis (mitochondrial glycerol-3-phosphate acyltransferase, diacylglycerol O-acyltransferase 1 and 2) and fatty acid (FA) oxidation (carnitine palmitoyltransferase 1A, C-4 to C-12 straight chain acyl-CoA dehydrogenase, very long chain acyl-CoA dehydrogenase) between bulls and steers. No differences in gene expression for very-low-density lipoprotein (VLDL) secretion, including apolipoprotein B mRNA and microsomal triglyceride transfer protein (MTTP) protein, were observed in the liver although MTTP mRNA levels were higher in steers compared to bulls. In conclusion, FA synthesis may contribute to increased hepatic lipid deposition in steers following castration. However, hepatic lipid metabolism, including triglyceride synthesis, FA oxidation, and VLDL secretion, was not significantly altered by castration. Our results suggest that hepatic lipid metabolism does not significantly contribute to increased body fat deposition in steers following castration.