Effects of treatment with sucrose in drinking water on liver histology, lipogenesis and lipogenic gene expression in rats fed high-fiber diet

doi:10.1016/j.plefa.2016.11.001

Prostaglandins, Leukotrienes and Essential Fatty Acids

Volume 116, January 2017, Pages 1-8

https://doi.org/10.1016/j.plefa.2016.11.001 Get rights and content

Highlights

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A number of αSMA immunoreactive cells increases in hepatic tissue after long-term sucrose treatment.
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Long-term sucrose treatment changes fatty acid profile of different phospholipid classes including cardiolipin.
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Linoleic and linolenic acid concentrations decreases after long-term sucrose treatment.
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Long-term sucrose treatment decreases phospholipid content of arachidonic acid, but not docosahexaenoic acid.
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Expressions of Δ5-desaturase and elongase 5 are decreased, while expressions of Δ9-desaturase and SREBP1c are increased after long-term sucrose treatment.

Abstract

We studied the influence of sucrose in drinking water on liver histology, fatty acid profile and lipogenic genes expression in rats maintained on high-fiber. The experimental groups were: control group (water) and sucrose group (sucrose solution in drinking water, 30% w/v). Liver histology of sucrose treated rats revealed steatosis and increased number of αSMA immunoreactive cells without the signs of fibrosis. Sucrose treatment increased de novo lipogenesis, lipid peroxidation and MUFA content and decreased PUFA content, C18:2n6 and C20:4n6 content in total phospholipids and phosphatidylethanolamine and C18:2n6 content in cardiolipin. RT-qPCR revealed increase in Δ-9-desaturase and SREBP1c gene expression and decrease in the Δ-5-desaturase and elongase 5 expression. Treatment with sucrose extensively changes fatty acid composition of hepatic lipid and phospholipid classes including cardiolipin, increases oxidative stress and causes pathological changes in liver in rats maintained on high-fiber diet.

Introduction

There are three different sources of whole body fatty acids: food, de novo lipogenesis and bioconversion. Fatty acids generated de novo, as well as fatty acids derived from the food, are bioconverted by series of desaturation, elongation and β-oxidation steps into different SFA, MUFA and PUFA. The regulation of desaturases (Δ9D, Δ6D, Δ5D) and elongases (Elovl2, Elovl5 and Elovl6) is complex and it involves induced expression by different metabolites (glucose), hormones (insulin) and transcriptional factors (peroxisome proliferator-activated receptors α, PPARα; sterol response element-binding protein-1c, SREBP-1c; liver X receptor, LXR; carbohydrate-regulatory element binding protein, ChREBP; MAX-like factor X, MLX) [1], [2]. Nutrition (substrate availability) and competition for rate-limiting enzymes as well as lipid oxidation and hormonal status, could substantially contribute or even override other regulatory mechanisms [3].

Metabolic diseases, such as diabetes, obesity or metabolic syndrome, are characterized with changes in lipogenesis and fatty acid concentrations in different tissues. In insulin dependent diabetes mellitus (IDDM), changes includes the decrease in mRNA expression of desaturases [4] and elongases [5]. Moreover, expression of different transcriptional factors, which are part of fatty acid synthesis regulation system, is also changed [1], [6]. In experimental insulin resistance and non-insulin dependent diabetes mellitus (NIDDM) fatty acid metabolism is more complex [7] and it depends on experimental model used: spontaneously diabetic rats [8], high fructose [9], high glucose [10], high sucrose [11] or high fat diet and obese animal models [1].

High intake of simple sugars via the beverages is nowadays not always coupled with high fat intake, which is predominant model for metabolic syndrome investigations, but also with dietary restriction and high-fiber diets. Therefore, present work was undertaken to study the influence of long-term treatment with sucrose in drinking water in rats by measuring the fatty acid profile of liver and adipose tissue and the expression of lipogenic genes in rats fed high-fiber diet.

Section snippets

Animals and diet

The research protocol was approved by the National Ethics Committee (EP 13/2015) and Veterinary Directorate, Ministry of Agriculture, Republic of Croatia. Male Wistar rats with an average initial body weight of 220±10 g were used over the period of 20 weeks. The rats were placed in polycarbonate cages in a controlled environment at a temperature of 22±1 °C and a 12 h cycle of light/dark. The experimental groups were formed according to the following treatments: control group (water) and sucrose

Body weights and non-fasting blood glucose values

As shown in Fig. 1A, earlier in the experiment (8th week), the Sucrose group had higher body weight compared to the Control group. Nevertheless, at the end of the study (20th week), the difference in mean body weights were not significantly different between the treatments.

Non-fasting mean blood glucose concentrations in the experimental groups were equivalent till the 16th week of experiment (Fig. 1B). From the 16th week till the end of the experiment, the Sucrose group had higher mean blood

Discussion

This study confirmed that long-term intake of large amounts of sucrose via the drinking water results in increased levels of glucose in blood. In Wistar rats, fed with normal laboratory chow, hyperglycemia can be noticed at the 4th week of sucrose treatment, which is substantially earlier than in our trial [18]. Besides transient increase in body mass at the 8th week, there was no statistically significant difference in the weight between control and sucrose-fed rats. These results could be

Funding

This work has been supported by Croatian Science Foundation under the project (IP-2014-09-8992) awarded to Tomislav Mašek.

Acknowledgements

The authors have declared no conflict of interest.

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Effects of treatment with sucrose in drinking water on liver histology, lipogenesis and lipogenic gene expression in rats fed high-fiber diet

Highlights

Abstract

Introduction

Section snippets

Animals and diet

Body weights and non-fasting blood glucose values

Discussion

Funding

Acknowledgements

J. Lipid Res.

Prostaglandins, Leukot. Essent. Fat. Acids

Prostaglandins, Leukot. Essent. Fat. Acids

Biochim. Et. Biophys. Acta (BBA) - Lipids Lipid Metab.

Biochimie

Chem. Phys. Lipids

Clin. Chim. Acta

Comp. Biochem. Physiol. Part C: Toxicol. Pharmacol.

J. Biol. Chem.

Exp. Toxicol. Pathol.

J. Nutr. Biochem.

J. Biol. Chem.

Chem. Phys. Lipids

Biochim. Biophys. Acta (BBA) - Mol. Cell Biol. Lipids

Exp. Gerontol.

Fatty acid–regulated transcription factors in the liver

Annu. Rev. Nutr.