Lipid profile of rats fed high-fat diets based on flaxseed, peanut, trout, or chicken skin

OBJECTIVE: Dietary saturated fatty acids are associated with coronary disease. Conversely, dietary monounsaturated polyunsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) seem to exert a protective effect. This study evaluated the lipid profile of rats fed high-fat (HF) diets, with fat added as different sources of PUFA (flaxseed and trout), MUFA (peanut), and saturated fatty acid (chicken skin). METHODS: Adult male Wistar rats were placed into six dietary groups (n = 10): control (normal); high fat, with 1% cholesterol, 10% soy oil, and 5% lard; and four groups fed similar HF diets, with 10% lipid as trout, flaxseed, peanut, or chicken skin. After 28 d the animals were killed. Blood, livers, and adipose tissue samples were collected. RESULTS: A higher level (P < 0.05) of total serum cholesterol was observed in rats fed the normal diet (93.57 +/- 14.95 mg/dL) compared with those fed the HF diet (67.57 +/- 12.54 mg/dL). Total cholesterol levels in rats fed the flaxseed diet were lower (P < 0.05) than in rats fed the other fats. No difference was observed in cholesterol levels between groups fed the peanut and chicken skin diets (P > 0.05). Animals fed the peanut diet showed decreased body weight gain than did animals in the other treatment groups. There were large lipid and cholesterol depositions in livers of rats fed the HF diet. Lipid deposition in adipose tissue followed the same dietary fatty acid profile, i.e., high levels of omega-3 PUFA in the flaxseed group, high levels of MUFA in the peanut and chicken skin groups and high levels of omega-6 PUFA in the trout group. CONCLUSIONS: These data indicate that flaxseed is promising for dietary manipulation of hyperlipidemia.     

Combined effects of dietary conjugated linoleic acid and sesamin triacylglycerol and ketone body production in rat liver

The effects of a combination of dietary conjugated linoleic acid (CLA) supplemented with sesamin on hepatic ketogenesis and triacylglycerol secretion were compared using the livers of rats fed diets containing 1% CLA or linoleic acid (LA) in combination with 0.2% sesamin for 14 d, respectively. The feeding of CLA, as compared to LA, caused a significant reduction in the weight of perirenal adipose tissue but not that of epididymal adipose tissue, and affected neither growth parameters nor hepatic lipid concentration. Hepatic production of ketone bodies was consistently higher in rats fed CLA than in those fed LA, while triacylglycerol secretion was reversed. No significant difference was noted in the hepatic secretion of cholesterol among the groups. Although there was no effect of the dietary combination of CLA with sesamin on adipose tissue weight, hepatic lipid parameters and ketone body production were observed: i.e., triacylglycerol secretion tended to be reduced. These results suggest that the dietary combination of CLA with sesamin may be an effective approach for lowering serum triacylglycerol levels. The decreased hepatic secretion of triacylglycerol is, in part, due to enhanced fatty acid oxidation in the liver.     

不同脂肪酸构成比对小鼠血脂影响的实验研究

目的:以小鼠饲料正常脂肪摄入量7.84%为基础,比较不同脂肪酸构成比对小鼠血脂水平的影响。方法:以小鼠正常饲料脂肪及脂肪酸构成为对照,分别设S/M/P比值为1∶1.7∶1.2和1∶1∶1的饲料,其中n-6/n-3比值在1～10∶1各设计4组,共10组, 喂小鼠10 w,测定血脂水平。结果: S/M/P为1∶1.7∶1.2, n-6/n-3在1～5∶1时TC和TC/HDL-C水平显著低于8∶1和10∶1组(P<0.05); S/M/P为1∶1∶1,n-6/n-3为1∶1时的TC和LDL-C水平显著低于其余各比值组(P<0.05);当n-6/n-3为10∶1时,S/M/P为1∶1.7∶1.2的TC、LDL-C、HDL-C以及TC/HDL-C和LDL-C/HDL-C水平均显著低于1∶1∶2组(P<0.05),S/M/P为1∶1∶2的LDL-C和TC/HDL-C水平显著低于1∶1∶1组(P<0.05)。结论: S/M/P现状1∶1.7∶1.2时,n-6/n-3在1～5∶1可维持血脂在较低水平;如脂肪酸构成比为1∶1∶1时,维持较低血脂所需的n-6/n-3为1∶1;在现状膳食n-6/n-3为10∶1时,S/M/P在1∶1.7∶1.2有利于维持低血脂。     

