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Choline intake in pregnancy and lactation modifies liver transcriptome profile in the offspring of female rats with nonalcoholic fatty liver disease

ABSTRACT: Choline intake in pregnancy and lactation modifies liver transcriptome profile in the offspring of female rats with nonalcoholic fatty liver disease

PROVIDER: PRJNA937659 | ENA |

REPOSITORIES: ENA

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Choline intake in pregnancy and lactation modifies liver transcriptome profile in the offspring of female rats with nonalcoholic fatty liver disease

Project description:The aim of the study was to analyze the impact of choline intake during pregnancy and/or lactation on histological alternation and gene expression profile in the liver of NAFLD dam progeny. We hypothesized that offspring of mothers suffering from non-alcoholic fatty liver (NAFLD) is more prone to develop fatty liver, because of suboptimal intrauterine environment. The performed analyses included histological examination of liver tissue obtained from 24-day-old male rats, which were offspring of dams with fatty liver: provided with proper choline amount during pregnancy and lactation (NN), fed a choline-deficient diet during these both periods (DD), deprived with choline only during pregnancy (DN) or only during lactation (ND). The global gene expression profile was analyzed by using microarray approach (Affymetrix® Rat Gene 2.1 ST Array Strip).

2024-05-20 | GSE225805 | GEO

Transcriptional profiling of mouse liver tissue following control, choline and methonine/choline deficient diet intervention

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Project description:Nonalcoholic fatty liver disease (NAFLD) associated with type 2 diabetes (T2D) easily progresses toward severe forms of nonalcoholic steatohepatitis (NASH) and fibrosis, and the underlying mechanism is under active investigation. Here, we established the role of transcription factor 7-like 2 (TCF7L2), the most significant T2D susceptibility gene, in NAFLD development and progression. Hepatic TCF7L2 expression was decreased in liver biopsies of patients with NAFLD. Based on the major risk factors for NAFLD development, liver-specific TCF7L2 knockout mice were subjected to a high-fat diet providing fatty acids (FAs) and refeeding/high-carbohydrate diet stimulating de novo lipogenesis. Hepatic TCF7L2 deficiency significantly increased the lipid synthetic pathways and hepatic TG accumulation by preferentially metabolizing carbohydrates than FAs. Mechanistically, TCF7L2 regulated miRNAs targeting SREBF1c and enhanced proteasome-mediated MLXIPL (ChREBP) degradation. Our findings will deepen the pathophysiological mechanism of NAFLD associated with dietary carbohydrate and diabetes, and will provide a potential target for treatment of NAFLD.

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Effects of maternal choline intake on placental gene expression

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Microarray analysis of choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model.

Project description:Nonalcoholic Fatty Liver Disease (NAFLD) is a broad spectrum of liver disorders ranging from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. The choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model has traditionally been used to understand the molecular mechanisms of disease development and progression. Although this animal model shows a similar course of disease progression to human NAFLD, it does not develop comorbidities such as obesity and type 2 diabetes. Therefore, its relevance to human NAFLD (what aspects of the disease etiology are recapitulated in this model?) is not fully understood. We applied microarray analysis to characterize its pathophysiology, and evaluate the similarity across species.

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Nonalcoholic fatty liver, but not nonalcoholic steatohepatitis is a protective factor to tetrachloroethylene-associated kidney effects in male C57BL/6J mice

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