Differential expression of lipoprotein lipase gene in tissues of the rat model with visceral obesity and postprandial hyperlipidemia

Postprandial hyperlipidemia is frequently accompanied with intra-abdominal visceral accumulation in human subjects. We have found that the decreased lipoprotein lipase (LPL) mass and activity is negatively associated with the amount of visceral fat accumulation. Here, we studied the postprandial hyperlipidemia using the OLETF rat, a model with visceral obesity, in order to clarify the molecular mechanism causing postprandial hyperlipidemia accompanied with visceral obesity. At the same age of 32 weeks, the OLETF rats showed obviously higher plasma leptin, total cholesterol, triglyceride, and HDL-cholesterol levels than the control LETO rats, although the plasma glucose level was not significantly different. Fat-loading test revealed the delayed metabolism of exogenous fat in the OLETF rats compared to the LETO rats, similar to human subjects with visceral obesity. In the obese rats, plasma levels of LPL mass and activities were 60 and 49% of control rats. The expression of LPL gene was decreased in subcutaneous adipose tissues and skeletal muscle of OLETF rats to 40 and 52% compared to those of LETO rats. In OLETF rats, plasma tumor necrosis factor-alpha (TNF-alpha) and insulin levels were increased to 2.0- and 2.3-folds compared to those in control rats. Furthermore, plasma insulin and TNF-alpha levels in OLETF rats were negatively correlated with the expression levels of LPL gene in subcutaneous fat and muscle. These results indicate that decreased LPL mass and activity in the animal model with visceral obesity is possibly caused by decreased expression of LPL gene in tissues mediated by the increased levels of insulin and TNF-alpha. The different expression of LPL gene in tissues associated with the increased levels of insulin and TNF-alpha possibly elucidate the underlying mechanisms involving the postprandial hyperlipidemia observed in visceral obesity.     

Endothelial function and myogenic reactivity in small mesenteric arteries of hyperlipidemic pregnant rats

Supraphysiological increases in serum triglycerides and cholesterol often occur during pregnancy, but their effects on vascular function are poorly understood. Intraperitoneal injection of the nontoxic surfactant poloxamer 407 (P-407) results in sustained elevation of triglycerides and cholesterol. We asked if P-407-induced hyperlipidemia during late pregnancy adversely affects mesenteric resistance artery vasodilator function. On days 13-15 of pregnancy, rats were given a single intraperitoneal injection of P-407, sterile water vehicle, or non-lipid-altering pluronic F-88 (P-88). Four days postinjection, serum triglycerides, cholesterol, free fatty acids, and the lipid peroxidation product malondialdehyde were significantly increased in P-407-treated rats. Mesenteric arteries from P-407-treated rats displayed significant increases in myogenic reactivity (constrictor responses to step increases in intraluminal pressure). The nitric oxide (NO) blocker N(alpha)-methyl-L-arginine increased the myogenic response in control but not in P-407 arteries, normalizing group differences. Endothelial removal increased myogenic reactivity beyond that of prior NO synthase inhibition in controls and potentiated myogenic reactivity in P-407 arteries such that responses again converged. Relaxation responses to the endothelium-dependent vasodilator methacholine did not differ. We conclude that that P-407-induced hyperlipidemia during pregnancy increases myogenic reactivity due to selective attenuation of an NO-mediated vasodilator component of the myogenic response.     

