• Animal Bioscience
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• 제35권1호
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• pp.22-28
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• 2022

Objective: Endoplasmic reticulum (ER) stress engages the unfolded protein response (UPR) that serves as an important mechanism for modulating hepatic fatty acid oxidation and lipogenesis. Chronic fasting in mice induced the UPR activation to regulate lipid metabolism. However, there is no direct evidence of whether negative energy balance (NEB) induces ER stress in the liver of cows. This study aimed to elucidate the relationship between the NEB attributed to feed deprivation and ER stress in bovine hepatocytes. Methods: Blood samples and liver biopsy tissues were collected from 6 non-lactating cows before and after their starvation for 48 h. The blood non-esterified fatty acids (NEFA), β-hydroxybutyric acid (BHBA) and glucose level were analyzed. Real-time quantitative polymerase chain reaction and Western blotting were used to explore the regulation of genes associated with UPR and lipid metabolism. Results: The starvation increased the plasma BHBA and NEFA levels and decreased the glucose level. Additionally, the starvation caused significant increases in the mRNA expression level of spliced X-box binding protein 1 (XBP1s) and the protein level of phosphorylated inositol-requiring kinase 1 alpha (p-IRE1α; an upstream protein of XBP1) in the liver. The mRNA expression levels of peroxisome proliferator-activated receptor alpha and its target fatty acid oxidation- and ketogenesis-related genes were significantly upregulated by the starvation-mediated NEB. Furthermore, we found that the mRNA expression levels of lipogenic genes were not significantly changed after starvation. Conclusion: These findings suggest that in the initial stage of NEB in dairy cows, the liver coordinates an adaptive response by activating the IRE1 arm of the UPR to enhance ketogenesis, thereby avoiding a fatty liver status.

• 한국식품영양과학회지
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• 제23권2호
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• pp.198-204
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• 1994

This study was carried out to investigate the effect of the feeding mixture of linesed oil, rich in n-3 PUFA and the sunflower seed oil, rich in n-6 PUFA on the lipid metabolism in the dietary hypprlidemic rats. After male Sprague-Dawley rats were induced hyperlipidemia by feeding the diet containing lard, butter, and cholesterol for 3 weeks, then they were fed with the diet containing lard 3.0% and butter 12.0% for control, the mixture in different proportion of both linseed oil and sunflower seed oil, and antihyperlipidemic durgs for 2 weeks. Analysis of the lipid component and the fatty acid composition of the liver showed following results. Concentration s of the total cholesterol and phospholipid in liver were significantly higher in group 2 (olive oil 12.0%) and lower in the other groups than in the control group, especially lower in groups 3 (cholestyramine 2.0%) and 9 (sunflower seed oil 12.0%) . Concentration of triglyceride was lower in the other groups except group 4 (liparoid), especially lowe rin group 9 than in the control group. In the fatty acid composition of liver lipids, C18:2 was the major fatty acid. Contents of n-6 PUFA increased , while those of n-3 PUFA decreased in groups composition of the test lipids. From the data on concentration s of total cholesterol. Phospholipid and triglyceride in liver, we concluded that the feeding mixed with 3.0% lard and 12.0 % sunflower seed oil were most effective for the improvement of the live lipids. The fatty acid composition in liver lipids were affected by the fatty acid composition of the test lipids.

• BMB Reports
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• 제30권1호
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• pp.1-6
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• 1997

The ability of Hep-G2 cells to process $[^{125}I]LDL$ under basal conditions was investigated. The receptor-binding and internalization of $[^{125}I]LDL$ increased with the time of incubation in a saturable manner. After 4 h of incubation, 31.4 ng of $[^{125}I]LDL$ was cell bound. The cells rapidly internalized $[^{125}I]LDL$ via specific, receptor-mediated endocytosis. The amount of internalized $[^{125}I]LDL$ reached a maximun of 96.7 ng at 2 h of incubation and remained constant for the next 2 h. The rate of degradation of internalized $[^{125}I]LDL$ proceeded in a linear manner over the entire 4 h of incubation after an initial lag period. The effects of individial fatty acids (C18:0. C18:1, C18:2. and C18:3), differing in their degree of unsaturation. on the receptor-binding, internalization and degradation of $[^{125}I]LDL$ were also investigated. Inclusion of 1.0 mM of each fatty acid into the culture medium significantly increased $[^{125}I]LDL$ metabolism in Hep-G2 cells. Among the fatty acids tested, stearic acid had the least effect on the receptor-binding activity. There were no significant differences among the unsaturated fatty acids in LDL-receptor binding. The effect of individual fatty acids on the $[^{125}I]LDL$ uptake was similar to that of the receptor-binding. showing a significantly lower effect with stearic acid. The amount of degraded material of internalized $[^{125}I]LDL$ was the lowest with stearic acid when it was compared with unsaturated fatty acids.

