Beta-glucan fractions from barley and oats are similarly antiatherogenic in hypercholesterolemic Syrian golden hamsters

The cholesterol-lowering activities of oats and barley are commonly attributed to the beta-glucan fractions. Although beta-glucan is present in both grains and appears to be chemically similar, the effect of source on cholesterol-lowering activity has not been evaluated. In the present study, the antiatherogenic properties of beta-glucan concentrates from oats and barley were evaluated in Syrian golden F(1)B hamsters consuming a semipurified hypercholesterolemic diet (HCD) containing cholesterol (0.15 g/100 g), hydrogenated coconut oil (20 g/100 g) and cellulose (15 g/100 g). After a 2-wk lead-in period, control hamsters were fed the HCD, whereas experimental hamsters consumed HCD formulated to include beta-glucan (2, 4, or 8 g/100 g) by addition of beta-glucan concentrate prepared from oats or barley at the expense of cellulose. Compared with control hamsters, dose-dependent decreases that were similar in magnitude in plasma total and LDL cholesterol concentrations were observed in hamsters fed beta-glucan from either source at wk 3, 6 and 9. Compared with controls, liver cholesterol concentrations were also reduced (P < 0.05) in hamsters consuming 8 g/100 g oat or barley beta-glucan. In agreement with previously proposed mechanisms, total fecal neutral sterol concentrations were significantly increased (P < 0.05) in hamsters consuming 8 g/100 g barley or oat beta-glucan. Aortic cholesterol ester concentrations were significantly reduced (P < 0.05) in hamsters fed 8 g/100 g beta-glucan from barley or oats. Although aortic total cholesterol and cholesterol ester concentrations were significantly correlated with LDL cholesterol (r = 0.565, P < 0.004 and r = 0.706, P < 0.0001, respectively), this association could explain only half of the variability. This study demonstrated that the cholesterol-lowering potency of beta-glucan is approximately identical whether its origin was oats or barley.     

Dietary soy and soy isoflavones have gender-specific effects on plasma lipids and isoflavones in golden Syrian f(1)b hybrid hamsters

The specific components of soy responsible for its beneficial effects on plasma lipids are unknown. Golden Syrian F(1)B Hybrid hamsters (75 male, 74 female) were evaluated for the effect of dietary soy and soy isoflavones on plasma lipids. They were fed the following diets for 16 wk: casein/lactalbumin (C/L), soy protein with isoflavones [Soy(+)], soy protein with isoflavones removed [Soy(-)], Soy(-) plus isoflavone extract (IF), and C/L + IF. At necropsy, plasma total cholesterol, HDL cholesterol (HDLC), LDL + VLDL cholesterol (LDL + VLDLC), isoflavones, and uterine and accessory gland weights were measured. Male hamsters fed the three soy-containing diets had lower LDL + VLDLC concentrations than those fed the two C/L diets (P < 0.01), and those fed Soy(-) + IF did not differ from those fed Soy(+). In females, diet did not affect plasma LDL + VLDLC concentration. Females fed Soy(+) or Soy(-) had higher HDLC (P < 0.05) than those fed C/L. HDLC was not affected by diet in males. Due to higher equol production (P < 0.01), males had greater plasma isoflavone concentrations (P < 0.01) than females. There was a positive association between plasma total isoflavones and LDL + VLDLC (r = 0.65, P < 0.05) in females. These data suggest gender differences in plasma lipid and isoflavone responses to soy- based diets in Syrian F(1)B Hybrid hamsters, which offer an opportunity to explore effects of sex hormones on isoflavone metabolism and the effects of isoflavones on lipid metabolism.     

