Our data showed that 2-AAA played an important role in regulating glycolipid metabolism independent of diet and exercise, implying that improving the level of 2-AAA in vivo could be developed as a strategy in the treatment of obesity or diabetes.
In the present study, we first found that adapentpronitrile significantly ameliorated neuronal injury and decreased amyloid precursor protein (APP) and amyloid beta (Aβ) expression in the hippocampus and cortex in the high fat diet/STZ rat model of diabetes.
Patients seen by APP s were more likely to have diabetes mellitus (37% versus 33%) and heart failure (20% versus 16%), be discharged to a nursing facility (21% versus 13%) and had more outpatient visits within 90 days post-discharge (median 6 versus 5, P<0.01 for all) than those seen by physicians only.
In this study, we have examined the expression and processing of pancreatic APP to test the hypothesis that APP may play a role in pancreatic function and the pathophysiology of diabetes.
Taken together, our findings provide a mechanistic link between diabetes and AD, and is consistent with the notion that geniposide might play an important role on APP processing via enhancing insulin signaling and may convey a therapeutic benefit in AD.
Formaldehyde level was analyzed by high-performance liquid chromatography (with fluorescence detection) in human urine from dementia patients (n=141), patients with hypertension (n=33) or diabetes (n=16) and healthy individuals (n=38), autopsy hippocampus samples from Alzheimer's disease (AD) patients and brains of three types of AD animal model: namely, senescence accelerated mice (SAMP8), APP-transgenic mice and APP/PS1-transgenic mice.
Our results indicate that the pathologic features of AD are exaggerated in the brain of APP transgenic mice that have concurrent insulin-deficient diabetes, and underscore a possible mechanism of brain dysfunction common to AD and diabetes.