Lipid Metabolism and Antioxidant Status in Sucrose vs. Potato-Fed Rats

Robert, Laëtitia; Narcy, Agnès; Rayssiguier, Yves; Mazur, Andrzej; Rémésy, Christian

doi:10.1080/07315724.2008.10719682

Cited by 30 publications

(13 citation statements)

References 49 publications

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“…The only exception was serum cholesterol, which was diminished to a lesser degree in MCD-starch mice than MCDsucrose mice. Serum cholesterol was lower in starch-fed control (MCS) mice than sucrose-fed control mice, consistent with previous reports documenting the hypocholesterolemic nature of complex dietary carbohydrate (28)(29)(30). Why this same effect was not observed in the MCD groups with different dietary carbohydrate is unknown.…”

Section: Resultssupporting

confidence: 78%

Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis

Pickens

Yan

et al. 2009

Journal of Lipid Research

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Diets devoid of methionine and choline [methionine choline-defi cient (MCD)] cause hepatic steatosis and infl ammation that mimics nonalcoholic steatohepatitis in human beings ( 1-3 ). MCD feeding reportedly induces hepatic steatosis through a dual process involving enhanced uptake of fatty acids by the liver as well as impaired secretion of hepatic triglyceride (TG) ( 2 ). Stimulation of fatty acid uptake in MCD-fed animals correlates with hepatic upregulation of fatty acid transport proteins. Suppression of hepatic TG secretion is due to the reduced availability of methionine and choline for phospholipid synthesis, which is critical to the formation of TG-rich VLDL particles ( 4, 5 ). Notably, commercial MCD formulas (MP Biomedicals, Harlan Teklad, and Dyets) not only lack methionine and choline but are also enriched in sucrose and fat. These nutrients can themselves stimulate hepatic lipid accumulation ( 6-8 ); thus, they may accentuate the hepatic lipid accumulation caused by methionine and choline deprivation alone.The role of dietary fat as a determinant of liver injury in the MCD model has been the subject of recent investigation. Somewhat unexpectedly, studies have shown that the fat content of the MCD formula can be varied over a wide range (10% to 40% of calories) without any impact on the amount of TG that accumulates in the liver ( 9, 10 ). Even more surprising is that dietary fat does not affect MCDmediated hepatocellular injury based on biochemical or Abstract Methionine-choline-defi cient (MCD) diets cause steatohepatitis in rodents and are used to study the pathophysiology of fatty liver disease in human beings. The most widely used commercial MCD formulas not only lack methionine and choline but also contain excess sucrose and fat. The objective of this study was to determine whether dietary sucrose in the MCD formula plays a role in the pathogenesis of MCD-related liver disease. We prepared two custom MCD formulas, one containing sucrose as the principal carbohydrate and the other substituting sucrose with starch. Mice fed the sucrose-enriched formula developed typical features of MCD-related liver disease, including hepatic steatosis, hepatocellular apoptosis, alanine aminotransferase elevation, lipid peroxidation, and hepatic infl ammation. In contrast, mice fed MCD-starch were signifi cantly protected against liver injury. MCD-sucrose and MCD-starch mice displayed identical diet-related abnormalities in hepatic fatty acid uptake and triglyceride secretion. Hepatic de novo lipogenesis and triglyceride synthesis, however, were 2 times higher in MCD-sucrose mice than MCDstarch mice ( P < 0.01). Hepatic lipid analysis revealed accumulation of excess saturated fatty acids in MCD-sucrose mice that correlated with hepatocellular injury. Overall, the results indicate that dietary sucrose is critical to the pathogenesis of MCD-mediated steatohepatitis. They suggest that saturated fatty acids, which are products of de novo lipogenesis, are mediators of hepatic toxicity in this model of liver disease. ...

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Section: Resultssupporting

confidence: 78%

Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis

Pickens

Yan

et al. 2009

Journal of Lipid Research

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“…Likewise, higher levels of liver and serum triglycerides were found in the HS group, as described in other studies [17,37,38] . Although fructose is considered a hypertriglyceridemic sugar and is thought to account for the hypertriglyceridemic effect of sucrose [39] , sucrose intake appears to be also associated with increased triglyceride levels in humans [40] .…”

Section: Discussionsupporting

confidence: 73%

“…The main dietary carbohydrates, starch or sucrose, may differentially affect lipid metabolism and the antioxidant status in rats, by potentially impacting on triglyceride clearance and because of the supply of antioxidant micronutrients provided by complex sugars in comparison to the refined ones [37] . It could probably be related to an increase in liver lipogenesis, converting sugar surplus into triglycerides.…”

Section: Discussionmentioning

confidence: 99%

A High-Sucrose Isocaloric Pair-Fed Model Induces Obesity and Impairs NDUFB6 Gene Function in Rat Adipose Tissue

et al. 2009

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Background/Aim: Changes in dietary macronutrient content are involved in altered energy metabolism and obesity development. However, there are controversial views about the obesogenic effects of high-sucrose (HS) diets, which usually lead to obesity and insulin resistance but are sometimes associated with reduced weight gain. The aim of this study was to investigate the effect of consumption of a pair-fed HS diet on weight gain and energy homeostasis in rats, as well as to assess the effects on expression of the NADH dehydrogenase (ubiquinone) 1β subcomplex 6 (NDUFB6) gene in adipose tissue. Methods/Results: Although both dietary groups, i.e. HS and control, were pair-fed (isoenergetic feeding), the HS diet increased adiposity and decreased plasma total and high-density lipoprotein cholesterol levels. While no significant differences were found with regard to serum glucose, insulin, adiponectin, free fatty acids and liver malondialdehyde, a slight increase in serum and liver triglycerides was observed. Interestingly, the gene expression of NDUFB6, an inner mitochondrial membrane protein involved in mitochondrial electron transport, was reduced in epididymal adipose tissue when compared to the control-fed group. Conclusion: These results suggest, apparently for the first time, that high-sugar diets appear to induce mitochondrial dysfunction in adipose tissue, which may be related to greater weight gain and metabolic impairment.

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“…Another study on the lipid-lowering effect of potato in rats showed that feeding rats a potato-enriched diet led to a decrease in cholesterol and triglyceride levels in plasma, decreased cholesterol level in the liver and improved antioxidant status (Robert et al, 2006, Robert et al, 2008. These results suggest that potato consumption may enhance antioxidant defense and improve the lipid metabolism.…”

Section: Carotenoids and Polyphenolsmentioning

confidence: 81%

Potato Antioxidant Compounds: Impact of Cultivation Methods and Relevance for Diet and Health

Evers¹,

Deußer²

2012

Nutrition, Well-Being and Health

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Lipid Metabolism and Antioxidant Status in Sucrose vs. Potato-Fed Rats

Cited by 30 publications

References 49 publications

Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis

Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis

A High-Sucrose Isocaloric Pair-Fed Model Induces Obesity and Impairs NDUFB6 Gene Function in Rat Adipose Tissue

Potato Antioxidant Compounds: Impact of Cultivation Methods and Relevance for Diet and Health

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