The levels of plasma low density lipoprotein are independent of cholesterol ester transfer protein in fish-oil fed F1B hamsters

BACKGROUND: Cholesterol ester transfer protein (CETP) plays a major role in regulating the levels of LDL- and HDL-cholesterol. We previously observed a fish-oil-induced elevation of low-density lipoprotein (LDL)-and very-low-density lipoprotein (VLDL)-cholesterol concentrations and a decrease in high-density lipoprotein (HDL)-cholesterol concentration in F1B hamsters. The molecular mechanism/s by which fish oil induces hyperlipidaemic effect was investigated in this study. We examined whether the effects of dietary fish oil on plasma lipoprotein concentrations are due to fish-oil-induced alterations in plasma CETP activity. MIX diet, a diet supplemented with a mixture of lard and safflower oil, was used as the control diet. RESULTS: We found that fish oil feeding in hamsters reduced CETP mass as well as CETP activity. Increasing the dietary fat level of fish-oil from 5% to 20% (w/w) led to a further decrease in CETP mass. Supplementation with dietary cholesterol increased both CETP mass and CETP activity in fish-oil and MIX-diet fed hamsters. However, there was no correlation between CETP mass as well as CETP activity and LDL-cholesterol concentrations. CONCLUSION: These findings suggest that cholesterol ester transfer between HDL and LDL is not likely to play a major role in determining fish-oil-induced changes in LDL- and HDL-cholesterol concentrations in F1B hamsters. A possible role of reduced clearance of LDL-particles as well as dietary fat level and dietary cholesterol dependent changes in LDL-lipid composition have been discussed.     

Butter naturally enriched in conjugated linoleic acid and vaccenic acid alters tissue fatty acids and improves the plasma lipoprotein profile in cholesterol-fed hamsters

Butter, which is naturally enriched in cis-9, trans-11 conjugated linoleic acid (rumenic acid; RA) and vaccenic acid (VA), has been shown to be an effective anticarcinogen in studies with animal models; however, there has been no examination of the effects of a naturally derived source of VA and RA on atherosclerosis-related biomarkers. The current study was designed to determine the effect of a diet containing VA/RA-enriched butter on plasma lipoproteins and tissue fatty acid profiles in cholesterol-fed hamsters. Male Golden Syrian hamsters were fed diets containing 0.2% cholesterol and 20% added fat as: 1) Control, 20% standard butter (CT); 2) 5% standard butter + 15% VA/RA-enriched butter (EB); 3) 15% standard butter + 5% partially-hydrogenated vegetable oil (VO). After 4 wk, plasma lipoproteins were isolated, cholesterol quantified, and tissue fatty acid profiles determined. Tissue concentrations of VA and RA were increased by consumption of the EB diet compared with both the CT and VO diets, whereas the VO diet increased their concentration compared with the CT diet only. Total and LDL cholesterol concentrations were significantly reduced in hamsters fed EB and VO compared with CT, whereas VLDL cholesterol concentrations were reduced in hamsters fed EB compared with those fed CT and VO. HDL cholesterol concentrations did not differ among treatments. The ratio of potentially atherogenic lipoproteins [VLDL + intermediate density lipoproteins (IDL) + LDL] to antiatherogenic HDL was significantly lower in hamsters fed VA/RA-enriched butter (0.60) than in those fed either control diet (1.70) or the diet containing partially hydrogenated vegetable oil (1.04). Thus, increasing the VA/RA concentration of butter results in a plasma lipoprotein cholesterol profile that is associated with a reduced risk of atherosclerosis.     

The hypocholesterolemic effect of dietary soybean protein vs. casein in hamsters fed cholesterol-free or cholesterol-enriched semipurified diets

Golden Syrian hamsters fed a cholesterol-free diet containing 25% casein had higher plasma total triglyceride and cholesterol levels and VLDL + LDL cholesterol levels than animals fed a 25% soybean protein diet. Hamsters fed the cholesterol-free casein diet also had higher HDL cholesterol levels than animals fed the soybean protein diet, but these differences were not statistically significant. Addition of cholesterol to the diets caused even greater mean differences between the animals fed different types of protein, but the increased inter-animal variability of response to the added cholesterol resulted in less statistically significant differences. Although less responsive than the nonhybrid Golden Syrian hamsters, hybrid F1B hamsters showed similar effects of dietary casein vs. soybean protein on plasma lipids. These results indicate that the hamster may be a useful model to examine the effect of different types of protein and the interaction with dietary cholesterol on various plasma lipids and lipoproteins.     

