Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

Deaciuc, Ion V.; Song, Zhenyuan; Peng, Xuejun; Barve, Shirish; Song, Ming; He, Qing-Yu; Knudsen, Thomas B.; Singh, Amar V.; McClain, Craig J.

doi:10.1007/s12072-007-9025-2

Cited by 9 publications

(5 citation statements)

References 43 publications

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“…Consistent with our findings of circulating levels of lipids, sucrose feeding alone did not induce NAFLD, nor did it affect hepatic outcomes when added to a high-fat diet. Contrary to our results, 60–70 % sucrose promoted development of hepatic steatosis in both rats [ 49 – 51 ] and mice [ 52 , 53 ]. However, while levels of hepatic inflammatory cytokines were increased [ 49 ], hepatic triglycerides were not significantly elevated [ 49 , 51 ].…”

Section: Discussioncontrasting

confidence: 99%

High-fat but not sucrose intake is essential for induction of dyslipidemia and non-alcoholic steatohepatitis in guinea pigs

et al. 2016

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BackgroundNon-alcoholic fatty liver disease (NAFLD) and dyslipidemia are closely related. Diet plays an important role in the progression of these diseases, but the role of specific dietary components is not completely understood. Therefore, we investigated the role of dietary sucrose and fat/cholesterol on the development of dyslipidemia and NAFLD.MethodsSeventy female guinea pigs were block-randomized (based on weight) into five groups and fed a normal chow diet (control: 4 % fat), a very high-sucrose diet (vHS: 4 % fat, 25 % sucrose), a high-fat diet (HF: 20 % fat, 0.35 % cholesterol), a high-fat/high-sucrose diet (HFHS: 20 % fat, 15 % sucrose, 0.35 % cholesterol) or a high-fat/very high-sucrose diet (HFvHS: 20 % fat, 25 % sucrose, 0.35 % cholesterol) for 16 and 25 weeks.ResultsAll three high-fat diets induced dyslipidemia with increased concentrations of plasma cholesterol (p < 0.0001), LDL-C (p < 0.0001) and VLDL-C (p < 0.05) compared to control and vHS. Contrary to this, plasma triglycerides were increased in control and vHS compared to high-fat fed animals (p < 0.01), while circulating levels of free fatty acids were even between groups. Histological evaluation of liver sections revealed non-alcoholic steatohepatitis (NASH) with progressive inflammation and bridging fibrosis in high-fat fed animals. Accordingly, hepatic triglycerides (p < 0.05) and cholesterol (p < 0.0001) was increased alongside elevated levels of alanine and aspartate aminotransferase (p < 0.01) compared to control and vHS.ConclusionCollectively, our results suggest that intake of fat and cholesterol, but not sucrose, are the main factors driving the development and progression of dyslipidemia and NAFLD/NASH.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0110-1) contains supplementary material, which is available to authorized users.

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Section: Discussioncontrasting

confidence: 99%

High-fat but not sucrose intake is essential for induction of dyslipidemia and non-alcoholic steatohepatitis in guinea pigs

et al. 2016

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“…In one study, a high-fat diet induced obesity and clear-cut diabetes with significantly increased fasting blood glucose (>240 mg/dL) and insulin levels [30] in C57BL/6J mice. Similarly, in a separate study, 16 weeks of a high-sucrose diet induced obesity and hepatosteatosis with increased blood glucose and insulin levels in C57BL/6J mice [31]. In our study, the HFD also induced obesity, glucose intolerance, and impaired insulin secretion in response to glucose in NSY mice.…”

