Diet-induced dyslipidemia impairs reverse cholesterol transport in hamsters

Tréguier, Morgan; Briand, François; Boubacar, Adamou; André, Agnès; Magot, T.; Nguyen, Patrick; Krempf, Michel; Sulpice, Thierry; Ouguerram, Khadija

doi:10.1111/j.1365-2362.2011.02478.x

Cited by 26 publications

(29 citation statements)

References 29 publications

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“…A recent report showed that diet-induced dyslipidemia impaired macrophage-to-feces RCT in hamsters fed a low-fat diet containing 0.3% cholesterol, although it did cause a pronounced increase in HDL-C. 51 Hamsters express CETP, but the HFHC diet also promoted RCT in our CETP transgenic mice. The differences in these results may be attributable to the specific diet-induced changes in the liver gene expression profile of hamsters.…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that the observed increased macrophage-specific RCT is an insufficient, compensatory mechanism to protect against atherosclerosis development. Therefore, HFHC diet-mediated effects on HDL antiinflammatory activity, 49 non-HDL-C, and fat cells and macrophage inflammation 50 appear to be the major contributor to atherosclerosis in these mice.A recent report showed that diet-induced dyslipidemia impaired macrophage-to-feces RCT in hamsters fed a low-fat diet containing 0.3% cholesterol, although it did cause a pronounced increase in HDL-C. 51 Hamsters express CETP, but the HFHC diet also promoted RCT in our CETP transgenic mice. The differences in these results may be attributable to the specific diet-induced changes in the liver gene expression profile of hamsters.…”

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confidence: 99%

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The Cholesterol Content of Western Diets Plays a Major Role in the Paradoxical Increase in High-Density Lipoprotein Cholesterol and Upregulates the Macrophage Reverse Cholesterol Transport Pathway

Escolà‐Gil

Llaverı́as

Julve

et al. 2011

ATVB

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Objective-A high-saturated fatty acid-and cholesterol-containing (HFHC) diet is considered to be a major risk factor for cardiovascular disease. The present study aimed to determine the effects of this Western-type diet on high-density lipoprotein (HDL) metabolism and reverse cholesterol transport (RCT) from macrophages to feces. Methods and Results-Experiments were carried out in mice fed a low-fat, low-cholesterol diet, an HFHC diet, or an HFHC diet without added cholesterol (high-saturated fatty acid and low-cholesterol [HFLC]). The HFHC diet caused a significant increase in plasma cholesterol, HDL cholesterol, and liver cholesterol and enhanced macrophage-derived [ 3 H]cholesterol flux to feces by 3-to 4-fold. These effects were greatly reduced in mice fed the HFLC diet. This HFHC diet-mediated induction of RCT was sex independent and was not associated with obesity or insulin resistance. The HFHC diet caused 1.4-and 3-fold increases in [ 3 H]cholesterol efflux to plasma and HDL-derived [ 3 H]tracer fecal excretion, respectively. Unlike a low-fat, low-cholesterol and HFLC diets, the HFHC diet increased liver ABCG5/G8 expression. The effect of the HFHC diet on fecal macrophage-derived [ 3 H]cholesterol excretion was totally blunted in ABCG5/G8-deficient mice. Conclusion-Despite its deleterious effects on atherosclerosis, the HFHC diet promoted a sustained compensatory macrophage-to-feces RCT. Our data provide direct evidence of the crucial role of dietary cholesterol signaling through liver ABCG5/G8 upregulation in the HFHC diet-mediated induction of macrophage-specific RCT. ietary saturated fat intake has been associated with an increased risk of atherosclerotic cardiovascular disease and metabolic diseases, such as obesity and type 2 diabetes. 1,2 This effect is thought to be mediated by an increase in plasma cholesterol, mainly low-density lipoprotein cholesterol. 3 However, both dietary saturated fat and cholesterol intake are known to raise plasma high-density lipoprotein cholesterol (HDL-C) levels. 4 -8 Several epidemiological studies and 1 meta-analysis of 60 controlled trials showed a positive correlation between high saturated fat intake and HDL-C. 9 -11 In an attempt to determine the mechanism underlying this paradoxical observation, several studies reported that a low saturated fat and cholesterol intake reduced HDL-C levels by reducing the apolipoprotein A-I secretion rate. [12][13][14] However, other studies found this effect to be associated with decreased apolipoprotein A-I fractional catabolic rates. 15,16 Also, when dietary cholesterol was increased along with total and saturated fat, increases in large high-density lipoprotein (HDL) subpopulations and HDL apolipoprotein E amounts were observed. 7,17 Macrophage-specific reverse cholesterol transport (RCT) is thought to be one of the most important HDL-mediated cardioprotective mechanisms. 18 HDL plays a critical role in cholesterol efflux from macrophages, the first step in RCT. 18 However, despite the reported changes in HDL compositi...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The Cholesterol Content of Western Diets Plays a Major Role in the Paradoxical Increase in High-Density Lipoprotein Cholesterol and Upregulates the Macrophage Reverse Cholesterol Transport Pathway