Hamsters and guinea pigs differ in their plasma lipoprotein cholesterol distribution when fed diets varying in animal protein, soluble fiber, or cholesterol content.

There were two objectives to these studies: 1) to compare the lipoprotein cholesterol distribution in two animal models in response to different dietary treatments and 2) to assess whether the hypercholesterolemia induced by high cholesterol intake could be reversed by consumption of vegetable-protein and/or dietary fiber. Guinea pigs, which carry the majority of plasma cholesterol in LDL, and hamsters, with a higher distribution of cholesterol in HDL, were evaluated in three different studies. In Study 1, animals were fed semi-purified diets for 4 wk with proportions of 60:40, 20:80 or 0:100 (w/w) of casein/ soybean protein. Hamsters and guinea pigs that consumed 100% soybean protein had lower plasma total cholesterol (TC) than those fed diets containing casein (P < 0.01). In Study 2, three doses of dietary pectin (2.7, 5.4, or 10.7 g/100g) added in place of cellulose were tested. Intake of 10.7 g/100 g pectin resulted in the lowest plasma TC concentrations for both species (P < 0.01). Although the TC lowering was similar in studies 1 and 2, the lipoprotein cholesterol distribution differed. Whereas the differences in plasma cholesterol were in LDL in guinea pigs, hamsters exhibited differences in both non-HDL and HDL cholesterol. In study 3, animals were fed 100% soybean protein, 10.7 g/100 g pectin, and three doses of dietary cholesterol: 0.04, 0.08, or 0.16 g/100 g, which is equivalent to 300, 600, or 1,200 mg/d in humans. Guinea pigs and hamsters had the highest plasma LDL and hepatic cholesterol concentrations when they consumed 0.16 g/100 g of cholesterol (P < 0.01). However, intake of 0.08 g/100 g of cholesterol resulted in lower plasma LDL cholesterol concentrations than did consuming high animal protein (60:40 casein/ soy) or low soluble fiber (2.7 g/100 g). Relatively high levels of dietary cholesterol combined with vegetable protein and soluble fiber resulted in desirable lipoprotein profiles in animal models that significantly differ in their lipoprotein cholesterol distribution.     

Avenanthramides and phenolic acids from oats are bioavailable and act synergistically with vitamin C to enhance hamster and human LDL resistance to oxidation

The intake of phenolic acids and related polyphenolic compounds has been inversely associated with the risk of heart disease, but limited information is available about their bioavailability or mechanisms of action. Polyphenolics, principally avenanthramides, and simple phenolic acids in oat bran phenol-rich powder were dissolved in HCl:H(2)O:methanol (1:19:80) and characterized by HPLC with electrochemical detection. The bioavailability of these oat phenolics was examined in BioF1B hamsters. Hamsters were gavaged with saline containing 0.25 g oat bran phenol-rich powder (40 micromol phenolics), and blood was collected between 20 and 120 min. Peak plasma concentrations of avenanthramides A and B, p-coumaric, p-hydroxybenzoic, vanillic, ferulic, sinapic, and syringic acids appeared at 40 min. Although absorbed oat phenolics did not enhance ex vivo resistance of LDL to Cu(2+)-induced oxidation, in vitro addition of ascorbic acid synergistically extended the lag time of the 60-min sample from 137 to 216 min (P < or = 0.05), unmasking the bioactivity of the oat phenolics from the oral dose. The antioxidant capability of oat phenolics to protect human LDL against oxidation induced by 10 micromol/L Cu(2+) was also determined in vitro. Oat phenolics from 0.52 to 1.95 micromol/L increased the lag time to LDL oxidation in a dose-dependent manner (P < or = 0.0001). Combining the oat phenolics with 5 micromol/L ascorbic acid extended the lag time in a synergistic fashion (P < or = 0.005). Thus, oat phenolics, including avenanthramides, are bioavailable in hamsters and interact synergistically with vitamin C to protect LDL during oxidation.     