• Nutrition Research and Practice
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• 제10권5호
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• pp.477-486
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• 2016

BACKGROUND/OBJECTIVES: Consumption of pine nut oil (PNO) was shown to reduce weight gain and attenuate hepatic steatosis in mice fed a high-fat diet (HFD). The aim of this study was to examine the effects of PNO on both intestinal and hepatic lipid metabolism in mice fed control or HFD. MATERIALS/METHODS: Five-week-old C57BL/6 mice were fed control diets containing 10% energy fat from either Soybean Oil (SBO) or PNO, or HFD containing 15% energy fat from lard and 30% energy fat from SBO or PNO for 12 weeks. Expression of genes related to intestinal fatty acid (FA) uptake and channeling (Cd36, Fatp4, Acsl5, Acbp), intestinal chylomicron synthesis (Mtp, ApoB48, ApoA4), hepatic lipid uptake and channeling (Lrp1, Fatp5, Acsl1, Acbp), hepatic triacylglycerol (TAG) lipolysis and FA oxidation (Atgl, Cpt1a, Acadl, Ehhadh, Acaa1), as well as very low-density lipoprotein (VLDL) assembly (ApoB100) were determined by real-time PCR. RESULTS: In intestine, significantly lower Cd36 mRNA expression (P<0.05) and a tendency of lower ApoA4 mRNA levels (P = 0.07) was observed in PNO-fed mice, indicating that PNO consumption may decrease intestinal FA uptake and chylomicron assembly. PNO consumption tended to result in higher hepatic mRNA levels of Atgl (P = 0.08) and Cpt1a (P = 0.05). Significantly higher hepatic mRNA levels of Acadl and ApoB100 were detected in mice fed PNO diet (P<0.05). These results suggest that PNO could increase hepatic TAG metabolism; mitochondrial fatty acid oxidation and VLDL assembly. CONCLUSIONS: PNO replacement in the diet might function in prevention of excessive lipid uptake by intestine and improve hepatic lipid metabolism in both control diet and HFD fed mice.

• BMB Reports
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• 제35권5호
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• pp.494-497
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• 2002

The present study explored the short-term effects of dietary conjugated-linoleic acid (CLA) on liver lipid metabolism in starved/refed Otsuka Long Evans Tokushima Fatty (OLETF) rats. Male OLETF rats (12 weeks old) were starved for 24 hours, then refed for 48 hours with either a CLA diet [7.5% CLA and 7.5% Safflower oil (SAF)] or a SAF control diet (15% SAF). The results demonstrated a 30% reduction of hepatic triglyceride (TG) concentration in the CLA group when compared to the control group. Liver cholesterol concentration was also 26% lower in the CLA fed rats. The activity of mitochondrial carnitine palmitoyltransferase, the rate-limiting enzyme of fatty acid oxidation, was moderately elevated by 1.2-fold in the livers of the CLA group when compared to the control. In contrast, phosphatidate phosphohydrolase, the rate-limiting enzyme for TG synthesis, was found to be 20% lower in the livers of the CLA-fed rats. Therefore, dietary CLA evidently lowers liver lipid concentrations through a reduced TG synthesis and enhanced fatty acid oxidation in starved/refed OLETF rats.