参麦注射液对高脂血症大鼠血脂的调节作用

目的：通过观察参麦注射液对高脂血症模型大鼠的血脂水平和一系列相关生化指标的影响,探讨其对高脂血症模型大鼠血脂的调节作用。方法：30只SPF级雄性SD大鼠用基础饲料适应性喂养1周,随机分为3组（n=10）：对照组,模型对照组,参麦注射液组。对照组用基础饲料喂养,模型对照组和参麦注射液组用高脂饲料喂养,每周测定动物体重一次。参麦注射液组每天给予2次参麦注射液10 ml/kg,连续灌胃45 d。之后测定大鼠血清总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）、超氧化物歧化酶（SOD）、谷胱甘肽过氧物酶（GSH-Px）、丙二醛（MDA）、脂蛋白酯酶（LPL）和肝酯酶（HL）活性。结果：模型对照组大鼠体重、血清中TC、TG、LDL-C和MDA水平较对照组明显升高（P<0.01）,而HDL-C、SOD、GSH-Px、LPL和HL水平明显降低（P<0.01）。参麦注射液组大鼠体重、血清中TC、TG、LDL-C和MDA水平较模型对照组明显降低（P<0.01）,而HDL-C、SOD、GSH-Px、LPL和HL水平明显升高（P<0.05,P<0.01）。结论：参麦注射液对高脂模型大鼠的血脂具有较明显的调节作用,并具有抗脂质过氧化的作用。     

Major involvement of mTOR in the PPARγ-induced stimulation of adipose tissue lipid uptake and fat accretion

Evidence points to a role of the mammalian target of rapamycin (mTOR) signaling pathway as a regulator of adiposity, yet its involvement as a mediator of the positive actions of peroxisome proliferator-activated receptor (PPAR)γ agonism on lipemia, fat accretion, lipid uptake, and its major determinant lipoprotein lipase (LPL) remains to be elucidated. Herein we evaluated the plasma lipid profile, triacylglycerol (TAG) secretion rates, and adipose tissue LPL-dependent lipid uptake, LPL expression/activity, and expression profile of other lipid metabolism genes in rats treated with the PPARγ agonist rosiglitazone (15 mg/kg/day) in combination or not with the mTOR inhibitor rapamycin (2 mg/kg/day) for 15 days. Rosiglitazone stimulated adipose tissue mTOR complex 1 and AMPK and induced TAG-derived lipid uptake (136%), LPL mRNA/activity (2- to 6-fold), and fat accretion in subcutaneous (but not visceral) white adipose tissue (WAT; 50%) and in brown adipose tissue (BAT; 266%). Chronic mTOR inhibition attenuated the upregulation of lipid uptake, LPL expression/activity, and fat accretion induced by PPARγ activation in both subcutaneous WAT and BAT, which resulted in hyperlipidemia. In contrast, rapamycin did not affect most of the other WAT lipogenic genes upregulated by rosiglitazone. Together these findings demonstrate that mTOR is a major regulator of adipose tissue LPL-mediated lipid uptake and a critical mediator of the hypolipidemic and lipogenic actions of PPARγ activation.     

Relationships between hepatic stearoyl-CoA desaturase-1 activity and mRNA expression with liver fat content in humans

Stearoyl-CoA desaturase-1 (SCD1) has gained much interest as a future drug target to treat fatty liver and its consequences. However, there are few and inconsistent human data about expression and activity of this important enzyme. We investigated activity and expression of SCD1 and their relationships with liver fat (LF) content in human liver samples. Fifty subjects undergoing liver surgery were studied. SCD1 activity was estimated from the ratio of oleate (C18:1) to stearate (C18:0) within lipid subfractions. Furthermore, SCD1 mRNA expression and LF content were measured. Similarly to previous studies, we observed a strong positive correlation between LF content and the C18:1/C18:0 ratio in the combined fatty acid (FA) fractions (r = 0.96, P < 0.0001), which could be interpreted as higher SCD1 activity with increasing LF. However, hepatic SCD1 mRNA expression did not correlate with LF (r = 0.16, P = 0.13). To solve these conflicting data, we analyzed the FA composition of hepatic lipid subfractions. With increasing LF content the amount of FAs from the triglyceride (TG) fraction increased (r = 0.96, P < 0.0001), whereas the FAs from the phospholipid (PL) fraction remained unchanged (r = -0.17, P = 0.19). Of these two major lipid fractions, the C18:1/C18:0 ratio in TG was 16-fold higher than in PL. Supporting the SCD1 mRNA expression data, the C18:1/C18:0 ratio of the TG or PL fraction did not correlate with LF (r = 0.26, P = 0.12 and r = 0.08, P = 0.29). We provide novel information that SCD1 activity and mRNA expression appear not to be elevated in subjects with high LF content. We suggest that the FA composition of lipid subclasses, rather than of mixed lipids, should be analyzed to estimate SCD1 activity.     

