Metabolic Brain Disease

, Volume 28, Issue 4, pp 597–604 | Cite as

Association between the characteristics of metabolic syndrome and Alzheimer’s disease

  • Hui-Ting Yang
  • Yi-Jing Sheen
  • Chuen-Der Kao
  • Chin-An Chang
  • Ya-Chun Hu
  • Jiann-Liang Lin
Original Paper

Abstract

Various epidemiological studies have shown that type 2 diabetes and metabolic syndrome are highly correlated with Alzheimer’s disease (AD). Here, we sought to assess the impact of metabolic syndrome characteristics on the progression of AD. Five-week-old male, spontaneously hypertensive (n = 32) and Wistar Kyoto (abbreviated WKY; n = 8) rats were divided into 5 groups (each n = 8): WKY, hypertension (HTN), streptozotocin-induced diabetes (STZ), high-fat diet (HFD), and STZ + high-fat diet-induced diabetes mellitus (DM). All animals were sacrificed and samples of the blood, liver, and brain were collected for further biological analysis. During the 15-week period of induction, the STZ and DM groups (animals injected with low-dose STZ) had significantly higher fasting glucose levels; the HFD group had elevated insulin levels, but normal blood glucose levels. The HFD and DM groups had hypercholesterolemia and higher hepatic levels of triglycerides and cholesterol. Additionally, correlations between HFD and elevated brain amyloid-beta 42 (Aβ-42), hyperglycemia and down-regulation of brain insulin receptor, and serum Aβ-42 and hepatic triglyceride concentrations (r2 = 0.41, p < 0.05) were observed. Serum C-reactive protein and malondialdehyde did not appear to have a significant influence on the association with biomarkers of AD. Thus, our study demonstrated that rats with characteristics of metabolic syndrome had a large number of biomarkers predicting AD; however, no relationship between traditional inflammatory and oxidative markers and AD was found. Further studies are necessary to prove that these findings in rats are relevant to AD processes in humans.

Keywords

Metabolic syndrome Alzheimer’s disease (AD) Amyloid precursor protein (APP) Amyloid beta-42 (Aβ-42) 

Notes

Acknowledgments

This study was supported by grants from the Taichung Hospital Department of Health, Executive Yuan, Taiwan. We would like to thank Editage for providing editorial assistance.

Conflict of Interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Hui-Ting Yang
    • 1
  • Yi-Jing Sheen
    • 2
  • Chuen-Der Kao
    • 3
  • Chin-An Chang
    • 4
  • Ya-Chun Hu
    • 1
  • Jiann-Liang Lin
    • 2
  1. 1.Department of NutritionChina Medical UniversityTaichungRepublic of China
  2. 2.Division of Endocrinology and Metabolism, Department of Internal MedicineTaichung Hospital Department of HealthTaichungRepublic of China
  3. 3.Division of Neurology, Department of Internal MedicineTaichung Hospital Department of HealthTaichungRepublic of China
  4. 4.Graduate Institute of Biochemical Sciences and TechnologyChaoyang University of TechnologyTaichungRepublic of China

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