Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet

Nishikawa, Satomi; Sugimoto, Jiro; Okada, Mitsuru; Sakairi, Tetsuya; Takagi, Shigeaki

doi:10.1177/0192623311422078

Cited by 38 publications

(29 citation statements)

References 18 publications

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“…Moreover, as we have previously observed, LCFA uptake and lipid deposition in the liver are directly related to CD36 expression, suggesting a causative role for increased CD36 expression in the pathogenesis of type 2 diabetes [18]. Similar findings were observed by several other rodent studies [22,23] and have recently been confirmed in liver biopsies of patients with NAFLD, highlighting the clinical relevance of CD36 in human liver diseases associated with obesity and type 2 diabetes [24]. Its role in age-associated NAFLD is, however, not yet known.…”

Section: Introductionsupporting

confidence: 85%

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Sheedfar

Sung

Aparicio-Vergara

et al. 2014

Aging

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CD36 has been associated with obesity and diabetes in human liver diseases, however, its role in age-associated nonalcoholic fatty liver disease (NAFLD) is unknown. Therefore, liver biopsies were collected from individuals with histologically normal livers (n=30), and from patients diagnosed with simple steatosis (NAS; n=26). Patients were divided into two groups according to age and liver biopsy samples were immunostained for CD36. NAFLD parameters were examined in young (12-week) and middle-aged (52-week) C57BL/6J mice, some fed with chow-diet and some fed with low-fat (LFD; 10% kcal fat) or high-fat diet (HFD; 60% kcal fat) for 12-weeks. CD36 expression was positively associated with age in individuals with normal livers but not in NAS patients. However, CD36 was predominantly located at the plasma membrane of hepatocytes in aged NAS patients as compared to young. In chow-fed mice, aging, despite an increase in hepatic CD36 expression, was not associated with the development of NAFLD. However, middle-aged mice did exhibit the development of HFD-induced NAFLD, mediated by an increase of CD36 on the membrane. Enhanced CD36-mediated hepatic fat uptake may contribute to an accelerated progression of NAFLD in mice and humans. Therapies to prevent the increase in CD36 expression and/or CD36 from anchoring at the membrane may prevent the development of NAFLD.

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Section: Introductionsupporting

confidence: 85%

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Sheedfar

Sung

Aparicio-Vergara

et al. 2014

Aging

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“…As these studies were conducted with laboratory animals and diverse diets, we would not expect a full overlap of genes that respond to the changed environment, but there are important matches. For example, seven metabolic genes ( Acox1 , Acsl1 , Cyp39a1 , Cyp4a14 , Dgka , Hsd17b12 , Scp2 ) and two transcription factors ( Ppara , Srebf1 ), which responded significantly to the metabolic demand of a high-fat diet [69], were differently marked in our study (gene set >94%tile). Similarly, metabolic genes Acsl1 , Ddc , G6pc , Pck1 , nuclear factors Hnf4a , Nrbf2 , Ppara , Srebf1 , immune and cell cycle genes Irf1 , Il1r1 , Pcna , and signal transduction genes Gna11 , Rgs2 were differentially expressed in mouse liver tissue after a high-fat diet [68] and differently marked in our mice.…”

Section: Discussioncontrasting

confidence: 50%

Genome-Wide Quantitative Analysis of Histone H3 Lysine 4 Trimethylation in Wild House Mouse Liver: Environmental Change Causes Epigenetic Plasticity

et al. 2014

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In mammals, exposure to toxic or disease-causing environments can change epigenetic marks that are inherited independently of the intrauterine environment. Such inheritance of molecular phenotypes may be adaptive. However, studies demonstrating molecular evidence for epigenetic inheritance have so far relied on extreme treatments, and are confined to inbred animals. We therefore investigated whether epigenomic changes could be detected after a non-drastic change in the environment of an outbred organism. We kept two populations of wild-caught house mice (Mus musculus domesticus) for several generations in semi-natural enclosures on either standard diet and light cycle, or on an energy-enriched diet with longer daylight to simulate summer. As epigenetic marker for active chromatin we quantified genome-wide histone-3 lysine-4 trimethylation (H3K4me3) from liver samples by chromatin immunoprecipitation and high-throughput sequencing as well as by quantitative polymerase chain reaction. The treatment caused a significant increase of H3K4me3 at metabolic genes such as lipid and cholesterol regulators, monooxygenases, and a bile acid transporter. In addition, genes involved in immune processes, cell cycle, and transcription and translation processes were also differently marked. When we transferred young mice of both populations to cages and bred them under standard conditions, most of the H3K4me3 differences were lost. The few loci with stable H3K4me3 changes did not cluster in metabolic functional categories. This is, to our knowledge, the first quantitative study of an epigenetic marker in an outbred mammalian organism. We demonstrate genome-wide epigenetic plasticity in response to a realistic environmental stimulus. In contrast to disease models, the bulk of the epigenomic changes we observed were not heritable.

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“…Variations in these experimental parameters may explain why previous studies have characterised the 129 and DBA/2 strains as either prone to obesity and insulin resistance, as shown in our comparison [1,7], or relatively resistant to the effects accompanying an HFD [1,7,46]. Similarly, BALB/c mice have been previously reported as being either prone [47] or resistant [48] to dietinduced hepatic lipid accumulation. The strength of the present study is that all strains of mice were studied at the same time, under the same experimental conditions.…”

Section: Discussionmentioning

confidence: 48%

Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding

et al. 2013

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Aims/hypothesis Metabolic disorders are commonly investigated using knockout and transgenic mouse models. A variety of mouse strains have been used for this purpose. However, mouse strains can differ in their inherent propensities to develop metabolic disease, which may affect the experimental outcomes of metabolic studies. We have investigated straindependent differences in the susceptibility to diet-induced obesity and insulin resistance in five commonly used inbred mouse strains (C57BL/6J, 129X1/SvJ, BALB/c, DBA/2 and FVB/N). Methods Mice were fed either a low-fat or a high-fat diet (HFD) for 8 weeks. Whole-body energy expenditure and body composition were then determined. Tissues were used to measure markers of mitochondrial metabolism, inflammation, oxidative stress and lipid accumulation. Results BL6, 129X1, DBA/2 and FVB/N mice were all susceptible to varying degrees to HFD-induced obesity, glucose intolerance and insulin resistance, but BALB/c mice exhibited some protection from these detrimental effects. This protection could not be explained by differences in mitochondrial metabolism or oxidative stress in liver or muscle, or inflammation in adipose tissue. Interestingly, in contrast with the other strains, BALB/c mice did not accumulate excess lipid (triacylglycerols and diacylglycerols) in the liver; this is potentially related to lower fatty acid uptake rather than differences in lipogenesis or lipid oxidation. Conclusions/interpretation Collectively, our findings indicate that most mouse strains develop metabolic defects on an HFD. However, there are inherent differences between strains, and thus the genetic background needs to be considered carefully in metabolic studies. Keywords

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Gene Expression in Livers of BALB/C and C57BL/6J Mice Fed a High-Fat Diet

Cited by 38 publications

References 18 publications

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Genome-Wide Quantitative Analysis of Histone H3 Lysine 4 Trimethylation in Wild House Mouse Liver: Environmental Change Causes Epigenetic Plasticity

Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding

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