High-cholesterol diets impair short-term retention of memory in alloxan-induced diabetic mice, but not acquisition of memory nor retention of memory in prediabetic mice.
Whether high-cholesterol diets (HCD) induce a high incidence of memory deficits in diabetes requires to be established; if so, whether they induce impairments of memory acquired in the pre-diabetic stage as well as in the diabetic stage also needs to be elucidated, and part of the related mechanisms involved in this dysfunction should be determined. The mice were grouped into: normal mice fed normal diets (NN), diabetic mice fed normal diets (DN), normal mice fed HCD (NH), and diabetic mice fed HCD (DH). Animals were subjected to Morris water maze testing: 1) Learning in the pre-diabetic stage and memory retrieval in the diabetic stage; 2) Learning and memory retrieval in the diabetic stage. Following water maze testing, biochemical parameters were estimated in the animals. The results showed that significant impairments of memory retrieval, acquired in the diabetic stage, were observed only in DH group, neither in DN nor NH group in a short term compared with NN group. Biochemical parameters including fasting blood glucose, lipid peroxidation productions and acetylcholinesterase activities in frontal cortex and hippocampus increased more rapidly in DH group than those in the rest. These results indicate that HCD impair the diabetic retention of memory, but neither the diabetic acquisition of memory nor the pre-diabetic retention of memory in diabetic mice in a short term. Controlled HCD may be a strategy to prevent the loss of memory in diabetic individuals after they have acquired new information.[1]References
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