维生素C通过调控脂肪形成相关基因的转录促进猪前体脂肪细胞的增殖与分化

探讨维生素C（Vit C）诱导猪前体脂肪细胞增殖分化最佳浓度及在分化过程中,5种脂肪形成相关基因peroxisome proliferator activated receptor gamma(PPARγ)和retinoid X receptor alpha(RXRα),脂肪细胞分化标志基因lipoprotein lipase (LPL),生脂基因phosphoenolpyruvate carboxykinase(PEPCK)、stearoyl CoA desaturase(SCD) mRNA表达时序性的变化. 以3　d龄猪前体脂肪细胞为实验对象,用Vit C诱导猪前体脂肪细胞增殖分化,分别在增殖分化第2、4、6和8 d收获细胞,利用MTT测定其增殖程度;油红O染色提取法检测其脂肪含量;采用SQ RT PCR法检测脂肪生成相关基因PPARγ、RXRα、LPL、PEPCK和SCD mRNA表达的变化. 结果显示,PPARγ mRNA在诱导分化第2 d时有低水平表达,在诱导分化过程中表达量逐步升高,在终末分化阶段仍保持高水平表达;RXRα mRNA在诱导分化第2和4 d表达量很低,诱导分化第6 d时表达增加.在诱导分化第8 d,RXRα mRNA表达与第6 d相比差异不显著,直至终末分化. 脂肪细胞分化标志基因LPL在第2 d开始表达,第4和6 d逐步升高,在终末分化阶段仍保持高水平的表达;生脂基因PEPCK和SCD mRNA在第2和4 d开始表达,第6和8 d仍保持高水平的表达. 研究结果表明,100 μmol/L的Vit C促进猪前体脂肪细胞增殖能力最强;250 μmol/L Vit C能显著促进猪前体脂肪细胞分化. 其作用机制可能是通过对转录因子PPARγ和RXRα及标志基因LPL mRNA时序性表达的调控来进行的,促进生脂基因的表达,从而诱导脂肪细胞的分化.     

The lipogenic enzymes DGAT1, FAS, and LPL in adipose tissue: effects of obesity, insulin resistance, and TZD treatment

Acyl-coenzyme A:diacylglycerol transferase (DGAT), fatty acid synthetase (FAS), and LPL are three enzymes important in adipose tissue triglyceride accumulation. To study the relationship of DGAT1, FAS, and LPL with insulin, we examined adipose mRNA expression of these genes in subjects with a wide range of insulin sensitivity (SI). DGAT1 and FAS (but not LPL) expression were strongly correlated with SI. In addition, the expression of DGAT1 and FAS (but not LPL) were higher in normal glucose-tolerant subjects compared with subjects with impaired glucose tolerance (IGT) (P < 0.005). To study the effects of insulin sensitizers, subjects with IGT were treated with pioglitazone or metformin for 10 weeks, and lipogenic enzymes were measured in adipose tissue. After pioglitazone treatment, DGAT1 expression was increased by 33 +/- 10% (P < 0.05) and FAS expression increased by 63 +/- 8% (P < 0.05); however, LPL expression was not altered. DGAT1, FAS, and LPL mRNA expression were not significantly changed after metformin treatment. The treatment of mice with rosiglitazone also resulted in an increase in adipose expression of DGAT1 by 2- to 3-fold, as did the treatment of 3T3 F442A adipocytes in vitro with thiazolidinediones. These data support a more global concept suggesting that adipose lipid storage functions to prevent peripheral lipotoxicity.     