Hamsters predisposed to sucrose-induced cholesterol gallstones (LPN strain) are more resistant to excess dietary cholesterol than hamsters that are not sensitive to cholelithiasis induction

We compared the effects of cholesterol feeding in male hamsters from two strains with different propensities to sucrose-induced cholelithiasis; Laboratoire de Physiologie de la Nutrition (LPN) hamsters are predisposed to developing biliary cholesterol gallstones, whereas Janvier (JAN) hamsters are not. When fed a basal control diet, LPN hamsters had a lower cholesterolemia (-21%, P = 0.01) than JAN hamsters, and a higher activity of 3-hydroxy-3-methyl glutaryl coenzyme A reductase in liver (+148%, P = 0.018) and intestine (+281%, P < 0.0001). After feeding the same diet enriched with 0.3% cholesterol for 5 wk, cholesterolemia increased more dramatically in JAN hamsters (+235%, P < 0.001) than in LPN hamsters (+108%, P < 0.001), as did the liver concentration of cholesterol, which reached 152.30 +/- 13.00 and 44.41 +/- 9.06 micromol/g, respectively. Only JAN hamsters displayed hepatomegaly, with an increased cholesterol saturation index of the gallbladder bile (+100%, P < 0.01), due to the cholesterol challenge. In liver, cholesterol feeding reduced cholesterol 7alpha-hydroxylase activity and mRNA level, and stimulated sterol 27-hydroxylase and oxysterol 7alpha-hydroxylase activities. Hepatic levels of LDL receptor decreased by approximately 60% in both strains, whereas HDL receptor scavenger class B type 1 (SR-BI) levels were unaffected by dietary cholesterol. The greater resistance of LPN hamsters to the hypercholesterolemic diet can be explained by a lower capacity to store cholesterol in the liver and greater efficiency in reducing the activity of 3-hydroxy-3-methyl glutaryl coenzyme A reductase in response to cholesterol feeding [from 11263 to 261 pmol/(min x organ) in LPN hamsters and from 4530 to 694 pmol/(min x organ) in JAN hamsters]. These results highlight the usefulness of this two-strain model, which offers some analogy with the inverse association between the predisposition to cholelithiasis and the risk of atherosclerosis in humans.     

Flavonoids from almond skins are bioavailable and act synergistically with vitamins C and E to enhance hamster and human LDL resistance to oxidation

Consumption of tree nuts such as almonds has been associated with a reduced risk of coronary heart disease. Flavonoids, found predominantly in the skin of almonds, may contribute to their putative health benefit, but their bioactivity and bioavailability have not previously been studied. Almond skin flavonoids (ASF) were extracted with HCl:H2O:methanol (1:19:80) and their content of catechins and flavonols identified by HPLC with electrochemical detection. ASF bioactivity was assessed in vitro by their capacity to increase the resistance of human LDL to oxidation induced by 10 micromol/L Cu2+. ASF from 0.18 to 1.44 mumol gallic acid equivalent (GAE)/L increased the lag time to LDL oxidation in a dose-dependent manner (P < or = 0.0001). Combining ASF with vitamin E or ascorbic acid extended the lag time >200% of the expected additive value (P < or = 0.05). The bioavailability and in vivo antioxidant activity of 40 micromol ASF were examined in BioF1B hamsters. Peak plasma concentrations of catechin, epicatechin, and flavonols (quercetin, kaempferol, and isorhamnetin) occurred at 60, 120, and 180 min, respectively. The concentration of isorhamnetin was significantly elevated in liver at 180 min. Absorbed ASF enhanced the ex vivo resistance of hamster LDL collected at 60 min to oxidation by 18.0% (P = 0.028), and the in vitro addition of 5.5 micromol/L vitamin E synergistically extended the lag time of the 60-min sample by 52.5% (P < or = 0.05). Thus, ASF possess antioxidant capacity in vitro; they are bioavailable and act in synergy with vitamins C and E to protect LDL against oxidation in hamsters.     