• Journal of Nutrition and Health
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• 제29권5호
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• pp.499-506
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• 1996

It has been established that hypercholesterolemia is a major risk factor for atherosclerosis. Recent data showed that the incidence of hypercholesterolemia increase in Korea. n-3 Fatty acids lower serum triglyceride profoundly but the effect on serum cholesterol is not clear. This study was performed to assess the effects of low and moderate supplementation of marine n-3 fatty fish on serum cholesterol in young healthy korean woman. Nineteen subjects were divided into two groups. Each group receive an experimental diet supplemented with either 100g (group I) or 200g mackeral(Scomber japonicus) fish(group II) for 1-week. The diet was designed to avoid in which the amount of n-6 fatty acids would be much greater than that of n-3 fatty acids. MUFA, SFA intakes were similar in the two diets. The ratio of n-6/n-3 fatty acids was 1 : 1.l for group I, 1 : 2.51 for group II. The average daily n-3 fatty acids consumption from fish was 3.87g/day (1.03g EPA, 2.84g DHA)for group I, 7.74g/day (2.06g EPA, 5.68g DHA) for group II. Blood samples were obtained 2 times before experimental diet, immediately after experimental diet for 1-week. After experimental diet for 1-week, the serum total-cholesterol levels decreased significantly (16.4$\pm$15.1mg/dl, p<0.01) in group II and lowered slightly (13.7$\pm$25.8mg/dl)in group I. There were no significant changes from baseline to the end of the study in serum HDL-cholesteol, LDL-cholesterol, HDL-C/T-C ratio, and LDC-C/HDL-C ratio. The results suggest that the moderate levels of marine n-3 fatty fish consumption could improve serum cholesterol in normal subjects, therefore in might be of value in the prevention of atherosclerosis. However the clinical usefulness of moderate n-3 fatty fish consumption of hypercholesterolemic subjects will require further study. Also further studies are required to elucidate the long-term effects of low n-3 fatty fish consumtion.

• 한국응용과학기술학회지
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• 제13권3호
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• pp.15-24
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• 1996

Essentiality was proposed in the field of lipid by Burr and Burr in 1929. When rats were raised on the fat-free diet, their growth retarded and their skin and tails showed the characteristic deficient symptoms, which were relieved by the addition of ${\omega}6(n-6)$ polyunsaturated fatty acids as linoleic(LA) and arachidonic(AA) acids to the basal diet. LA is dehydrogenated to ${\gamma}-linolenic$ acid(GLNA) by ${\Delta}6$ desaturase, then GLNA is 2 carbon chain elongated by elongase to $dihomo-{\gamma}-linolenic$ acid(DGLNA), which is desaturated by ${\Delta}5$ desaturase to AA. These acids are called LA family or ${\omega}6(n-6)$ polyunsaturated fatty acids(PUFA). ${\alpha}-Linolenic$ acid(ALNA) is converted through the series of desaturation and elongation steps to docosahexaenic acid(DHA) via eicosapentaenoic acid(EPA). These acids belong to ALNA family or ${\omega}3(n-3)$PUFA. Human who consume large amounts of EPA and DHA, which are present in fatty fish and fish oils, have increased levels of these two fatty acids in their plasma and tissue lipids at the expense of LA and AA. Alternately, vegetarians, whose intake of LA in high, have more elevated levels of LA and AA and lower levels of EPA and DHA in plasma lipids and in cell membranes than omnivores. AA and EPA are metabolized to substances called eicosanoids. Those derived form AA are known as prostanocids(prostaglandins and prostacyclins) of the 2-types and leukotrienes of the 4-series, whereas those derived from EPA are known as prostanoids of the 3-types and leukotrienes of the 5-series. DGLNA is a precursor of the 1-types of prostaglandins. The metabolites of AA and EPA have competitive functions. Ingestion of EPA from fish or fish oil replaces AA from membrane phospholipids in practically all cells. So this leads to a more physiological state characterized by the production of proatanoids and leukotrienes that have antithrombic, antichemotactic, antivasoconstrictive and antiinflammatory properties. It is evident that ${\omega}3$ fatty acids can affect a number of chronic diseases through eicosanoids alone.