Sulfamethizole attenuates poloxamer 407-induced atherosclerotic neointima formation via inhibition of mTOR in C57BL/6 mice

Mammalian target of Rapamycin C1 (mTORC1) inhibition limits plaque progression in atherosclerosis. The present study evaluated the protective effect of sulfamethizole on poloxamer 407-induced atherosclerotic neointima formation in C57BL/6 mice via mTOR inhibition. Poloxamer 407 (P-407) (0.5 g/kg body weight) was administered intraperitoneally to male C57BL/6 mice every third day for 148 days to induce chronic hyperlipidemia. From Day 121 to 148, animals were additionally administered Sulfamethizole (5, 10, and 50 mg/kg, p.o.), Rapamycin (0.5 mg/kg, positive control), or vehicle (1 ml/kg). Plasma lipid levels were measured on Days 120 and 148. Upon sacrifice, histological studies were performed, and aortic tissue interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and mTOR levels were evaluated. A molecular docking study was carried out to mimic the interaction of sulfamethizole with mTOR protein. Chronic P-407 administration significantly (p < 0.001) elevated plasma lipid levels, compared with those of the normal control group. Chronic hyperlipidemia resulted in increased tunica intima thickness, collagen deposition, and IL-6, TNF-α, and mTOR levels. Treatment with Sulfamethizole attenuated these parameters significantly in a dose-dependent manner. Molecular docking studies showed a significant interaction of Sulfamethizole with mTOR. In conclusion, this study suggests that sulfamethizole significantly limits poloxamer 407-induced atherosclerotic neointima formation in C57BL/6 mice via mTOR inhibition.     

Feeding a High Concentrate Diet Down-Regulates Expression of ACACA,LPL and SCD and Modifies Milk Composition in Lactating Goats

High concentrate diets are fed to early and mid-lactation stages dairy ruminants to meet the energy demands for high milk production in modern milk industry. The present study evaluated the effects of a high concentrate diet on milk fat and milk composition, especially, cis-9, trans-11 CLA content in milk and gene expression of lactating goats. Eight mid-lactating goats with rumen fistula were randomly assigned into a high concentrate diet (HCD) group and low concentrate diet (LCD) group. High concentrate diet feeding significantly increased lipopolysaccharides (LPS) in plasma and decreased milk fat content, vaccenic acid (VA) and cis-9, trans-11 CLA in milk of the lactating goats. The mRNA expression levels of sterol regulatory element binding protein B 1c (SREBP1c), lipoprotein lipase (LPL), fatty acid synthetase (FASN) and acetyl-CoA carboxylase α (ACACA, ACCα) involving in lipid metabolism were analyzed, and ACACA and LPL all decreased in their expression level in the mammary glands of goats fed a high concentrate diet. DNA methylation rate of stearoyl-CoA desaturase (SCD) was elevated and decreased, and SCD mRNA and protein expression was reduced significantly in the mammary glands of goats fed a high concentrate diet. In conclusion, feeding a high concentrate diet to lactating goats decreases milk fat and reduced expression of SCD in the mammary gland, which finally induced cis-9, trans-11 CLA content in milk.     

山楂降脂汤对高脂血症大鼠血脂水平的调节和血管内皮保护作用

目的观察山楂降脂汤对高脂血症大鼠血脂水平调节和血管内皮的保护作用,以及对肝组织的影响。方法采用高脂饲料饲喂法建立高脂血症大鼠模型,通过山楂降脂汤高、中、低剂量和阳性对照药血脂康分别灌胃,观察大鼠的一般情况及肝、肾组织的病理变化,检测大鼠丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、总胆固醇（TCHO）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、一氧化氮（NO）和内皮素-1（ET-1）的含量。结果山楂降脂汤高、中、低剂量均能显著降低模型大鼠血液ALT、AST、UA、TCHO、TC、LDL-C、ET-1含量（P〈0.05,P〈0.01）,提高HDL-C、NO含量（P〈0.05,P〈0.01）,其中山楂降脂汤的作用随剂量递增。结论山楂降脂汤能显著调节机体的血脂水平,有效预防高脂血症和保护血管内皮细胞功能。     