Hydroxypropylmethylcellulose, Viscosity, and Plasma Cholesterol Control

The mechanism for the lowering of plasma cholesterol by water-soluble nonstarch polysaccharides (NSP) could involve alteration of intestinal viscosity leading to attenuated fat and steroid digestion and absorption. Alternatively, there may be direct inhibition of hepatic cholesterol synthesis by short-chain fatty acids produced by large bowel bacterial fermentation. A synthetic NSP, hydroxypropylmethylcellulose (HPMC), has been shown to lower plasma low-density lipoprotein (LDL) cholesterol in humans. This polysaccharide is not fermented by the large bowel microflora and has been shown to lower the plasma and liver cholesterol in hamsters, with no change noted in hepatic sterol synthesis. In further studies with hamsters, a linear relationship has been identified between plasma cholesterol and the logarithm of hydroxymethylcellulose viscosity. Only a relatively small increment in viscosity was necessary to achieve a maximal effect, suggesting that intestinal digestion may be quite sensitive to increased NSP intake.     

Dietary Cholesterol Affects Plasma Lipid Levels,the Intravascular Processing of Lipoproteins and Reverse Cholesterol Transport without Increasing the Risk for Heart Disease

The associations between dietary cholesterol and heart disease are highly controversial. While epidemiological studies and clinical interventions have shown the lack of correlation between cholesterol intake and cardiovascular disease (CVD) risk, there is still concern among health practitioners and the general population regarding dietary cholesterol. In this review, several clinical studies utilizing cholesterol challenges are analyzed in terms of changes that occur in lipoprotein metabolism resulting from excess consumption of cholesterol. Dietary cholesterol has been shown to increase both LDL and HDL in those individuals who respond to a cholesterol challenge without altering the LDL cholesterol/HDL cholesterol ratio, a key marker of CVD risk. Further, dietary cholesterol has been shown to increase only HDL with no changes in LDL with average cholesterol consumption and during weight loss interventions. Ingestion of cholesterol has also been shown to increase the size of both LDL and HDL particles with the associated implications of a less atherogenic LDL particle as well as more functional HDL in reverse cholesterol transport. Other changes observed in lipoprotein metabolism are a greater number of large LDL and decreases in small LDL subfractions. All this information put together points to specific roles of dietary cholesterol in substantially altering intravascular processing of lipoproteins as well as reverse cholesterol transport.     

Hamsters fed diets high in saturated fat have increased cholesterol accumulation and cytokine production in the aortic arch compared with cholesterol-fed hamsters with moderately elevated plasma non-HDL cholesterol concentrations

There is growing evidence that dietary fatty acids and/or dietary cholesterol could have a direct role on inflammatory diseases such as atherosclerosis. F(1)B Golden Syrian hamsters (Mesocricetus auratus), in 2 groups of 72, were fed for 10 wk a semipurified diet containing either 20 g/100 g hydrogenated coconut oil without cholesterol or cocoa butter (20 g/100 g) with cholesterol (0.15 g/100 g). After the 10-wk treatment period, plasma was collected from food-deprived hamsters (16 h) for plasma lipid measurements. Hamsters were then ranked according to their plasma VLDL and LDL cholesterol (non-HDL-C) concentrations with 1.86 mmol/L as the cut-off point between low (Low; n = 36) and medium (Med; n = 36) concentrations for each treatment. Hamsters in the Low and Medium groups fed cholesterol (Low-chol) had significantly lower plasma total cholesterol (TC) concentrations than hamsters in the Low group fed coconut oil (Low-CO). However, this difference for the Medium group was reflected in significantly lower plasma HDL cholesterol (HDL-C) concentrations. Hamsters in the Low-CO group had significantly higher aortic total and esterified cholesterol concentrations than hamsters in the Low-chol group. Hamsters in the Low-chol group had significantly higher aortic tumor necrosis factor-alpha concentrations than hamsters in the Low-CO group. Hamsters in the Med-CO group had significantly higher aortic interleukin-1beta concentrations than hamsters in the Med-chol group. In conclusion, the present study suggests that dietary cholesterol and saturated fatty acids could have an effect on atherosclerosis not only beyond their role in affecting plasma lipoproteins but also through increased production of inflammatory cytokines in the arterial wall.     