Effect of dietary n-3 and n-6 oils with and without food restriction on activity of antioxidant enzymes and lipid peroxidation in livers of cyclophosphamide treated autoimmune-prone NZB/W female mice

OBJECTIVE: Cyclophosphamide (CTX), an alkylating agent, is extensively used in the treatment of lupus nephritis, but its administration has been associated with free radical mediated oxidative stress. The present study was designed to investigate the effect of dietary corn oil (CO), fish oil (FO) and food restriction (FR) on the activities of hepatic antioxidant enzymes, fatty acid composition and lipid peroxidation following CTX administration in autoimmune-prone NZB/W female mice. METHODS: Autoimmune-prone NZB/W female mice were fed either ad libitum (AL) or food restricted (60% of AL intake), semipurified diets containing 5% CO or 5% FO supplemented with equal levels of antioxidants and injected with either phosphate buffered saline (PBS), or CTX (50 mg/kg body weight) every 10 days. Proteinuria was measured biweekly. The treatment was stopped at 10 months and diets were continued until the mice were killed at 12 months. Fatty acid composition, activity of antioxidant enzymes and lipid peroxidation were analyzed in liver homogenates, and anti-DNA antibodies were analyzed in the serum. RESULTS: Mice in the FO/AL dietary group exhibited significantly higher liver catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities compared to the CO/AL dietary group. CTX significantly decreased SOD and GSH-Px activity in the FO/AL group and CAT and GSH-Px in the CO/AL group. In AL fed mice given CTX, activities of CAT, GSH-Px and GST were significantly higher in mice fed FO diets than in mice fed CO diets. FR increased the activity of enzymes in both the CO and FO diet groups. In FR mice, CTX decreased CAT and GSH-Px activity in both the CO and FO dietary groups, but glutathione S-transferase (GST) only in the CO group. The decrease in SOD activity was not significant in either of the restricted groups. CTX significantly increased generation of thiobarbituric acid reactive substances (TBARS) in both AL groups. FR significantly decreased lipid peroxidation in both the CO and FO groups, with or without CTX. CTX decreased serum anti-DNA antibody levels in both the CO and FO dietary groups. FR also decreased antibody titer in both the CO and FO dietary groups, and it was decreased further with CTX treatment. FO fed animals had higher levels of n-3 fatty acids, whereas CO fed animals had high levels of n-6 fatty acids. CTX significantly increased 20:4 and decreased 18:1 in CO/AL fed animals, whereas it increased 18:1 and decreased 22:6 in FO/AL fed animals. CONCLUSIONS: Results obtained in the present study suggests that FO and, more significantly, FO combined with FR can have a beneficial effect in hepatic tissues subjected to CTX induced oxidative stress by regulating the activity of antioxidant enzymes. In addition, the study also indicates that n-3 and n-6 dietary lipids are susceptible to lipid peroxidation, particularly in the presence of a prooxidant like CTX, and that FR is beneficial in decreasing lipid peroxidation. The study also suggests that FO and CTX can have additive effects in preventing kidney disease in NZB/W mice.     

Punicic acid was metabolised and incorporated in the form of conjugated linoleic acid in different rat tissues

The objective of this study was to evaluate the effects of a supplementation of pomegranate seed oil (PSO), being rich in punicic acid, on the biochemical parameters of healthy rats. PSO was given to the animals intragastrically for 40?days at concentrations of 1%, 2% and 4%. There were no changes in their total body weight gain, their serum biochemical markers, or in the oxidative stress in their tissues. However, the TBARS values were reduced in the brains of the animals, noting that no significant amounts of conjugated fatty acids were found in this tissue. Conjugated linoleic acid (CLA) was present in all the other tissues studied. The results obtained have demonstrated that punicic acid from PSO was metabolised and incorporated in the form of CLA in different rat tissues. It did not cause alterations in their lipid metabolism, nor did it participate in the processes of oxidation inhibition.     

