Liver Regeneration Is Impaired in Mice with Acute Exposure to a Very Low Carbohydrate Diet
| Autor: | Hao Chen, Yan-die Lin, Hao Li, Yun Cai, Wu Sun |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Male
STAT3 Transcription Factor 0301 basic medicine medicine.medical_specialty Physiology medicine.medical_treatment Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine Dietary Carbohydrates medicine Animals Hepatectomy Beta oxidation Mice Inbred BALB C Triglyceride Interleukin-6 Tumor Necrosis Factor-alpha Chemistry Regeneration (biology) Gastroenterology Lipid metabolism Metabolism Animal Feed Liver regeneration Diet Liver Regeneration 030104 developmental biology Endocrinology Gene Expression Regulation 030211 gastroenterology & hepatology Transcriptome Signal Transduction Ketogenic diet |
| Zdroj: | Digestive Diseases and Sciences. 62:1256-1264 |
| ISSN: | 1573-2568 0163-2116 |
| Popis: | The metabolic response to hepatic insufficiency has been implicated in the regulators of normal liver regeneration. Modulation of nutritional factors has been demonstrated to affect liver regeneration. Diets containing very low carbohydrate and high fat levels cause a unique metabolic state, the effect of which on liver regeneration is unknown. Mice were placed on standard mice chow (ND) or a very low carbohydrate diet (VLCD) after 70% partial hepatectomy (PH). After 48 h, mice on VLCD were placed back to ND. The serum metabolic profiles, hepatic lipid content, and gene expression profile were examined. The dynamics of liver regeneration were detected at timed points. Activation of signaling pathways was examined. VLCD feeding caused hypoglycemia and elevation of serum β-hydroxybutyrate and free fatty acids in mice after PH. It increased hepatic triglyceride contents, enhanced fatty acid oxidation, and reduced lipid synthesis. Mice on VLCD exhibited diminished hepatocellular mitotic frequency, a reduced BrdU incorporation and liver mass regeneration ratio, and delayed expression of PCNA. Expressions of IL-6 and TNFα in liver and serum were downregulated. Meanwhile, phosphorylation of STAT3, Erk, and AKT was delayed compared with controls. VLCD feeding delayed liver regeneration, probably because of the suppression of TNFα-IL-6-STAT3 signaling and delayed activation of Erk and AKT induced by the unique metabolic effects of this diet. |
| Databáze: | OpenAIRE |
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