ANTI-LOW-DENSITY LIPOPROTEIN ANTIBODIES IN ALCOHOLICS WITHOUT AND WITH LIVER DISEASE AND IN SOCIAL DRINKERS

Antibodies directed to native and to in-vitro acetaldehyde-modified(ethylated) low-density lipoproteins (LDL) were determined in28 alcoholic subjects divided into two groups: one with do clinicalnor laboratory evidence of liver involvement and the secondwith histologically proven alcohol-related liver disease. Thecontrol group consisted of 18 individuals who drank alcoholsocially. In the individuals with alcoholic liver disease igGreactivity against both native and ethylated LDL was significantlyhigher than in alcoholic individuals without liver injury. Highlevels of IgG reactivity in individuals with alcoholic liverdisease were also observed against malondialdehyde-modified,methylated, acetylated and carbamylated LDL. A selective highanti-ethylated LDL IgG reactivity was observed in 11% of controlsubjects.     

CARDIAC CARNITINE-BINDING PROTEIN

Carnitine uptake by the heart is facilitated by a cardiac camitine-binding protein (CBP). A genetically cardiomyopathy strain of hamsters has altered CBP and a less effective carnitine transport system.,     

Effect of esterified 4-desmethylsterols and -stanols or 4,4'-dimethylsterols on cholesterol and bile acid metabolism in hamsters

4-Desmethylsterols and -stanols reduce plasma total cholesterol (TC) and LDL cholesterol by inhibition of intestinal cholesterol absorption, while the cholesterol-lowering potential of 4,4'-dimethylsterols is less well defined. The present study aimed to compare the effects of 4-desmethylsterols, -stanols, and 4,4'-dimethylsterols on plasma and hepatic cholesterol, sterol excretion and bile acid metabolism. Male golden Syrian hamsters were fed diets containing 13 g/100 g fat, 008 g/100 g cholesterol and 0 (control), 0.24 or 0.48% (w/w) esterified 4-desmethylsterols (sterols) and esterified hydrogenated 4-desmethylsterols (stanols) from common vegetable oils or esterified 4,4'-dimethylsterols from rice bran oil for 5 weeks. Sterol and stanol esters at the dose of 0.24% were equally effective and significantly (P<0.05) lowered TC by 15%, while 0.24% 4,4-dimethylsterols reduced TC by 10%. Liver total and esterified cholesterol concentrations were significantly (P<0.05) lowered by 40, 22, 43 and 31% in hamsters fed 0.48% sterols, 0.24% stanols, 0.48% stanols or 0.48% dimethylsterols, respectively. Daily faecal bile acid excretion and hepatic cholesterol 7alpha-hydroxylase activity were not altered, indicating that sterols, stanols and dimethylsterols had no effect on the intestinal re-absorption of bile acids or on hepatic bile acid synthesis. Daily excretion of cholesterol was significantly higher in hamsters fed esterified sterols and stanols, but was only slightly increased in those fed dimethylsterols. The results indicate that esterified sterols and stanols were equally effective in lowering plasma TC and LDL cholesterol, while dimethylsterol esters caused a weaker cholesterol-lowering effect. Sterols and stanols achieve their cholesterol-lowering effect by stimulating faecal cholesterol excretion through inhibiting intestinal cholesterol absorption, but do not affect bile acid excretion. Other mechanisms need to be considered to explain the effect on plasma and hepatic cholesterol of dimethylsterols.     

