The metabolic response to a high-fat diet reveals obesity-prone and -resistant phenotypes in mice with distinct mRNA-seq transcriptome profiles

Jy, Choi; Ra, McGregor; Ey, Kwon; Kim, Yoon Jun; Han, Yang; Jh, Park; Kw, Lee; Sj, Kim; J, Kim; Yun, Jong Won; Choi, Man‐Yeon

doi:10.1038/ijo.2016.70

Cited by 25 publications

(19 citation statements)

References 41 publications

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“…4A). Interestingly, we found that −/− Y mice had a similar expression profile to those on a high-fat diet (HFD) (32), which verified that Elovl2 ablation resulted in fatty acid accumulation (SI Appendix, Fig. S5A).…”

Section: Rna-seq Analysis Indicates Various Metabolic and Aging-relatedsupporting

confidence: 64%

RETRACTED: Impaired lipid metabolism by age-dependent DNA methylation alterations accelerates aging

Wang

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Epigenetic alterations and metabolic dysfunction are two hallmarks of aging. However, the mechanism of how their interaction regulates aging, particularly in mammals, remains largely unknown. Here we show ELOVL fatty acid elongase 2 (Elovl2), a gene whose epigenetic alterations are most highly correlated with age prediction, contributes to aging by regulating lipid metabolism. Impaired Elovl2 function disturbs lipid synthesis with increased endoplasmic reticulum stress and mitochondrial dysfunction, leading to key accelerated aging phenotypes. Restoration of mitochondrial activity can rescue age-related macular degeneration (AMD) phenotypes induced by Elovl2 deficiency in human retinal pigmental epithelial (RPE) cells. We revealed an epigenetic–metabolism axis contributing to aging and potentially to antiaging therapy.

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Section: Rna-seq Analysis Indicates Various Metabolic and Aging-relatedsupporting

confidence: 64%

RETRACTED: Impaired lipid metabolism by age-dependent DNA methylation alterations accelerates aging

Wang

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…EAE impairs hepatic development and increases the propensity for hepatic stress. The liver is the primary metabolic organ of the body, and alterations in its response to HFHC diet are a risk factor for the development of metabolic syndrome (54). Therefore, we examined the impact of EAE on hepatic development using fluorescent reporter lines and in situ hybridization.…”

Section: Resultsmentioning

confidence: 99%

Fetal alcohol spectrum disorder predisposes to metabolic abnormalities in adulthood

Weeks¹,

Bossé²,

Oderberg³

et al. 2020

Journal of Clinical Investigation

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“…In fact, numerous studies based on single strains have shown that a subset of the most commonly used rodent strains, namely, the inbred C57Bl/6 mice and the outbred Sprague-Dawley rats, do not respond to HFD feeding. 68,212 Importantly, studies evaluating a large collection of inbred strains not only provide better understanding of this variation but also mimic the diversity observed in human populations. One such study compared the metabolic responses to HFD in males and females of 43 inbred mouse strains.…”

Section: Prediabetesmentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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Diet is a critical element determining human health and diseases, and unbalanced food habits are major risk factors for the development of obesity and related metabolic disorders. Despite technological and pharmacological advances, as well as intensification of awareness campaigns, the prevalence of metabolic disorders worldwide is still increasing. Thus, novel therapeutic approaches with increased efficacy are urgently required, which often depends on cellular and molecular investigations using robust animal models. In the absence of perfect rodent models, those induced by excessive consumption of fat and sugars better replicate the key aspects that are the root causes of human metabolic diseases. However, the results obtained using these models cannot be directly compared, particularly because of the use of different dietary protocols, and animal species and strains, among other confounding factors. This review article revisits diet-induced models of obesity and related metabolic disorders, namely, metabolic syndrome, prediabetes, diabetes and nonalcoholic fatty liver disease. A critical analysis focused on the main pathophysiological features of rodent models, as opposed to the criteria defined for humans, is provided as a practical guide with a translational perspective for the establishment of animal models of obesity-related metabolic diseases.

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The metabolic response to a high-fat diet reveals obesity-prone and -resistant phenotypes in mice with distinct mRNA-seq transcriptome profiles

Abstract: Taken altogether, the results provide robust evidence of major divergence in the transcriptomes, phenotypes and metabolic processes between obesity susceptibility and obesity resistance in the HFD-fed C57BL/6J mice.

Cited by 25 publications

References 41 publications

RETRACTED: Impaired lipid metabolism by age-dependent DNA methylation alterations accelerates aging

RETRACTED: Impaired lipid metabolism by age-dependent DNA methylation alterations accelerates aging

Fetal alcohol spectrum disorder predisposes to metabolic abnormalities in adulthood

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

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