Different dietary fats influence serum and tissue lipids and anti-cardiolipin antibody levels in autoimmune-prone NZB/W F1 mice

To investigate the influence of different dietary fats on lipids and anti-cardiolipin antibody levels, autoimmune NZB/W F1 mice were fed on diets containing 200 g dietary fat as palm oil, lard-soyabean oil (1:1, w/w), soyabean oil, rapeseed oil or fish oil/kg. In addition, each dietary fat group was divided into an early-feeding group with feeding from 2 months of age, and a late-feeding group with feeding from 5 months of age. Serum levels of triacylglycerol, phospholipid, cholesterol and anti-cardiolipin antibody were measured at regular intervals, and mice were killed at the age of 7 months for analysis of hepatic lipid and fatty acids. The results showed that hepatic triacylglycerol and cholesterol contents were lower in mice fed on fish oil than in those fed on palm oil. In contrast, hepatic phospholipid content was higher in mice of the fish oil group than in those of the other four dietary fat groups. Composition profiles for both hepatic and renal oleic acid (18: 1n-9), linoleic acid (18: 2n-6) and eicosapentaenoic acid (20: 5n-3) were similar to those of the dietary fats in mice of both early-feeding and late-feeding groups. Fish oil intake decreased arachidonic acid (20: 4n-6) concentration in kidney tissue but not in liver tissue. Serum triacylglycerol, cholesterol and phospholipid levels were lower in mice fed on fish oil than in those fed on palm oil. Immunoglobulin (Ig) M anti-cardiolipin antibody was lower for the fish oil group than for the other groups. The IgG anti-cardiolipin antibody level was significantly lower in mice fed on fish oil compared with that of the palm oil group only in the early-feeding group. There was a positive correlation between serum IgM anti-cardiolipin antibody and phospholipid levels (early-feeding group r 0.902, P < 0.05; late-feeding group r 0.894, P < 0.05). These findings suggest dietary fish oil may affect both lipid levels and anti-cardiolipin antibody, contributing to alleviation of the autoimmune process in autoimmune-prone NZB x NZW F1 mice.     

Lymphocyte activation, cell-mediated cytotoxicity and their relationship to dietary fat-enhanced mammary tumorigenesis in C3H/OUJ mice

The effects of dietary soybean oil (SBO) concentration (5 vs. 20% by weight) on mammary tumorigenesis, mitogen-induced blastogenesis, cell-mediated cytotoxicity and serum and lymphocyte fatty acid composition were studied in C3H/OUJ female mice. Weanling mice fed 20% SBO for 9 mo had a higher incidence (89 vs. 65%) and greater average size (2.9 vs. 1.9 g) of mammary tumor virus type S breast tumors than mice fed 5% SBO. The response of isolated splenocytes to the T-cell mitogens concanavalin A and phytohemagglutinin was 20-25% lower in mice fed 20% SBO than in mice fed 5% SBO for 20 wk. There was no effect of SBO concentration on the splenocyte response to lipopolysaccharide E55:B5, a B-cell mitogen, or to pokeweed mitogen, and B- and T-cell mitogen. Cell-mediated cytotoxicity to allogenic P815 tumor cells was 20% lower in mice fed 20% SBO than in mice fed 5% SBO for 12 wk. The lower cell-mediated immunity associated with 20% SBO was not due to changes in the fatty acid composition of the two major splenocyte membrane phospholipids, phosphatidylcholine and phosphatidylethanolamine. However, serum levels of linoleic acid were higher in mice fed 20% SBO. Raising dietary SBO from 5 to 20% by weight was associated with increased mammary tumorigenesis, reduced T-cell blastogenesis and lower cell-mediated cytotoxicity.     