Reduction in cholesterol absorption is enhanced by stearate-enriched plant sterol esters in hamsters

Consumption of plant sterol esters reduces plasma LDL cholesterol concentration by inhibiting intestinal cholesterol absorption. Commercially available plant sterol esters are prepared by esterifying free sterols to fatty acids from edible plant oils such as canola, soybean, and sunflower. To determine the influence of the fatty acid moiety on cholesterol metabolism, plant sterol esters were made with fatty acids from soybean oil (SO), beef tallow (BT), or purified stearic acid (SA) and fed to male hamsters for 4 wk. A control group fed no plant sterol esters was also included. Hamsters fed BT and SA had significantly lower cholesterol absorption and decreased concentrations of plasma non-HDL cholesterol and liver esterified cholesterol, and significantly greater fecal sterol excretion than SO and control hamsters. Cholesterol absorption was lowest in hamsters fed SA (7.5%), whereas it was 72.9% in control hamsters. Cholesterol absorption was correlated with fecal sterol excretion (r = -0.72, P < 0.001), liver cholesterol concentration (r = 0.88, P < 0.001), and plasma non-HDL cholesterol concentration (r = 0.85, P < 0.001). A multiple regression model that included each sterol ester type vs. cholesterol absorption indicated that intake of steryl stearate was the only dietary component that contributed significantly to the model (R2 = -0.75, P < 0.001). Therefore, our results demonstrate that BT and SA are more effective than SO in reducing cholesterol absorption, liver cholesterol, and plasma non-HDL cholesterol concentration, suggesting that cardioprotective benefits can be achieved by consuming stearate-enriched plant sterol esters.     

The natural concentration of the conjugated linoleic acid, cis-9,trans-11, in milk fat has antiatherogenic effects in hyperlipidemic hamsters

Milk fat is usually considered to be proatherogenic, although its fatty acid composition can vary, due mainly to farming conditions. No study has evaluated whether such variation can modify the atherogenic properties of dairy fat. Aortic lipid deposition and related risk factors were examined in Syrian hamsters fed diets for 12 wk containing 200 g/kg of 2 commercial milk fats [high content of saturated fatty acids (HSF) and low content of saturated fatty acids (LSF)] contrasting, respectively, in total saturated fatty acids (72 vs. 67 g/100 g), 18:1, trans (4.24 vs. 7.26 g/100g), and conjugated linoleic acid (mainly cis-9,trans-11 or rumenic acid; 0.39 vs. 2.59 g/100 g). Hamsters fed the LSF-diet had 25% less aortic cholesteryl-ester deposition than those fed the HSF-diet; this was accompanied by an improved plasma cholesterol profile (lower LDL cholesterol and LDL:HDL cholesterol ratio), a lower local inflammatory status (aortic gene expression of cyclooxygenase-2), and lower aortic gene expression of vascular cell adhesion molecule-1 (all P < 0.05). Supplementation of the LSF-diet with rumenic acid (up to 9 g/kg) amplified the antiatherogenic effect of the original LSF-diet compared with the HSF-diet, i.e., less aortic cholesterol loading, increased reverse cholesterol transport potential (higher plasma HDL cholesterol concentration and ATP-binding cassette, subfamily A, transporter 1 gene expression in aorta), and decreased LDL-peroxidability index and gene expression of proinflammatory IL-1beta in the aorta (all P < 0.05). In conclusion, our results suggest that the atherogenic potential of milk fat can be greatly reduced in products with a naturally high abundance of rumenic acid, and argue for increasing this fatty acid in milk.     

THYROIDITIS AND EXCESS IODINE

The reaction of hyperplastic thyroid glands of hamsters to iodine at higher than required levels is of two types: a thyroiditis and an inhibition of colloid reaccumulation.     

The hypocholesterolemic effect of lemon peels,lemon pectin,and the waste stream material of lemon peels in hybrid F<Subscript>1</Subscript>B hamsters

