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eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

Autor: Woo-Gyun Choi, Jaeseok Han, Ji-Hyeon Kim, Mi-Jeong Kim, Jae-Woo Park, Benbo Song, Hee-Jeong Cha, Hye-Seon Choi, Hun-Taeg Chung, In-Kyu Lee, Tae-Sik Park, Maria Hatzoglou, Hueng-Sik Choi, Hyun Ju Yoo, Randal J. Kaufman, Sung Hoon Back

Publikováno v: Nutrition & Metabolism, Vol 14, Iss 1, Pp 1-21 (2017)

Abstract Background Dietary fructose can rapidly cause fatty liver in animals through de novo lipogenesis (DNL) and contribute to the development and severity of nonalcoholic fatty liver disease (NAFLD). In response to diverse cellular insults includ

Externí odkaz: https://doaj.org/article/622f68c66e374394b6921639e0484074

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Glucagon Receptor Antagonism-Mediated β-Cell Regeneration as an Effective Anti-Diabetic Therapy

Publikováno v: SSRN Electronic Journal.

Type 1 Diabetes (T1D) is a chronic disease with potentially severe complications, and β-cell deficiency underlies this disease. Despite active research, no therapy to date has been able to induce β-cell regeneration in humans. Here, we discovered t

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::ba4f36146e0d14cfbdef1799482a61fe
https://doi.org/10.2139/ssrn.3844996

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Glucagon-receptor-antagonism-mediated β-cell regeneration as an effective anti-diabetic therapy

Publikováno v: Cell Reports. 39:110872

Type 1 diabetes mellitus (T1D) is a chronic disease with potentially severe complications, and β-cell deficiency underlies this disease. Despite active research, no therapy to date has been able to induce β-cell regeneration in humans. Here, we dis

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8e2383421e75ecb35f5dcb96db24609f
https://doi.org/10.1016/j.celrep.2022.110872

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Antioxidants Complement the Requirement for Protein Chaperone Function to Maintain β-Cell Function and Glucose Homeostasis

Autor: Vamsi K. Kodali, Anita Pottekat, Justin R. Hassler, Benbo Song, Sung Hoon Back, Subramaniam Pennathur, Jiun Kim, Jaeseok Han, Randal J. Kaufman, Shiyu Wang, Michael G. Katze, Miao Wang

Publikováno v: Diabetes

Proinsulin misfolding in the endoplasmic reticulum (ER) initiates a cell death response, although the mechanism(s) remains unknown. To provide insight into how protein misfolding may cause β-cell failure, we analyzed mice with the deletion of P58IPK

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::68c5ed8622b2f1a4ed9f57495a17e712
https://doi.org/10.2337/db14-1357

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Additional file 1: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

Autor: Woo-Gyun Choi, Jaeseok Han, Ji-Hyeon Kim, Kim, Mi-Jeong, Park, Jae-Woo, Benbo Song, Cha, Hee-Jeong, Hye-Seon Choi, Hun-Taeg Chung, Lee, In-Kyu, Park, Tae-Sik, Hatzoglou, Maria, Hueng-Sik Choi, Yoo, Hyun, Kaufman, Randal, Back, Sung

eIF2α phosphorylation in hepatocytes is dispensable for survival of adult mice. (a) Diagram depicting the four genotypes of mice used in these experiments. S/A and A/A represent heterozygous and homozygous eIF2α Ser51Ala (*) mutation(s) in exon 2 o

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Additional file 9: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

The levels of eIF2α phosphorylation in the livers of adult mice after 5 weeks of HFrD. Western blot analysis of liver lysates from 4-month-old Cont. and A/A Hep mice fed an RD or an HFrD for 5 wks. The * indicates non-specific bands in the Western b

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Additional file 4: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

Hepatocyte death and fibrosis in 13 month-old A/A Hep mice fed a regular diet (RD) or a 60% high fructose diet (HFrD) for 5 wks (a) Hematoxylin and eosin (H&E)-stained images of liver tissue sections from 13-month-old Cont. (A/A-fTg) (n = 5) and A/A

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Additional file 6: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

eIF2α phosphorylation in adult mice prevents hepatocyte death induced by a long-term HFrD. (a) Hematoxylin and eosin (H&E)-stained images of paraffin-embedded liver sections from 7-month-old Cont. and A/A Hep mice fed an RD or an HFrD for 16 wks. In

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Additional file 7: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

The severity of HFrD-mediated damage is higher in middle-aged A/A Hep mice. (a) The data (serum ALT level, necrotic cell #, TUNEL positive cell #, and cleaved caspase 3 positive cell # of RD-fed adult A/A Hep mice from Fig. 3a–d and RD-fed middle-a

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Additional file 8: of eIF2α phosphorylation is required to prevent hepatocyte death and liver fibrosis in mice challenged with a high fructose diet

A high fructose diet increases expression of proapoptotic genes in liver tissues of A/A Hep mice. (a) Quantitative real-time PCR analysis to assess the expression of selected genes (anti/proapoptotic genes) in liver tissues from 7-month-old Cont. and

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