Effect of dietary tung oil on the growth and lipid metabolism of laying hens

The influence of dietary tung oil, containing a high level of alpha-eleostearic acid (cis-9, trans-11, trans-13-octadecatrienoic acid, EA) on growth, egg production, and lipid and fatty acid compositions in tissues and egg yolks of laying hens was studied in White Leghorn hens. Forty-week-old hens were divided into three groups of eight birds each and fed diets containing 0, 0.5, or 1.0% tung oil for 6 wk. The average body weight, feed consumption, rate of egg production, and weights of eggs and yolks were not affected. The weight of adipose tissue was remarkably small in hens fed tung oil, whereas the yolk lipid content did not change. Triglyceride level in heart and adipose tissue decreased in hens fed tung oil, and the level of linolenic acid (C18:3) in all tissues was decreased. Alpha-EA was not almost deposited in the tissues and egg yolk of hens fed tung oil, but conjugated linoleic acid (CLA) was detected in all tissues and egg yolks. The level of CLA in the tissues was significantly higher with increased dietary tung oil. The order of CLA level in tissue lipids was adipose tissue>liver>heart>breast muscle. Especially, the level of CLA in the lipids of adipose tissue and egg yolks of hens fed 1.0% tung oil was 2.0% of the total fatty acid. These results supposed that dietary tung oil affected the lipid metabolism of laying hens and could modify the lipid and fatty acid composition in tissues and eggs.     

维生素E对老龄小鼠脾细胞转化反应及肝脏脂质过氧化作用的影响

本文报告了维生素E(VE)对老龄小鼠免疫反应及肝脏脂质过氧化作用的影响。3个月幼龄小鼠和18个月老龄小鼠各饲以含VE 500ppm和30ppm饲料8周后,测定血清中VE浓度,脾细胞转化反应和肝脏过氧化脂质(LPO)含量。结果表明,饲以合500PPmVE饲料的老龄小鼠脾细胞对刀豆蛋白A(ConA)和脂多糖(LPS)的反应及血清VE浓度均比饲以含30ppmVE饲料者显著增高(P<0.01),肝脏LPO含量却明显降低(P<0.01),膳食VE对老龄小鼠血清VE及肝脏LPO的影响明显高于幼龄鼠。     

Modulation of body fat and serum leptin levels by dietary conjugated linoleic acid in Sprague-Dawley rats fed various fat-level diets

OBJECTIVES: In this study, we examined the effect of dietary conjugated linoleic acid (CLA) on body fat levels in Sprague-Dawley rats. METHODS: Rats were fed AIN-93G type diets containing 4%, 7%, and 10% fats with or without 1.5% CLA. RESULTS: Three weeks after the onset of the experimental period, the weights of perirenal white adipose tissue were lower in CLA-fed rats. The weights of epididymal white adipose tissue also were lower in CLA-fed rats than in control rats, but this effect disappeared with increased dietary fat level. Serum leptin levels tended to be lower in the CLA group, especially the low-fat diet group, than in the control group. There were significant positive correlations between serum leptin level and weights of perirenal and epididymal white adipose tissues in control groups, but these correlations were weaker in the CLA groups. Serum tumor necrosis factor-alpha levels also tended to be lower in CLA-fed rats, and this tendency was most remarkable in the rats fed 7% fat diets. CONCLUSION: In conclusion, dietary CLA, especially the low-fat diet, reduced body fat without hepatic injury to Sprague-Dawley rats.     

Ameliorative effect of myricetin on insulin resistance in mice fed a high-fat,high-sucrose diet

BACKGROUND/OBJECTIVES

Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance.

MATERIALS/METHODS

Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined.

RESULTS

Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in mice fed the HFHS diet.

CONCLUSIONS

These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.     