Summary Background We found in preliminary studies with hamsters that citrus peels have a cholesterol lowering effect comparable to that of pectin extracted from these peels. Aim of the study We wanted to examine whether the cholesterol lowering effect of the peels could be completely accounted for by the pectin in the peels. Methods We fed cholesterol enriched (0.1 %,w/w) semipurified diets containing 3 % (w/w) of cellulose, lemon peels, lemon pectin, and the waste stream material of the lemon peels to hybrid F₁B hamsters for a period of 8 weeks. The waste stream of the lemon peels is the left over after extraction of the lemon pectin. Results Feeding the semipurified diets resulted in an increase of plasma cholesterol levels in all the dietary groups after 2 and 4 weeks on the diets. Cholesterol concentrations in the cellulose fed hamsters continued to increase after 4 weeks on the diet, whereas cholesterol levels in the other groups had reached a plateau. As a consequence, the plasma cholesterol levels in the hamsters fed the peels (5.59 ± 0.74 mmol/L, mean ± SD, n = 14), pectin (5.19 ± 0.48 mmol/L), or waste stream (5.53 ± 0.94 mmol/L) were lower than those in the hamsters fed cellulose (6.71 ± 1.52 mmol/L) after 8 weeks on the diets. Differences in total plasma cholesterol were reflected in differences in both VLDL and LDL cholesterol concentration, but this effect was more distinct for the VLDL. There was no effect of the type of fiber on HDL cholesterol levels. Liver cholesterol concentrations paralleled the concentrations of plasma cholesterol and the liver cholesterol concentrations in the hamsters fed the peels (3.57 ± 1.01 μmol/g liver, mean ± SD, n = 14), pectin (4.86 ± 1.42), and the waste stream (4.96 ± 1.89) were lower than those in the cellulose group (7.19 ± 2.32). The hamsters fed the peels, pectin, or waste stream tended to have a higher excretion of fecal bile acids and neutral sterols then the cellulose fed hamsters. Conclusion The results of this study suggest that lemon peels and the waste stream of the lemon peels are as effective in lowering plasma and liver cholesterol in hamsters as the pectin extracted from the peels and that also compounds other than pectin are probably responsible for the cholesterol lowering effect of the citrus peels. Received: 20 September 2001, Accepted: 17 December 2001     

Dietary polyunsaturated to saturated fatty acid ratio alters hepatic LDL transport in cynomolgus macaques fed low cholesterol diets.

To determine effect of interaction between dietary cholesterol and triglyceride, i.e., polyunsaturated to saturated (P:S) fatty acid ratio, on LDL metabolism, male cynomolgus macaques were fed purified diets for 83 wk with cholesterol levels of 0.01, 0.06 and 0.50 mg/kJ and P:S ratios of 0.5 and 0.9, oleic acid constant. There were six groups of five animals each (cholesterol, mg/kJ--P:S ratio): Group 1, 0.01--0.5; Group 2, 0.01--0.9; Group 3, 0.06--0.5; Group 4, 0.06--0.9; Group 5, 0.50-0.5; Group 6, 0.50-0.9. LDL (1.019 less than d less than 1.063 kg/L) and glucosylated LDL were iodinated for turnover studies. Hepatic LDL transport was determined using 125I-tyramine-cellobiose-LDL as tracer. Plasma cholesterol increased in proportion to dietary cholesterol, and concentrations (mmol/L) at 77-78 wk were (mean +/- SEM): Group 1, 434 +/- 0.31; Group 2, 3.03 +/- 0.14; Group 3, 8.28 +/- 1.48; Group 4, 7.34 +/- 1.31; Group 5, 15.54 +/- 1.44; Group 6, 15.54 +/- 1.41. LDL cholesterol was 45% higher in Group 1 (2.43 mmol/L) than in Group 2 (1.68 mmol/L). In vivo studies showed that LDL clearance was suppressed by excess dietary cholesterol; receptor-independent LDL clearance was relatively constant. Hepatic LDL protein transport was greater in Group 2 (P:S 0.9) compared with Group 1 (P:S 0.5). The LDL protein synthetic rate was lower in Groups 2, 4 and 6 (P:S 0.9) relative to Groups 1, 3 and 5 (P:S 0.5). We conclude that in this model hepatic LDL receptor activity is altered by degree of saturation in dietary triglycerides when dietary cholesterol is minimal, and that saturated dietary triglycerides enhance LDL protein secretion when dietary cholesterol is ample.