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J Diabetes Complications. 2016 Jan-Feb;30(1):85-92. doi: 10.1016/j.jdiacomp.2015.10.008. Epub 2015 Oct 19.

Chronic fructose intake accelerates non-alcoholic fatty liver disease in the presence of essential hypertension.

Author information

1
Department of Physiological Sciences, Federal University of Espírito Santo, Av Marechal Campos 1468, Maruipe, 29042-755, Vitória, ES, Brazil.
2
Department of Morphology, Federal University of Espírito Santo, Av Marechal Campos 1468, Maruipe, 29042-755, Vitória, ES, Brazil.
3
Department of Pharmacy and Nutrition, Federal University of Espírito Santo, Rod Alto Universitário, Guararema, 29500-000, Alegre, ES, Brazil.
4
Department of Physiological Sciences, Federal University of Espírito Santo, Av Marechal Campos 1468, Maruipe, 29042-755, Vitória, ES, Brazil; Department of Pharmacy and Nutrition, Federal University of Espírito Santo, Rod Alto Universitário, Guararema, 29500-000, Alegre, ES, Brazil.
5
Department of Physiological Sciences, Federal University of Espírito Santo, Av Marechal Campos 1468, Maruipe, 29042-755, Vitória, ES, Brazil. Electronic address: marcelobaldo@ymail.com.

Abstract

BACKGROUND:

The growing epidemic of metabolic syndrome has been related to the increased use of fructose by the food industry. In fact, the use of fructose as an ingredient has increased in sweetened beverages, such as sodas and juices. We thus hypothesized that fructose intake by hypertensive rats would have a worse prognosis in developing metabolic disorder and non-alcoholic fatty liver disease.

METHODS:

Male Wistar and SHR rats aged 6weeks were given water or fructose (10%) for 6weeks. Blood glucose was measured every two weeks, and insulin and glucose sensitivity tests were assessed at the end of the follow-up. Systolic blood pressure was measure by plethysmography. Lean mass and abdominal fat mass were collected and weighed. Liver tissue was analyzed to determine interstitial fat deposition and fibrosis.

RESULTS:

Fasting glucose increased in animals that underwent a high fructose intake, independent of blood pressure levels. Also, insulin resistance was observed in normotensive and mostly in hypertensive rats after fructose intake. Fructose intake caused a 2.5-fold increase in triglycerides levels in both groups. Fructose intake did not change lean mass. However, we found that fructose intake significantly increased abdominal fat mass deposition in normotensive but not in hypertensive rats. Nevertheless, chronic fructose intake only increased fat deposition and fibrosis in the liver in hypertensive rats.

CONCLUSIONS:

We demonstrated that, in normotensive and hypertensive rats, fructose intake increased triglycerides and abdominal fat deposition, and caused insulin resistance. However, hypertensive rats that underwent fructose intake also developed interstitial fat deposition and fibrosis in liver.

KEYWORDS:

Fat liver disease; Fructose; Hypertension; Metabolic disorder; Visceral fat

PMID:
26597602
DOI:
10.1016/j.jdiacomp.2015.10.008
[Indexed for MEDLINE]

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