Replacing dietary fish oil by vegetable oils has little effect on lipogenesis, lipid transport and tissue lipid uptake in rainbow trout (Oncorhynchus mykiss)

In order to investigate the effects of dietary lipid sources on mechanisms involved in lipid deposition, two groups of rainbow trout were fed from first-feeding to the commercial size of 1 kg (for 62 weeks) with two diets differing only by lipid source: 100% fish oil or 100% blend of vegetable oils (55% rapeseed oil, 30% palm oil, 15% linseed oil). The activities and levels of gene expression of lipogenic enzymes (fatty acid synthetase, glucose-6-phosphate dehydrogenase and malic enzyme) in liver and of lipoprotein lipase in perivisceral adipose tissue, white muscle and liver were determined. Transport of lipid was studied by determining lipid composition of plasma and lipoprotein classes. We also examined the clearance of LDL by assaying the level of LDL receptor gene expression in several tissues. Total replacement of dietary fish oil by the blend of vegetable oils did not affect growth of rainbow trout and did not modify muscle lipid content. Hepatic lipogenesis and lipid uptake in perivisceral adipose tissue, white muscle and liver were also not modified by dietary treatments. Diets containing the blend of vegetable oils induced a decrease in plasma cholesterol and LDL. In trout fed the vegetable oils diet, expression of LDL receptor gene in the liver was down-regulated.     

Differential regulation of hepatic gene expression by starvation versus refeeding following a high-sucrose or high-fat diet

OBJECTIVES: The objective of this work was to determine the effects of starvation versus refeeding following a high-sucrose diet (HS) or high-fat diet (HF) on fatty acid metabolism in mice. METHODS: The mice were fed an AIN-76 control diet (CD), a modified HS, or an HF. The three dietary groups were subdivided into three groups each: those fed experimental diets for 12 wk, mice starved for 48 h after 12 wk on an experimental diet, and those with the same starvation treatment but with 72 h of refeeding after starvation, respectively. RESULTS: Serum total cholesterol levels of CD and HF groups decreased and then increased under starvation and refeeding states, respectively. Refeeding HS and HF increased serum levels of low-density lipoprotein (LDL) cholesterol compared with refeeding of the CD group. Starvation significantly increased hepatic levels of total cholesterol in the HS and HF groups compared with the CD group. Hepatic acyl coenzyme A (CoA) synthetase (ACS) levels in the CD and HS groups but not the HF group increased and then decreased under starved and refed states, respectively; an opposite regulation was observed in the HF group. Levels of hepatic acetyl-CoA carboxylase (ACC) in the HS and HF groups were significantly increased by refeeding. Hepatic levels of carnitine palmitoyltransferase-I mRNA were significantly enhanced by starvation and refeeding in the HS group but decreased in CD and then increased in the HF group. CONCLUSIONS: Changes in dietary energy nutrients, fasting, and refeeding affect hepatic ACS, CPT-I, and ACC mRNA expression, and these results will serve to enhance our understanding of the molecular mechanisms underlying regulation of fatty acid metabolism.     

Chitooligosaccharide ameliorates diet-induced obesity in mice and affects adipose gene expression involved in adipogenesis and inflammation

Chitooligosaccharide (CO) has been reported to have potential antiobestic effects in a few studies, but the antiobesity properties of CO and its related mechanisms in models of dietary obesity remain unclear. We investigated the effect of CO on body weight gain, size of adipocytes, adipokines, and lipid profiles in high-fat (HF) diet-induced obese mice and on the gene expression in adipose tissue using a complementary DNA microarray approach to test the hypothesis that CO supplementation would alleviate HF diet-induced obesity by the alteration of adipose tissue-specific gene expression. Male C57BL/6N mice were fed a normal diet (control), HF diet, or CO-supplemented HF diet (1% or 3%) for 5 months. Compared with the HF diet mice, mice fed the 3% CO-supplemented diet gained 15% less weight but did not display any change in food and energy intake. Chitooligosaccharide supplementation markedly improved serum and hepatic lipid profiles. Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3% CO. Microarray analysis showed that dietary CO supplementation modulated adipogenesis-related genes such as matrix metallopeptidases 3, 12, 13, and 14; tissue inhibitor of metalloproteinase 1; and cathepsin k in the adipose tissues. Twenty-five percent of the CO-responsive genes identified are involved in immune responses including the inflammatory response and cytokine production. These results suggest that CO supplementation may help ameliorate HF diet-induced weight gain and improve serum and liver lipid profile abnormalities, which are associated, at least in part, with altered adipose tissue gene expression involved in adipogenesis and inflammation.     

