A Murine Model of Obesity With Accelerated Atherosclerosis

King, Victoria; Hatch, Nicholas; Chan, Huei Wei; Beer, Maria C. de; Beer, Frederick C. de; Tannock, Lisa R.

doi:10.1038/oby.2009.176

Cited by 74 publications

(75 citation statements)

References 37 publications

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“…These changes in microbiota increased the capability to break down fiber into short chain fatty acids and to release additional energy, which could be converted into fat 28) . ApoE-deficient mice fed a high fat diet were recently found to exhibit a chronic level of inflammation, which may mediate the formation of atherosclerotic lesions 29) . The influence of probiotic bacteria was studied in patients with a high cholesterol level supplemented with L. plantarum 299v.…”

Section: Discussionmentioning

confidence: 99%

Absence of Microbiota (Germ-Free Conditions) Accelerates the Atherosclerosis in ApoE-Deficient Mice Fed Standard Low Cholesterol Diet

Štěpánková

Tonar

Bártová

et al. 2010

JAT

140

120

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Aim:The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice. Methods:The experiments were performed on ApoE / -deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3 − 4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods. Results: Conventionally reared ApoE / mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE / mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls. Conclusion: In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE / mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE / mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development. J Atheroscler Thromb, 2010; 17:796-804.

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Section: Discussionmentioning

confidence: 99%

Absence of Microbiota (Germ-Free Conditions) Accelerates the Atherosclerosis in ApoE-Deficient Mice Fed Standard Low Cholesterol Diet

Štěpánková

Tonar

Bártová

et al. 2010

JAT

140

120

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“…Specifically, we found that apoE -/-mice fed a high-fat diet (with 60% of the calories from fat) for 17 weeks have increased body weight and atherosclerosis (King et al, 2009). These high-fatfed apoE -/-mice are glucose intolerant and also display elevated systemic inflammation, as measured by increased serum amyloid A concentrations in the plasma.…”

Section: Apolipoprotein E (Apoe)-deficient Micementioning

confidence: 99%

Mouse models of the metabolic syndrome

Kennedy

Ellacott

King

et al. 2010

Disease Models &Amp; Mechanisms

Self Cite

233

224

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The metabolic syndrome (MetS) is characterized by obesity concomitant with other metabolic abnormalities such as hypertriglyceridemia, reduced high-density lipoprotein levels, elevated blood pressure and raised fasting glucose levels. The precise definition of MetS, the relationships of its metabolic features, and what initiates it, are debated. However, obesity is on the rise worldwide, and its association with these metabolic symptoms increases the risk for diabetes and cardiovascular disease (among many other diseases). Research needs to determine the mechanisms by which obesity and MetS increase the risk of disease. In light of this growing epidemic, it is imperative to develop animal models of MetS. These models will help determine the pathophysiological basis for MetS and how MetS increases the risk for other diseases. Among the various animal models available to study MetS, mice are the most commonly used for several reasons. First, there are several spontaneously occurring obese mouse strains that have been used for decades and that are very well characterized. Second, high-fat feeding studies require only months to induce MetS. Third, it is relatively easy to study the effects of single genes by developing transgenic or gene knockouts to determine the influence of a gene on MetS. For these reasons, this review will focus on the benefits and caveats of the most common mouse models of MetS. It is our hope that the reader will be able to use this review as a guide for the selection of mouse models for their own studies.

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“…The serum adiponectin concentration after 12 weeks of HF + PP feeding did not change significantly when compared with HF feeding. There was a report that ApoE-deficient mice fed high fat diet had a marked atherosclerotic lesion formation, but did not show significant difference in adipocytokine levels including adiponectin [40].…”

Section: Discussionmentioning

confidence: 99%

Persimmon (Diospyros Kaki Thunb ‘Saijo’) Peel Improved Dyslipidemia and its Related Production of Atherogenic Autoantigen Complexes in Low- Density Lipoprotein Receptor-Deficient Mice

Quan¹,

Kobayashi²,

Matsunami³

et al. 2012

TONUTRJ

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Abstract:Role of persimmon (Diospyros kaki, Thunb 'Saijo') peel was investigated on developing atherosclerosis in low-density lipoprotein receptor (LDLR)-deficient mice with emphasis on lipid metabolism, physio-biological oxidation, production of related atherogenic autoantigens, and production of anti-atherogenic natural antibodies. Male LDLRdeficient mice were fed high fat diet or high fat diet supplemented with 10% dried and powdered persimmon peel (PP) for 12 weeks. PP supplementation significantly prevented the increment of plasma cholesterol and triglyceride levels. High fat diet feeding increased plasma level of oxidized LDL/β2-glycoprotein I (oxLDL/β2GPI) complexes regarded as an atherogenic autoantigen, while PP supplementation significantly blocked the increment (p<0.05). After a 12-week feeding, atherosclerotic plaques in mice fed with diet supplemented with PP decreased by 70% as compared to that of mice fed the high fat diet (p<0.005). PP feeding also reduced urinary 11-dehydro-thromboxane B 2 , a stable metabolite of the platelet activation marker thromboxane A 2 , but level of IgM anti-oxLDL antibodies was not changed. Thus, these results obviously demonstrate that persimmon peel may have an anti-atherogenic property through normalization of lipid metabolism and reduced production of the atherogenic complexes.

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A Murine Model of Obesity With Accelerated Atherosclerosis

Cited by 74 publications

References 37 publications

Absence of Microbiota (Germ-Free Conditions) Accelerates the Atherosclerosis in ApoE-Deficient Mice Fed Standard Low Cholesterol Diet

Absence of Microbiota (Germ-Free Conditions) Accelerates the Atherosclerosis in ApoE-Deficient Mice Fed Standard Low Cholesterol Diet

Mouse models of the metabolic syndrome

Persimmon (Diospyros Kaki Thunb ‘Saijo’) Peel Improved Dyslipidemia and its Related Production of Atherogenic Autoantigen Complexes in Low- Density Lipoprotein Receptor-Deficient Mice

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