Kidney triglyceride accumulation in the fasted mouse is dependent upon serum free fatty acids

Lipid accumulation is a pathological feature of every type of kidney injury. Despite this striking histological feature, physiological accumulation of lipids in the kidney is poorly understood. We studied whether the accumulation of lipids in the fasted kidney are derived from lipoproteins or NEFAs. With overnight fasting, kidneys accumulated triglyceride, but had reduced levels of ceramide and glycosphingolipid species. Fasting led to a nearly 5-fold increase in kidney uptake of plasma [¹⁴C]oleic acid. Increasing circulating NEFAs using a β adrenergic receptor agonist caused a 15-fold greater accumulation of lipid in the kidney, while mice with reduced NEFAs due to adipose tissue deficiency of adipose triglyceride lipase had reduced triglycerides. Cluster of differentiation (Cd)36 mRNA increased 2-fold, and angiopoietin-like 4 (Angptl4), an LPL inhibitor, increased 10-fold. Fasting-induced kidney lipid accumulation was not affected by inhibition of LPL with poloxamer 407 or by use of mice with induced genetic LPL deletion. Despite the increase in CD36 expression with fasting, genetic loss of CD36 did not alter fatty acid uptake or triglyceride accumulation. Our data demonstrate that fasting-induced triglyceride accumulation in the kidney correlates with the plasma concentrations of NEFAs, but is not due to uptake of lipoprotein lipids and does not involve the fatty acid transporter, CD36.     

The effects of feeding condition and dietary lipid level on lipoprotein lipase gene expression in liver and visceral adipose tissue of red sea bream Pagrus major

The effects of feeding condition and dietary lipid level on lipoprotein lipase (LPL) gene expression in the liver and visceral adipose tissue of red sea bream Pagrus major were investigated by competitive polymerase chain reaction. Not only visceral adipose tissue but also liver of red sea bream showed substantial LPL gene expression. In the liver, starvation (at 48 h post-feeding) drastically stimulated LPL gene expression in the fish-fed low lipid diet, but had no effect in the fish fed high lipid diet. Dietary lipid level did not significantly affect the liver LPL mRNA level under fed condition (at 5 h post-feeding). In the visceral adipose tissue, LPL mRNA number per tissue weight was significantly higher in the fed condition than in the starved condition, irrespective of the dietary lipid levels. Dietary lipid levels did not affect the visceral adipose tissue LPL mRNA levels under fed or starved conditions. Our results demonstrate that both feeding conditions and dietary lipid levels alter the liver LPL mRNA levels, while only the feeding conditions but not dietary lipid levels cause changes in the visceral adipose LPL mRNA level. It was concluded that the liver and visceral adipose LPL gene expression of red sea bream seems to be regulated in a tissue-specific fashion by the nutritional state.     

SCD1 activity in muscle increases triglyceride PUFA content,exercise capacity,and PPARδ expression in mice

