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Yuzu extract prevents cognitive decline and impaired glucose homeostasis in β-amyloid-infused rats.
J Nutr 2013; 143(7):1093-9JN

Abstract

Our preliminary study revealed that dementia induced by β-amyloid accumulation impairs peripheral glucose homeostasis (unpublished). We therefore evaluated whether long-term oral consumption of yuzu (Citrus junos Tanaka) extract improves cognitive dysfunction and glucose homeostasis in β-amyloid-induced rats. Male rats received hippocampal CA1 infusions of β-amyloid (25-35) [plaque forming β-amyloid; Alzheimer disease (AD)] or β-amyloid (35-25) [non-plaque forming β-amyloid; C (non-Alzheimer disease control)] at a rate of 3.6 nmol/d for 14 d. AD rats were divided into 2 dietary groups that received either 3% lyophilized 70% ethanol extracts of yuzu (AD-Y) or 3% dextrin (AD-C) in high-fat diets (43% energy as fat). The AD-C group exhibited greater hippocampal β-amyloid deposition, which was not detected in the C group, and attenuated hippocampal insulin signaling. Yuzu treatment prevented β-amyloid accumulation, increased tau phosphorylation, and attenuated hippocampal insulin signaling observed in AD-C rats. Consistent with β-amyloid accumulation, the AD-C rats experienced cognitive dysfunction, which was prevented by yuzu. AD-C rats gained less weight than did C rats due to decreased feed consumption, and yuzu treatment prevented the decrease in feed consumption. Serum glucose concentrations were higher in AD-C than in C rats at 40-120 min after glucose loading during an oral-glucose-tolerance test, but not at 0-40 min. Serum insulin concentrations were highly elevated in AD-C rats but not enough to lower serum glucose to normal concentrations, indicating that rats in the AD-C group had insulin resistance and a borderline diabetic state. Although AD-C rats were profoundly insulin resistant, AD-Y rats exhibited normal first and second phases of glucose tolerance and insulin sensitivity and secretion. In conclusion, yuzu treatment prevented the cognitive dysfunction and impaired energy and glucose homeostasis induced by β-amyloid infusion.

Authors+Show Affiliations

Food Certification Center, Korean Food Research Institutes, Sungnam, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23719224

Citation

Yang, Hye Jeong, et al. "Yuzu Extract Prevents Cognitive Decline and Impaired Glucose Homeostasis in Β-amyloid-infused Rats." The Journal of Nutrition, vol. 143, no. 7, 2013, pp. 1093-9.
Yang HJ, Hwang JT, Kwon DY, et al. Yuzu extract prevents cognitive decline and impaired glucose homeostasis in β-amyloid-infused rats. J Nutr. 2013;143(7):1093-9.
Yang, H. J., Hwang, J. T., Kwon, D. Y., Kim, M. J., Kang, S., Moon, N. R., & Park, S. (2013). Yuzu extract prevents cognitive decline and impaired glucose homeostasis in β-amyloid-infused rats. The Journal of Nutrition, 143(7), pp. 1093-9. doi:10.3945/jn.112.173401.
Yang HJ, et al. Yuzu Extract Prevents Cognitive Decline and Impaired Glucose Homeostasis in Β-amyloid-infused Rats. J Nutr. 2013;143(7):1093-9. PubMed PMID: 23719224.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Yuzu extract prevents cognitive decline and impaired glucose homeostasis in β-amyloid-infused rats. AU - Yang,Hye Jeong, AU - Hwang,Jin Taek, AU - Kwon,Dae Young, AU - Kim,Min Jung, AU - Kang,Suna, AU - Moon,Na Rang, AU - Park,Sunmin, Y1 - 2013/05/29/ PY - 2013/5/31/entrez PY - 2013/5/31/pubmed PY - 2013/8/27/medline SP - 1093 EP - 9 JF - The Journal of nutrition JO - J. Nutr. VL - 143 IS - 7 N2 - Our preliminary study revealed that dementia induced by β-amyloid accumulation impairs peripheral glucose homeostasis (unpublished). We therefore evaluated whether long-term oral consumption of yuzu (Citrus junos Tanaka) extract improves cognitive dysfunction and glucose homeostasis in β-amyloid-induced rats. Male rats received hippocampal CA1 infusions of β-amyloid (25-35) [plaque forming β-amyloid; Alzheimer disease (AD)] or β-amyloid (35-25) [non-plaque forming β-amyloid; C (non-Alzheimer disease control)] at a rate of 3.6 nmol/d for 14 d. AD rats were divided into 2 dietary groups that received either 3% lyophilized 70% ethanol extracts of yuzu (AD-Y) or 3% dextrin (AD-C) in high-fat diets (43% energy as fat). The AD-C group exhibited greater hippocampal β-amyloid deposition, which was not detected in the C group, and attenuated hippocampal insulin signaling. Yuzu treatment prevented β-amyloid accumulation, increased tau phosphorylation, and attenuated hippocampal insulin signaling observed in AD-C rats. Consistent with β-amyloid accumulation, the AD-C rats experienced cognitive dysfunction, which was prevented by yuzu. AD-C rats gained less weight than did C rats due to decreased feed consumption, and yuzu treatment prevented the decrease in feed consumption. Serum glucose concentrations were higher in AD-C than in C rats at 40-120 min after glucose loading during an oral-glucose-tolerance test, but not at 0-40 min. Serum insulin concentrations were highly elevated in AD-C rats but not enough to lower serum glucose to normal concentrations, indicating that rats in the AD-C group had insulin resistance and a borderline diabetic state. Although AD-C rats were profoundly insulin resistant, AD-Y rats exhibited normal first and second phases of glucose tolerance and insulin sensitivity and secretion. In conclusion, yuzu treatment prevented the cognitive dysfunction and impaired energy and glucose homeostasis induced by β-amyloid infusion. SN - 1541-6100 UR - https://www.unboundmedicine.com/medline/citation/23719224/Yuzu_extract_prevents_cognitive_decline_and_impaired_glucose_homeostasis_in_β_amyloid_infused_rats_ L2 - https://academic.oup.com/jn/article-lookup/doi/10.3945/jn.112.173401 DB - PRIME DP - Unbound Medicine ER -