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Standardized chungkookjang, short‐term fermented soybeans with Bacillus lichemiformis, improves cognitive function and insulin resistance in β‐amyloid‐infused diabetic rats
Author(s) -
Park Sunmin,
Kang Suna,
Kim Hyun Jin,
Kwon Dae Young,
Daily James
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1079.14
Subject(s) - endocrinology , medicine , insulin resistance , insulin , type 2 diabetes , diabetes mellitus , chemistry , amyloid (mycology) , pathology
Both traditionally made chungkookjang (TFC, naturally fermented) and standardized chungkookjang (SFC, fermented by inoculating Bacillus lichemifomis for 48 h) have potent antidiabetic activities. It is interesting to investigate whether both chungkookjangs can protect against cognitive dysfunction in β‐amyloid‐infused diabetic rats since Alzheimer's disease is known as “brain diabetes”. Male rats with type 2 diabetes and an Alzheimer's‐like brain disorder induced by partial pancreatectomy and ICV β‐amyloid (25–35) infusion were fed either control diet, 10% cooked soybeans (CSB), 10% TFC, or SFC in a high fat diet for 8 weeks. Px rats infused β‐amyloid (35–25) as a normal‐control group. SFC, CSB and TFC improved cognitive function as measured by a water maze test in an ascending order. β‐amyloid deposition was much higher in the control rats than the normal‐control rats and SFC decreased its accumulation. Rats in the control group had lower whole body glucose infusion rates and increased hepatic glucose output at hyperinsulinemic state during euglycemic hyperinsulinemic clamp which was normalized by SFC. Interestingly, insulin secretion, especially at the second phase during hyperglycemic clamp, was higher in control rats in comparison to the normal control group while CSB, TFC, SFC lowered it. However, β‐cell mass was restored by SFC in β‐amyloid‐infused rats with reduced β‐cell mass by increased β‐cell apoptosis. In conclusion, cognitive dysfunction exacerbated insulin resistance and decreased β‐cell mass and SFC alleviated their exacerbation in β‐amyloid infused diabetic rats. The SFC‐improved memory loss may be due to increased genistein, daidzein, poly‐gamma‐glutamate, small peptides and other components in SFC.