Stearoyl-CoA desaturase (SCD)1 converts saturated fatty acids into monounsaturated fatty acids. Using muscle overexpression, we sought to determine the role of SCD1 expression in glucose and lipid metabolism and its effects on exercise capacity in mice. Wild-type C57Bl/6 (WT) and SCD1 muscle transgenic (SCD1-Tg) mice were generated, and expression of the SCD1 transgene was restricted to skeletal muscle. SCD1 overexpression was associated with increased triglyceride (TG) content. The fatty acid composition of the muscle revealed a significant increase in polyunsaturated fatty acid (PUFA) content of TG, including linoleate (18:2n6). Untrained SCD1-Tg mice also displayed significantly increased treadmill exercise capacity (WT = 6.6 ± 3 min, Tg = 71.9 ± 9.5 min; P = 0.0009). SCD1-Tg mice had decreased fasting plasma glucose, glucose transporter (GLUT)1 mRNA, fatty acid oxidation, mitochondrial content, and increased peroxisome proliferator-activated receptor (PPAR)δ and Pgc-1 protein expression in skeletal muscle. In vitro studies in C2C12 myocytes revealed that linoleate (18:2n6) and not oleate (18:1n9) caused a 3-fold increase in PPARδ and a 9-fold increase in CPT-1b with a subsequent increase in fat oxidation. The present model suggests that increasing delta-9 desaturase activity of muscle increases metabolic function, exercise capacity, and lipid oxidation likely through increased PUFA content, which increases PPARδ expression and activity. However, the mechanism of action that results in increased PUFA content of SCD1-Tg mice remains to be elucidated.     

饲料脂肪水平对瓦氏黄颡鱼生长及脂蛋白脂酶基因表达的影响

研究采用脂肪水平分别为4.7%、7.9%、10.9%、15.4%、18.9%的五种等氮配合饲料饲喂瓦氏黄颡鱼早期幼鱼,进行了为期30d的生长实验,探讨了瓦氏黄颡鱼早期幼鱼的脂肪需求。并克隆了瓦氏黄颡鱼脂蛋白脂酶(LPL)cDNA序列片段,采用实时荧光定量PCR研究了饲料脂肪水平对肝脏LPL基因表达水平的影响。结果表明,饲料脂肪水平从4.7%增加到10.9%显著促进了瓦氏黄颡鱼早期幼鱼的生长(P<0.05)。饲料脂肪水平显著影响了实验鱼的鱼体体成分,随着饲料脂肪水平的升高,鱼体干物质和脂肪含量显著增加而蛋白含量显著下降(P<0.05)。高脂诱导了瓦氏黄颡鱼肝脏LPL基因表达,摄食15.4%、18.9%这两组较高脂肪水平的实验鱼肝脏LPLmRNA表达水平显著升高(P<0.05)。根据特定生长率通过折线回归分析得出瓦氏黄颡鱼早期幼鱼最适脂肪水平为11.2%。       

FABP5-PPARγ信号通路对血管性痴呆大鼠学习记忆及脂质代谢的影响*

目的: 探讨脂肪酸结合蛋白5(FABP5)-过氧化物酶体增殖物激活受体γ(PPARγ)信号通路对血管性痴呆(VD)大鼠学习记忆及脂质代谢的影响及其作用机制。方法: ①采用双侧颈总动脉结扎法制备VD模型大鼠,设立正常对照组(WT组)、假手术组(sham组)及VD模型组;②设立WT组和WT+FABP5抑制剂组。4周后行Morris水迷宫实验检测大鼠空间学习记忆能力;采用RT-qPCR及Western blot方法测定脑内FABP5、PPARγ、p- PPARγ及脂蛋白脂肪酶(LPL)在转录水平和蛋白水平的表达;用试剂盒检测脑组织中总胆固醇(TC)、甘油三酯(TG)及游离脂肪酸(FFA)含量。结果: 与WT组和sham组相比,VD模型和FABP5抑制剂组大鼠学习记忆能力明显下降(P＜0.05, P＜0.01),脑内的FABP5、PPARγ、p- PPARγ及LPL在转录水平和蛋白水平上表达显著降低(P＜0.05, P＜ 0.01);脑内的TC、TG和FFA含量明显提高(P＜0.05, P＜0.01)。结论: FABP5可通过PPARγ和LPL影响VD大鼠的学习记忆和脂质代谢。     

Determining hepatic triglyceride production in mice: comparison of poloxamer 407 with Triton WR-1339