Dietary fat source regulates ob gene expression in white adipose tissue of rats under hyperphagic feeding

This work was designed to investigate the effect of different lipid sources on ob gene expression and serum leptin levels in rats with two different feeding protocols: (1) free access to food; or (2) energy-controlled feeding. Male Wistar rats were fed diets containing 40 % energy as fat (olive oil, sunflower oil or beef tallow), for 4 weeks. In Expt 1 rats had free access to food, and in Expt 2 rats were fed a controlled amount of food (16 g/d, equivalent to 300 kJ/d). Insulin and leptin were determined by ELISA and ob mRNA by Northern blot. When rats had free access to food, ob mRNA levels were higher in animals fed either olive oil or sunflower oil than in those fed beef tallow. In marked contrast with feeding ad libitum, no differences were found among dietary fat groups in rats fed energy-controlled diets. When both feeding protocols were compared, free access to food induced an increased expression of ob mRNA in perirenal and/or epididymal adipose tissues from rats fed either olive oil or sunflower oil, but not from rats fed beef tallow. Dietary lipid type did not induce modifications in serum leptin concentrations. A tendency to higher serum leptin levels was observed more in rats with free access to food than in rats fed energy-controlled feeding. No differences were found in insulin levels. Dietary fat type importantly affects ob mRNA expression in rat white adipose tissue under hyperphagic conditions. Further study is needed in order to elucidate the mechanism underlying this effect.     

High Dietary Fat Intake during Lactation Promotes the Development of Social Stress-Induced Obesity in the Offspring of Mice

This study examined how a maternal high-fat diet (HD) during lactation and exposure of offspring to isolation stress influence the susceptibility of offspring to the development of obesity. C57BL/6J mice were fed a commercial diet (CD) during pregnancy and a CD or HD during lactation. Male offspring were weaned at three weeks of age, fed a CD until seven weeks of age, and fed a CD or HD until 11 weeks of age. Offspring were housed alone (isolation stress) or at six per cage (ordinary circumstances). Thus, offspring were assigned to one of eight groups: dams fed a CD or HD during lactation and offspring fed a CD or HD and housed under ordinary circumstances or isolation stress. Serum corticosterone level was significantly elevated by isolation stress. High-fat feeding of offspring reduced their serum corticosterone level, which was significantly elevated by a maternal HD. A maternal HD and isolation stress had combined effects in elevating the serum corticosterone level. These findings suggest that a maternal HD during lactation enhances the stress sensitivity of offspring. White adipose tissue weights were significantly increased by a maternal HD and isolation stress and by their combination. In addition, significant adipocyte hypertrophy was induced by a maternal HD and isolation stress and exacerbated by their combination. Thus, a maternal HD and isolation stress promote visceral fat accumulation and adipocyte hypertrophy, accelerating the progression of obesity through their combined effects. The mechanism may involve enhanced fatty acid synthesis and lipid influx from blood into adipose tissue. These findings demonstrate that a maternal HD during lactation may increase the susceptibility of offspring to the development of stress-induced obesity.     

Serum lipid levels correlate with solid tumor weight in hepatoma-bearing rats fed dietary fish oil

The effects of dietary fish oil (FO) on serum lipid levels and tumor proliferation were studied in Donryu rats subcutaneously implanted with the ascites hepatoma cell line AH109A. Solid tumor weight was significantly less and serum total cholesterol (T-Ch) level significantly lower in the groups fed the FO diet both before and after AH109A implantation than in the groups fed the corn oil diet. There were no significant effects in the serum lipid levels and tumor proliferation in the groups fed the FO diet only before or after the hepatoma implantation. The serum triacylglyceride, phospholipid, nonesterified fatty acid, T-Ch, and very-low-density lipoprotein+low-density lipoprotein-Ch levels showed significant positive correlations with the solid tumor weight. These results suggest that dietary FO ingestion after hepatoma implantation suppresses tumor proliferation and reduces serum lipid levels along with suppressing tumor proliferation.     

