Raspberry ketone preserved cholinergic activity and antioxidant defense in obesity induced Alzheimer disease in rats.

Obesity is a proven risk factor for neurodegenerative disease like Alzheimer's disease (AD). Accumulating evidences suggested that nutritional interventions provide potential for prevention and treatment of AD. The present study aimed to investigate the effect of dietary treatment of obese rats with natural Raspberry ketone (RK) and their relationship with neurodegeneration. Obesity was first induced in 40 male Wistar rats (140-160 g) by feeding high fat diet (HFD) for 16 weeks. Obese rats were then assigned into 4 groups (n = 10 each). (O-AD) is obese induced AD group maintained on HFD for another 6 weeks. OCR is obese group received calorie restricted diet for 6 weeks. OCRRK is obese group received calorie restricted diet and RK (44 mg/kg body weight, daily, orally) for 6 weeks and OCRD is obese group received calorie restricted diet and orlistate (10 mg/kg body weight, daily orally) for 6 weeks. Another 10 normal rats received normal diet were used as normal control group (NC). Body weight, visceral white adipose tissue weight (WAT), lipid profile, oxidative stress markers, adiponectin, cholinergic activity and amyloid extracellular plaques were examined. In addition to histological changes in brain tissues were evaluated.Raspberry ketone (RK) via its antioxidant properties attenuated oxidative damage and dyslipidemia in O-AD group. It inhibited acetylcholinesterase enzyme (AchE) and hence increased acetylcholine level (Ach) in brain tissues of O-AD rats. It is also impeded the upregulation of beta-secretase-1 (BACE-1) and the accumulation of amyloid beta (Aß) plaques which crucially involved in AD. The combination of CR diet with RK was more effective than CR diet with orlistate (antiobese drug) in abrogating the neurodegenerative changes induced by obesity. Results from this study suggested that concomitant supplementation of RK with calorie restricted regimen effectively modulate the neurodegenerative changes induced by obesity and delay the progression of AD.

Effect of zinc gluconate, sage oil on inflammatory patterns and hyperglycemia in zinc deficient diabetic rats.

BACKGROUND: The relationship between zinc homeostasis and pancreatic function had been established. In this study we aimed firstly to configure the inflammatory pattern and hyperglycemia in zinc deficient diabetic rats. Secondly to illustrate the effect of two selected agents namely Zinc gluconate and sage oil (Salvia Officinalis, family Lamiaceae). METHODS: Rats were fed on Zinc deficient diet, deionized water for 28days along with Zinc level check up at intervals to achieve zinc deficient state then rats were rendered diabetic through receiving one dose of alloxan monohydrate (120mg/kg) body weight, classified later into 5 subgroups. RESULTS: Treatment with sage oil (0.042mg/kg IP) and Zinc gluconate orally (150mg/kg) body weight daily for 8 weeks significantly reduced serum glucose, C-reactive protein (CRP), Tumor necrosis factor alpha (TNF- α), interleukins-6 1 ß, inflammatory8 (IFN È£), pancreatic 1L1-ß along with an increase in serum Zinc and pancreatic Zinc transporter 8 (ZNT8). Histopathological results of pancreatic tissues showed a good correlation with the biochemical findings. CONCLUSIONS: Both sage oil and zinc gluconate induced an improvement in the glycemic and inflammatory states. This may be of value like the therapeutic agent for diabetes.