Abstract
In this paper, we first observed that there were differences in expressions of 11β-HSD1 and PPAR-γ, in hippocampi and hypothalami, among constant hyperglycemia group, control group and the fluctuant glycemia group, using Immunohistochemical analysis. However, whether in expression o f 11β-HSD1 or PPAR-γ, there were no statistic differences between the control group or the fluctuant glycemia group. So, we removed the fluctuant glycemia group, retaining only constant hyperglycemia group and control group, being fed for 8 weeks. After 8 weeks of induction, 11β-HSD1 expression increased and PPAR-γ expression decreased in the constant hyperglycemia group compared with control group, both in hippocampi and hypothalami, by Western Blot. The constant hyperglycemia group also showed impaired cognition in MORRIS watermaze, lower serum corticosterone level, and higher Serum ACTH concentration after 8 weeks. We inferred that the cognition impairment may be related to the abnormal expression of 11β-HSD1 and PPAR-γ in central nerves system. As for 11β-HSD1 is a regulating enzyme, converting the inactive 11-dehydrocorticosterone into the active glucocorticoid corticosterone, thus amplifying GC action in local tissues. It is also well known that high local GC levels can affect the cognitive function. In addition, PPAR-a protective receptor, which is related to cognition.
Highlights
Diabetes mellitus negatively affects the cognitive function, neurophysiology, and structure in the brain, which is referred as diabetic encephalopathy
Some studies have demonstrated that hyperglycemia, hyperlipidemia, the change of blood flow, and neurotrophic factors in diabetes [2,3,4,5] are involved in the pathophysiology of diabetic encephalopathy
It has been reported that abnormal elevation of 11β-HSD1 activity in brain may contribute to the development of Alzheimer’s disease (AD), which is characterized by cognitive impairment [10]
Summary
Diabetes mellitus negatively affects the cognitive function, neurophysiology, and structure in the brain, which is referred as diabetic encephalopathy. PPAR-γ is an isoform of PPARs, expressed mainly in adipose tissue. AD is related to the decreased levels of PPAR-γ in the brain [11]. These studies may suggest a hypothesis that the cognitive impairment in diabetes may be associated with the abnormal levels of 11β-HSD1 and PPAR-γ in the brain. We hypothesize that hyperglycemia would induce the variations of 11β-HSD1 and PPAR-γ expressions in hippocampus and hypothalamus, which are related to the cognitive impairment in diabetic rats. We demonstrated that the variations of 11β-HSD1 and PPARγ expressions in hippocampi and hypothalamic, respectively, in STZ-induced SD rats are detected by immunohistochemistry and western blot. The changes of cognitive function of these experimental diabetic rats had been detected by the Morris water maze during the experimental period, before the samples had been collected as well
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