Effects of CLA at different dietary fat levels on the nutritional status of rats during protein repletion

OBJECTIVE: Protein depletion is associated with decreased body weight gain, low nitrogen balance, intrahepatic lipid accumulation, and hypoalbuminemia. Because conjugated linoleic acid (CLA) can increase lean body mass, enhance feed efficiency, and modulate lipid metabolism, this study investigated the effects of CLA at two levels of dietary fat on energy efficiency, nitrogen retention, and plasmatic and hepatic lipid levels in rats during dietary protein repletion. METHODS: The animals were subjected to a moderate protein restriction for 14 d. After that, they were fed a protein repletion diet for 30 d, supplemented or not with CLA at recommended and high-fat levels. Energy efficiency, nitrogen balance, and nutritional parameters in serum and tissues were evaluated. RESULTS: Protein repletion improved most of the nutritional parameters evaluated independently of CLA supplementation at both fat levels. At recommended fat levels, CLA did not have any effect. At high-fat levels, energy efficiency increased more than 20% by fat accumulation in carcasses and epididymal pads, serum cholesterol increased (two-fold), and liver triacylglycerol accumulation remained elevated. However, at high-fat levels, CLA prevented lipid accumulation in liver and adipose tissue. CONCLUSION: Protein repletion improved the nutritional status of protein-restricted rats with minor effects of CLA at both dietary fat levels. However, when high-fat diets were given, CLA-enriched oil showed preventive effects on liver and adipose tissue lipid accumulation and no deleterious effects were observed. Because there are no studies dealing with CLA effects on protein repletion, this experimental model could improve nutritional interventions to overcome the protein-deficit stage.     

Adipose tissue fatty acid composition and its relations to diet and plasma lipid concentrations in hemodialysis patients

Adipose tissue fatty acid composition, serum lipid profile, and dietary intake of 37 patients on maintenance hemodialysis were studied. In August 1982, 1984, and 1986, analyses were carried out in 15 normotriglyceridemic (NTG) and 22 hypertriglyceridemic (HTG; type IV hyperlipidemia) patients. No correlations were found between dietary intake of polyunsaturated fatty acids (PUFAs), ratio of polyunsaturated to saturated fatty acids (P-S ratio), and carbohydrate content on the one hand and serum lipid concentrations on the other in the two groups. Adipose tissue linolenic acid correlated negatively with serum cholesterol in both groups. Strong correlations were found between dietary intake of PUFAs and adipose tissue linoleic acid content, between PUFAs and the double-bond index, between P-S ratio and adipose tissue linoleic acid content, and between P-S ratio and the double-bond index. No significant differences in dietary intake or adipose tissue fatty acid composition were observed between NTG and HTG patients. Thus, no evidence was found for exogenous dietary influences on serum lipid concentrations. The adipose tissue linoleic acid content did reflect the dietary intake of PUFAs.     

Abietic acid has an anti-obesity effect in mice fed a high-fat diet

We investigated the anti-obesity effect of abietic acid in mice fed a high-fat diet with emphasis on changes in adipogenesis in epididymal adipose tissues. Male C57BL/6J mice were divided into four groups and fed a normal diet, a high-fat diet (HFD), or HFD plus oral administration of abietic acid (20 mg/kg of body weight/day [LA] or 40 mg/kg of body weight/day [HA]) for 8 weeks. Compared with the HFD group, mice orally administered 40 mg of abietic acid/kg of body weight/day exhibited significantly decreased body weight and adipose tissue weights. Serum triglyceride concentrations in the HA group were significantly lower than those in the HFD group, as were the levels of serum insulin and leptin. Hematoxylin and eosin staining revealed that epididymal adipose tissue mass was decreased by abietic acid administration. Abietic acid also inhibited the protein expression of sterol regulatory element-binding protein-1c, CCAAT/enhancer-binding protein α, and CD36 in epididymal adipose tissues, which are up-regulated by HFDs. These data demonstrate that abietic acid has an anti-obesity effect in mice mediated by the regulation of adipogenesis.