Escolà‐Gil

Llaverı́as

Julve

et al. 2011

ATVB

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“…Meanwhile, an animal model that reflects the human situation (e.g., fat and fructose overconsumption) would be helpful to evaluate novel therapies targeting metabolic syndrome. We recently demonstrated the relevance of the hamster model for studying RCT (11)(12)(13), because this CETP-expressing species has a similar lipoprotein metabolism to humans (11). In the present study, Golden Syrian hamsters were fed a high fat/ fructose-enriched (HF) diet to induce the main features of human metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

High-Fat and Fructose Intake Induces Insulin Resistance, Dyslipidemia, and Liver Steatosis and Alters In Vivo Macrophage-to-Feces Reverse Cholesterol Transport in Hamsters

Briand

Thieblemont

Muzotte

et al. 2012

The Journal of Nutrition

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Reverse cholesterol transport (RCT) promotes the egress of cholesterol from peripheral tissues to the liver for biliary and fecal excretion. Although not demonstrated in vivo, RCT is thought to be impaired in patients with metabolic syndrome, in which liver steatosis prevalence is relatively high. Golden Syrian hamsters were fed a nonpurified (CON) diet and normal drinking water or a high-fat (HF) diet containing 27% fat, 0.5% cholesterol, and 0.25% deoxycholate as well as 10% fructose in drinking water for 4 wk. Compared to CON, the HF diet induced insulin resistance and dyslipidemia, with significantly higher plasma non-HDL-cholesterol concentrations and cholesteryl ester transfer protein activity. The HF diet induced severe liver steatosis, with significantly higher cholesterol and TG levels compared to CON. In vivo RCT was assessed by i.p. injecting ³H-cholesterol labeled macrophages. Compared to CON, HF hamsters had significantly greater ³H-tracer recoveries in plasma, but not HDL. After 72 h, ³H-tracer recovery in HF hamsters was 318% higher in liver and 75% lower in bile (P < 0.01), indicating that the HF diet impaired hepatic cholesterol fluxes. However, macrophage-derived cholesterol fecal excretion was 45% higher in HF hamsters than in CON hamsters. This effect was not related to intestinal cholesterol absorption, which was 89% higher in HF hamsters (P < 0.05), suggesting a possible upregulation of transintestinal cholesterol excretion. Our data indicate a significant increase in macrophage-derived cholesterol fecal excretion in a hamster model of metabolic syndrome, which may not compensate for the diet-induced dyslipidemia and liver steatosis.

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“…Except steroidogenic tissues, cells in general, are unable to metabolize cholesterol, so the non-esterified cholesterol excess is carried by the liver, to the biliary and fecal output. However, this mechanism may become inefficient, and cholesterol accumulates in the hepatocytes [40]. Indeed, HFS and HFS-PO animals had higher hepatic cholesterol accumulation and higher fecal output.…”

Section: Discussionmentioning

confidence: 99%

The Partial Replacement of Lard by Caryocar brasiliense Oil in a Western Diet improves Cardiovascular Risk Factors in Rats

Esteves¹

2017

F Nutr Reprt

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Diet-induced dyslipidemia impairs reverse cholesterol transport in hamsters

Abstract: Overall, these data demonstrate that diet-induced dyslipidemia severely impairs in vivo RCT in hamsters.

Cited by 26 publications

References 29 publications

The Cholesterol Content of Western Diets Plays a Major Role in the Paradoxical Increase in High-Density Lipoprotein Cholesterol and Upregulates the Macrophage Reverse Cholesterol Transport Pathway

The Cholesterol Content of Western Diets Plays a Major Role in the Paradoxical Increase in High-Density Lipoprotein Cholesterol and Upregulates the Macrophage Reverse Cholesterol Transport Pathway

High-Fat and Fructose Intake Induces Insulin Resistance, Dyslipidemia, and Liver Steatosis and Alters In Vivo Macrophage-to-Feces Reverse Cholesterol Transport in Hamsters

The Partial Replacement of Lard by Caryocar brasiliense Oil in a Western Diet improves Cardiovascular Risk Factors in Rats

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