A new model of acute liver steatosis induced in rats by fasting followed by refeeding a high carbohydrate-fat free diet. Biochemical and morphological analysis
Background/Aims: Dietary habits are often considered to be responsible for fatty liver, a common histological finding in human liver biopsies. The aim of the present work was to test the hypothesis that fasting followed by refeeding high carbohydrate-fat free diets in rats disrupts hepatic lipid hom...
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Published in | Journal of hepatology Vol. 26; no. 4; pp. 880 - 885 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Elsevier B.V
01.04.1997
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Background/Aims: Dietary habits are often considered to be responsible for fatty liver, a common histological finding in human liver biopsies. The aim of the present work was to test the hypothesis that fasting followed by refeeding high carbohydrate-fat free diets in rats disrupts hepatic lipid homeostatis, leading to liver lipid accumulation and morphological alterations.
Methods: Male Wistar rats were fasted for 48 h, then refed
ad libitum with a high carbohydrate-fat free diet.
Results: Six hours after refeeding, a slight micro-vascuolar steatosis, mainly located in zone I was observed, whereas later or in the process, macrovacuolar steatosis extended to all three zones of the hepatic lobules. The present paper also contributes information on the mechanism of fasting-high carbohydrate-fat free diet, diet-induced steatosis: we show that both circulating and
de novo hepatic synthesized fatty acid availabilities are implicated in the disequilibrium between triglyceride synthesis and secretion.
Conclusios: The results are discussed, taking into account the putative implication of carbohydrate-induced lipogenesis in human fatty liver, occurring in non-insulin-dependent diabetic or obese patients. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0168-8278 1600-0641 |
DOI: | 10.1016/S0168-8278(97)80256-5 |