• 대한약리학회지
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• 제2권1호
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• pp.99-109
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• 1966

It has been known that the pronounced hypotension resulting from hemorrhage gives rise to compensatory stimulation of the adrenosympathetic system, which leads to an increase of liberation of catecholamines from sympathetic nervous system and adrenal medulla. It is obvious, therefore, that numerous physiological and biochemical changes during the hemorrhagic hypotention might be mediated through the increased liberation of catecholamines. Although an extensive studies have been reported on changes of protein and carbohydrate metabolism in hemorrhagic shock a few studies on the changes of lipid metabolism have been reported. Levenson(1961) observed a marked increase of serum lipids content during hemorrhagic shock and also noticed a marked elevation of serum free fatty acids. He suggested that these effects were due to mobilization and accelerated metabolic breakdown of lipids which might be resulted by sympathetic stimulation as a cause. To elucidate the mechanism of this, author studied the change of serum free fatty acids and blood sugar with relation to catecholamines during experimentally induced hemorrhagic shock in dog. Healthy male mongrel dogs weighing approximately 15kg were used. Under the general anesthesia with pentobarbital, rapid hemorrhage was produced from the femoral artery maintaining blood pressure level of 40 mmHg measured by the manometer connected with the opposite femoral artery throughout the experiment. Serum free fatty acids(FFA) and blood sugar were measured by the methods of Dole(1956) and Folin-wu,(1920) respectively. Tissue catecholamine was measured by Shore and Olin method(1958) using Aminco-Bowman spectrophotofluorometer.

• BMB Reports
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• 제47권1호
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• pp.15-20
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• 2014

Intracellular lipid-binding proteins (LBPs) impact fatty acid homeostasis in various ways, including fatty acid transport into mitochondria. However, the physiological consequences caused by mutations in genes encoding LBPs remain largely uncharacterized. Here, we explore the metabolic consequences of lbp-5 gene deficiency in terms of energy homeostasis in Caenorhabditis elegans. In addition to increased fat storage, which has previously been reported, deletion of lbp-5 attenuated mitochondrial membrane potential and increased reactive oxygen species levels. Biochemical measurement coupled to proteomic analysis of the lbp-5(tm1618) mutant revealed highly increased rates of glycolysis in this mutant. These differential expression profile data support a novel metabolic adaptation of C. elegans, in which glycolysis is activated to compensate for the energy shortage due to the insufficient mitochondrial ${\beta}$-oxidation of fatty acids in lbp-5 mutant worms. This report marks the first demonstration of a unique metabolic adaptation that is a consequence of LBP-5 deficiency in C. elegans.

• Nutrition Research and Practice
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• 제5권6호
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• pp.511-519
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• 2011

Dietary intake of whole grains reduces the incidence of chronic diseases such as obesity, diabetes, cardiovascular disease, and cancer. In an earlier study, we showed that Panicum miliaceum L. extract (PME) exhibited the highest anti-lipogenic activity in 3T3-L1 cells among extracts of nine different cereal grains tested. In this study, we hypothesized that PME in the diet would lead to weight loss and augmentation of hyperlipidemia by regulating fatty acid metabolism. PME was fed to ob/ob mice at 0%, 0.5%, or 1% (w/w) for 4 weeks. After the experimental period, body weight changes, blood serum and lipid profiles, hepatic fatty acid metabolism-related gene expression, and white adipose tissue (WAT) fatty acid composition were determined. We found that the 1% PME diet, but not the 0.5%, effectively decreased body weight, liver weight, and blood triglyceride and total cholesterol levels (P < 0.05) compared to obese ob/ob mice on a normal diet. Hepatic lipogenic-related gene ($PPAR{\alpha}$, L-FABP, FAS, and SCD1) expression decreased, whereas lipolysis-related gene (CPT1) expression increased in animals fed the 1% PME diet (P < 0.05). Long chain fatty acid content and the ratio of C18:1/C18:0 fatty acids decreased significantly in adipose tissue of animals fed the 1% PME diet (P < 0.05). Serum inflammatory mediators also decreased significantly in animals fed the 1% PME diet compared to those of the ob/ob control group (P < 0.05). These results suggest that PME is useful in the chemoprevention or treatment of obesity and obesity-related disorders.