Abstract

Background. Nonalcoholic fatty liver disease (NAFLD) is one of the complications of the metabolic syndrome. It encompasses a wide range of disease spectrum from simple steatosis to liver cirrhosis. Structural alteration of hepatic mitochondria might be involved in the pathogenesis of NAFLD. Aims. In the present study, we used a newly established model of fructose-induced metabolic syndrome in male Wistar rats in order to investigate the ultrastructural changes in hepatic mitochondria that occur with fructose consumption and their association with NAFLD pathogenesis. Methods. The concentration of fructose-drinking water (FDW) used in this study was 20%. Six male Wistar rats were supplemented with FDW 20% for eight weeks. Body composition and metabolic parameters were measured before and after 8 weeks of FDW 20%. Histomorphology of the liver was evaluated and ultrastructural changes of mitochondria were assessed with transmission electron micrograph. Results. After 8 weeks of fructose consumption, the animals developed several features of the metabolic syndrome. Moreover, fructose consumption led to the development of macrovesicular hepatic steatosis and mitochondrial ultrastructural changes, such as increase in mitochondrial size, disruption of the cristae, and reduction of matrix density. Conclusion. We conclude that in male Wistar rat 8-week consumption of FDW 20% leads to NAFLD likely via mitochondrial structural alteration.

Highlights

  • Obesity and fatty liver diseases are global health problems which involve adults and children [1]

  • We hypothesized that the increase in the liver weight could be attributed to the higher numbers of lipid vacuoles depositions in the hepatocyte cytoplasm and the presence of fibrosis that may have changed the consistency of the liver following consumption of HFHC diet compared to fructose-drinking water (FDW) 20% only

  • The present study demonstrates that consumption of FDW 20% for eight weeks resulted in simple swelling of mitochondria rather than megamitochondria

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Summary

Introduction

Obesity and fatty liver diseases are global health problems which involve adults and children [1]. Causes not related to alcohol consumption which may cause fatty liver disease are obesity, diabetes mellitus type II, dyslipidemia, and hypertension, and it is known as nonalcoholic fatty liver disease (NAFLD) [1]. All these causes for NAFLD are components of the metabolic syndrome. Nonalcoholic fatty liver disease (NAFLD) is one of the complications of the metabolic syndrome. We used a newly established model of fructose-induced metabolic syndrome in male Wistar rats in order to investigate the ultrastructural changes in hepatic mitochondria that occur with fructose consumption and their association with NAFLD pathogenesis. We conclude that in male Wistar rat 8-week consumption of FDW 20% leads to NAFLD likely via mitochondrial structural alteration

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