Transcriptome Analysis of Skin from SMP30/GNL Knockout Mice Reveals the Effect of Ascorbic Acid Deficiency on Skin and Hair

Wakame, Koji; Komatsu, Kenichi; Nakata, Akifumi; Sato, Keisuke; Takaguri, Akira; Masutomi, Hirofumi; Nagashima, Takayuki; Uchiyama, Hiroo

doi:10.21873/invivo.11100

Cited by 6 publications

(9 citation statements)

References 15 publications

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“…Portions of the RNA samples were subjected to RNA sequencing (RNA-Seq) and corresponding qPCR analyses. RNA-Seq was performed as previously described [ 34 ]. Portions of the 100 ng of total RNA from the livers of the control, CDAA-HF-T(+), and CDAA-HF-T(−) groups (treated for 13 weeks, n = 3–4) were used for library preparation.…”

Section: Methodsmentioning

confidence: 99%

“…Sequencing libraries were generated using a TruSeq RNA Library Preparation Kit v2 (Illumina Inc., San Diego, CA, USA). Principal component analysis (PCA), differential expression analysis, generation of heat maps with hierarchical clustering of samples, and features and functional annotation analyses using Ingenuity Pathway Analysis (IPA) software (Ingenuity Systems, Qiagen Co., Ltd., CA, USA) were performed as previously described [ 34 ].…”

Section: Methodsmentioning

confidence: 99%

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A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet

et al. 2020

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Background Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Efforts have focused on reducing the intake of trans fatty acids (TFAs) because of potential hazards to human health and the increased risk for NASH. However, the health benefits of reducing dietary TFAs have not been fully elucidated. Here, the effects of TFAs vs. a substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF) were investigated. Methods Mice were fed CDAA-HF containing shortening with TFAs (CDAA-HF-T(+)), CDAA-HF containing shortening without TFAs (CDAA-HF-T(−)), or a control chow for 13 or 26 weeks. Results At week 13, NASH was induced in mice by feeding CDAA-HF-T(+) containing TFAs or CDAA-HF-T(−) containing no TFAs, but rather mostly saturated fatty acids (FAs), as evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced a greater extent of hepatocellular apoptosis at week 13. At week 26, proliferative (preneoplastic and non-neoplastic) nodular lesions were more pronounced in mice fed CDAA-HF-T(−) than CDAA-HF-T(+). Conclusions Replacement of dietary TFAs with a substitute promoted the development of proliferation lesions in the liver of a mouse NASH model, at least under the present conditions. Attention should be paid regarding use of TFA substitutes in foods for human consumption, and a balance of FAs is likely more important than the particular types of FAs.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet

et al. 2020

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“…Portions of the RNA samples were sequenced (RNA‐Seq) and analyzed via qPCR analyses. RNA‐Seq was conducted as described elsewhere [ 19 ]. Portions of the 100 ng of total RNA from the livers of the control, CDAHFD‐0.1, and CDAHFD‐0.6 groups (treated for 13 weeks, n = 3–4) were used for the library preparation.…”

Section: Methodsmentioning

confidence: 99%

Nonobese mice with nonalcoholic steatohepatitis fed on a choline‐deficient, l‐amino acid‐defined, high‐fat diet exhibit alterations in signaling pathways

et al. 2021

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Nonalcoholic steatohepatitis (NASH) is often associated with obesity, but some patients develop NASH without obesity. The physiological processes by which non-obese patients develop NASH and cirrhosis have not yet been determined. Here, we analyzed the effects of dietary methionine content on NASH induced in mice fed on a choline-deficient, methionine-lowered, L-amino acid-defined high-fat diet (CDAHFD). CDAHFD with insufficient methionine induced insulin sensitivity and enhanced NASH pathology, but without obesity. In contrast, CDAHFD with sufficient methionine induced steatosis, and unlike CDAHFD with insufficient methionine, also induced obesity and insulin resistance. Gene profile analysis revealed that the disease severity in CDAHFD may partially be due to upregulation of the Rho family GTPases pathway, and mitochondrial and nuclear receptor signal dysfunction. The signaling factors/pathways detected in this study may assist in future study of NASH regulation, especially its "non-obese" subtype.

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“…Portions of the RNA samples were subjected to RNA sequencing (RNA-Seq) and corresponding qPCR analyses. RNA-Seq was performed as previously described [27]. Portions of the 100 ng of total RNA from the livers of the control, CDAA-HF-T(+), and CDAA-HF-T(−) groups (treated for 13 weeks, n = 3-4) were used for library preparation.…”

Section: Rna Extraction and Analysismentioning

confidence: 99%

“…Sequencing libraries were generated using a TruSeq RNA Library Preparation Kit v2 (Illumina Inc., San Diego, CA, USA). The principal component analysis (PCA), differential expression analysis, generation of heat maps with hierarchical clustering of samples, and features and functional annotation analyses using Ingenuity Pathway Analysis (IPA) software (Ingenuity Systems, Qiagen Co., Ltd.) were performed as previously described [27].…”

Section: Rna Extraction and Analysismentioning

confidence: 99%

A Trans Fatty Acid Substitute Aggravates Nonalcoholic Steatohepatitis Induced in Mice by Feeding a Choline-Deficient, Methionine-Lowered, L-Amino Acid-Defined, High-Fat Diet

Suzuki-Kemuriyama

Abe

Uno

et al. 2020

Preprint

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Background: Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Trans fatty acid (TFA) is hazardous for human health and a risk factor of NASH; thus, efforts have focused on reducing its intake. However, the health benefits of reducing dietary TFA are not fully elucidated. We investigated effects of TFA and its substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF). Methods: Mice were fed CDAA-HF containing shortening with TFA (CDAA-HF-T(+)), CDAA-HF containing shortening with a TFA substitute (CDAA-HF-T(−)), or a control chow for 13/26 weeks. Results: CDAA-HF-T(+) contained TFA, whereas CDAA-HF-T(−) contained no TFA and much saturated fatty acids. CDAA-HF-T(+) and CDAA-HF-T(−) induced NASH in mice, evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced more hepatocellular apoptosis and proliferative (preneoplastic and non-neoplastic) nodular lesions than CDAA-HF-T(+). Conclusions: Thus, replacement of dietary TFA with its substitute does not prevent but aggravates nutritionally induced NASH in mice, at least under the present conditions. Attention should be paid regarding future TFA substitute use in humans, and a fatty acid balance is likely more important than the particular types of fatty acids.

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Transcriptome Analysis of Skin from SMP30/GNL Knockout Mice Reveals the Effect of Ascorbic Acid Deficiency on Skin and Hair

Cited by 6 publications

References 15 publications

A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet

A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet

Nonobese mice with nonalcoholic steatohepatitis fed on a choline‐deficient, l‐amino acid‐defined, high‐fat diet exhibit alterations in signaling pathways

A Trans Fatty Acid Substitute Aggravates Nonalcoholic Steatohepatitis Induced in Mice by Feeding a Choline-Deficient, Methionine-Lowered, L-Amino Acid-Defined, High-Fat Diet

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