Triglyceride (TG), a water-insoluble energy-rich lipid, is secreted by the liver as part of very low density lipoproteins (VLDLs) to supply energy to extrahepatic tissues. Overproduction of VLDL is associated with increased risk of cardiovascular heart disease; this has renewed an interest in factors that affect hepatic TG production. The TG production rate is determined by measuring temporal increases in plasma TG under conditions in which TG hydrolysis by lipoprotein lipase (LPL) is inhibited. The nonionic detergent, Triton WR-1339 (Triton), has commonly been used to inhibit LPL for this purpose. Triton, in addition to inhibition of TG hydrolysis, has properties that have the potential to adversely influence lipoprotein metabolism. Another nonionic detergent, poloxamer 407 (P-407), also inhibits LPL. In these studies, we demonstrate that P-407 is comparable to Triton in the determination of TG production but without the unwanted side effects of Triton.     

The association of lipoprotein lipase PvuII polymorphism and niacin intake in the prevalence of metabolic syndrome: a KMSRI-Seoul study

Lipoprotein lipase (LPL) polymorphism correlated with LPL activity is associated with plasma lipid and lipoprotein levels. We aimed to investigate the frequency of LPL PvuII polymorphism and effects of LPL PvuII polymorphism and niacin intake on the prevalence of metabolic syndrome (MetSyn) in Koreans. Lifestyle questionnaires, anthropometry, and dietary records were completed, and LPL PvuII polymorphism, LPL mass, and lipid profiles were determined in 548 Koreans (MetSyn: 278, Non-MetSyn: 270). The MetSyn group showed a significantly lower frequency of P1P1 (wild type) and a higher frequency of P1P2 (hetero type) than the non-MetSyn group. The P2P2 (mutant type) group significantly showed lower levels of HDLc and LPL mass and a higher level of TG than the P1P1 group. As niacin intake increased, LPL mass decreased in the P2P2 group (r ² = 0.07). In particular, the lowest niacin intake group (≤14.82 mg/day) increased more than 3 times with regard to a higher risk of MetSyn than the others in the P2P2 mutant groups. However, the MetSyn risk declined 74% at the optimal levels of niacin intake (14.83–17.80 mg/day) in the P2P2 group compared to those of the P1 allele group. The findings indicate that optimal levels of niacin intake effectively decreased Korean MetSyn prevalence in the P2P2 mutant group.     

Regulation of lipoprotein lipase gene expression by insulin and troglitazone in rainbow trout (Oncorhynchus mykiss) adipocyte cells in culture

Adipose tissue plays a central role regulating the balance between deposition and mobilization of lipid reserves. Lipoprotein lipase (LPL) is a key enzyme controlling lipid accumulation in mammals and fish. In the present study, we have examined the expression of LPL in rainbow trout cultured adipocytes and we have investigated the effect of troglitazone, a member of thiazolidinediones (TZDs), and insulin on its expression. LPL gene expression increased from day 1 until day 12 of culture, and the level was maintained up to day 21. The addition of insulin at 10 nM and 1.7 μM increased significantly LPL gene expression in undifferentiated cells (days 7 to 12 maintained in growth medium). Nevertheless, treatment of day 7 cells incubated in growth medium with troglitazone (5 μM) or troglitazone plus insulin (1 μM each), tended to enhance LPL expression. In addition, LPL mRNA levels increased significantly in the presence of 1 μM and 5 μM of troglitazone (days 7 to 12) when the cells were induced to differentiate by addition of differentiation medium. Although troglitazone alone (1 μM) did not stimulate lipid accumulation in the cells neither in growth nor in differentiation medium, the simultaneous presence of troglitazone (1 μM) and insulin (1 μM) increased significantly the content of triglycerides in adipocyte cells maintained in growth medium (days 7 to 12). These results indicate that insulin and troglitazone regulate LPL gene expression during adipocyte differentiation and suggest that both factors may have combined effects in the modulation of adipogenesis.