Section: Discussionsupporting

confidence: 79%

Analysis of hepatic gene expression profile in a spontaneous mouse model of type 2 diabetes under a high sucrose diet

et al. 2013

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Both genetic factors and diabetogenic environmental factors, such as a high-sucrose diet (HSD), are involved in the development of type 2 diabetes. In this study, the Nagoya-Shibata-Yasuda (NSY) mouse, an animal model of type 2 diabetes and C3H mice used as controls, were fed a HSD, a high-fat diet (HFD) or a regular diet (RD) from weaning. In C3H mice, HFD significantly increased body weight gain, but maintained glucose tolerance. In contrast, in NSY mice, HSD resulted in increased body weight gain and liver steatosis and increased glucose intolerance to a greater extent than HFD. Furthermore, we performed DNA microarray analysis to detect differences in hepatic gene expression levels in both strains under HSD. We then performed RT-PCR analysis on selected genes to evaluate basal expression level under RD and changes under HSD conditions. HSD-fed NSY, but not C3H mice, exhibited increased hepatic expression levels of Pparg2, an isoform of Pparg as well as G0s2, a target of Pparg, which are known to be adipocyte-specific genes. Compared to RD-fed C3H mice, hepatic expression levels of Kat2b (transcriptional regulation), Hsd3b5 (steroid hormone metabolism) and Cyp7b1 (bile acid metabolism) were initially lower in RD-fed NSY mice, and were further decreased in HSD-fed NSY mice. Expression of Metallothionein (Mt1) and Metallothionein 2 (Mt2) was significantly lower in NSY mice compared to C3H mice, irrespective of dietary condition. These data suggest that elucidation of this heterogeneity in response to HSD might contribute to further understanding of the gene-environment interactions leading to diabetes in humans.

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“…Furthermore, a recent study suggests that fructose, not glucose, is the primary cause of hepatic abnormality after chronic high-sucrose ingestion (22). Sucrose content in the low-protein diets in the present study was 40%, while most high-sucrose diets in previous studies contained 65-70% sucrose (19)(20)(21)(22). We can not, however, exclude the possibility that intake of sucrose influenced hepatic triglyceride deposition in the present study.…”

Section: Discussioncontrasting

confidence: 73%

“…High-sucrose diets have been shown to affect hepatic lipid metabolism (19)(20)(21)(22). Furthermore, a recent study suggests that fructose, not glucose, is the primary cause of hepatic abnormality after chronic high-sucrose ingestion (22).…”

Section: Discussionmentioning

confidence: 99%

Dietary Medium-Chain Triglycerides Attenuate Hepatic Lipid Deposition in Growing Rats with Protein Malnutrition

Kuwahata

Kubota

Amano

et al. 2011

J Nutr Sci Vitaminol

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SummaryThe objective of this study was to investigate the effects of dietary mediumchain triglycerides (MCT) on hepatic lipid accumulation in growing rats with protein malnutrition. Weaning rats were fed either a low-protein diet (3%, LP) or control protein diet (20%, CP), in combination with or without MCT. The four groups were as follows: CP-MCT, CP ϩ MCT, LP Ϫ MCT, and LP ϩ MCT. Rats in the CP Ϫ MCT, CP ϩ MCT and LP ϩ MCT groups were pair-fed their respective diets based on the amount of diet consumed by the LP Ϫ MCT group. Rats were fed each experimental diet for 30 d. Four weeks later, the respiratory quotient was higher in the LP Ϫ MCT group than those in the other groups during the fasting period. Hepatic triglyceride content increased in the LP groups compared with the CP groups. Hepatic triglyceride content in the LP ϩ MCT group, however, was significantly decreased compared with that in the LP Ϫ MCT group. Levels of carnitine palmitoyltransferase (CPT) 1a mRNA and CPT2 mRNA were significantly decreased in the livers of the LP Ϫ MCT group, as compared with corresponding mRNA levels of the other groups. These results suggest that ingestion of a low-protein diet caused fatty liver in growing rats. However, when rats were fed the low-protein diet with MCT, hepatic triglyceride deposition was attenuated, and mRNA levels encoding CPT1a and CPT2 were preserved at the levels of rats fed control protein diets.

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Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

Cited by 9 publications

References 43 publications

High-fat but not sucrose intake is essential for induction of dyslipidemia and non-alcoholic steatohepatitis in guinea pigs

High-fat but not sucrose intake is essential for induction of dyslipidemia and non-alcoholic steatohepatitis in guinea pigs

Analysis of hepatic gene expression profile in a spontaneous mouse model of type 2 diabetes under a high sucrose diet

Dietary Medium-Chain Triglycerides Attenuate Hepatic Lipid Deposition in Growing Rats with Protein Malnutrition

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