A High-Fructose-High-Coconut Oil Diet Induces Dysregulating Expressions of Hippocampal Leptin and Stearoyl-CoA Desaturase, and Spatial Memory Deficits in Rats.

Ching-I Lin,Shyh-Hsiang Lin,Tsui-Han Hsu,Chu-Fu Shen

doi:10.3390/nu9060619

Ching-I Lin, Shyh-Hsiang Lin + Show 2 more

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https://doi.org/10.3390/nu9060619

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Journal: Nutrients	Publication Date: Jun 16, 2017
Citations: 10	License type: CC BY 4.0

Affiliation: Kainan University, Taipei Medical University

Abstract

We investigated the effects of high-fructose-high-fat diets with different fat compositions on metabolic parameters, hippocampal-dependent cognitive function, and brain leptin (as well as stearoyl-CoA desaturase (SCD1) mRNA expressions). Thirty-two male Wistar rats were divided into 3 groups, a control group (n = 8), a high-fructose soybean oil group (37.5% of fat calories, n = 12), and a high-fructose coconut oil group (37.5% of fat calories, n = 12) for 20 weeks. By the end of the study, the coconut oil group exhibited significantly higher serum fasting glucose, fructosamine, insulin, leptin, and triglyceride levels compared to those of the control and soybean oil groups. However, hippocampal leptin expression and leptin receptor mRNA levels were significantly lower, while SCD1 mRNA was significantly higher in rats fed the high-fructose-high-coconut oil diet than in rats fed the other experimental diets. In addition, the coconut oil group spent significantly less time in the target quadrant on the probe test in the Morris water maze (MWM) task. Rats fed the high-fructose-high-coconut oil diet for 20 weeks were prone to develop hyperglycemia, hyperinsulinemia, hyperleptinemia, and hypertriglyceridemia. These metabolic consequences may contribute to hippocampal-dependent memory impairment, accompanied by a lower central leptin level, and a higher SCD1 gene expression in the brain.

Highlights

Environmental factors such as diet significantly contribute to the causation of chronic diseases including obesity and type 2 diabetes mellitus (T2DM) [1]
The biochemical analyses performed in the 20th week of dietary intake showed that the rats fed the high-fructose-high-coconut oil diet had significantly higher glucose, TG, insulin, and high-density lipoprotein (HDL) compared to the control group
LDL had increased in rats receiving the high-fructose-high-coconut oil diet compared to the control and high-fructose-high-soybean oil-fed rats, this change did not reach a statistical difference (Table 2)

Summary

Introduction

Environmental factors such as diet (i.e., excessive caloric intake) significantly contribute to the causation of chronic diseases including obesity and type 2 diabetes mellitus (T2DM) [1]. Individuals with obesity and/or T2DM may place themselves at an increased risk of developing memory deterioration and cognitive impairment, and, in turn, neurodegenerative diseases [2,3]. A dietary pattern which is similar to the typical Western diet (characterized by a high intake of meat, butter, high-fat dairy products, eggs, and refined sugar) was demonstrated to predict an increased risk of neurodegenerative disease, i.e., Alzheimer’s disease (AD) [4]. Among the components of a Western diet, high intakes of saturated fats and simple carbohydrates (e.g., refined sugar) have garnered much attention for their roles in the development of cognitive dysfunction and neurodegenerative diseases [5,6]. Animal studies suggest that a high-fat diet rich in saturated fatty acids (SFAs) can result in obesity as well as deficits in hippocampal-dependent learning and memory processes [7,8].

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