Early life exposure to hypercaloric diet impairs eating behavior during weaning: The role of BDNF signaling and astrocyte marks.

Literature shows that gestational and/or lactational exposure to hypercaloric diets induces long term effects on eating behavior and the involvement of neurochemical mechanisms. We hypothesized that the effects of hypercaloric diets in early development phases can precede an overweight or an obesity status. The aim of the present study was to evaluate the impact of gestational and lactational exposure to cafeteria diet on eating behavior and neurochemical parameters, BDNF signaling, epigenetic and astrocyte marks in the hippocampus and olfactory bulb during the weaning phase. Pregnant female rats were randomized between standard and cafeteria diet, the respective diet was maintained through the lactational period. The framework of feeding pattern, meal, and its microstructure, was observed in postnatal day 20. Exposure to cafeteria diet increased the number of meals, associated with a lower first inter-meal interval and higher consumption in both genders, without any changes in body weight. Diet exposure also reduced the number of grooming, a behavior typically found at the end of meals. Hypercaloric diet exposure reduced BDNF levels in the olfactory bulb and hippocampus from rats of both sexes and increased the content of the TrkB receptor in hippocampi. It was observed an increase in HDAC5 levels, an epigenetic mark. Still, early exposure to the hypercaloric diet reduced hippocampal GFAP and PPARγ levels, without any effect on NeuN content, indicating that alterations in astrocytes can precede those neuronal outcomes. Our results showed that changes in interrelated neurochemical signaling, BDNF, and astrocyte marks, induced by hypercaloric diet in early stages of development may be related to impairment in the temporal distribution of eating pattern and consequent amounts of consumed food during the weaning phase.

The amyloid precursor protein (APP) processing as a biological link between Alzheimer's disease and cancer.

Aging is a risk factor for several illnesses, such as Alzheimer's Disease and various cancers. However, an inverse correlation between malignancies and Alzheimer's Disease has been suggested. This review addressed the potential role of non-amyloidogenic and amyloidogenic pathways of amyloid precursor protein processing as a relevant biochemical mechanism to clarify this association. Amyloidogenic and non-amyloidogenic pathways have been related to Alzheimer's Disease and certain malignancies, respectively. Several known molecules involved in APP processing, including its regulation and final products, were summarized. Among them some candidate mechanisms emerged, such as extracellular-regulated kinase (Erk) and protein kinase C (PKC). Therefore, the imbalance of APP processing may be involved with the negative correlation between cancer and Alzheimer Disease.