In an ischemia rat model, accumulation of zinc was observed specifically in degenerating neurons in the hippocampus, and intraventricular injection of CaEDTA could reduce zinc accumulation and prevent hippocampal neurodegeneration. Administration of Ca-EDTA markedly attenuated the late rise in zinc and cell death in the hippocampal CA1 region at 3 days after ischemia in the gerbil. In the present study, we extended our experiments to assess the chelating effects of a zinc chelator, CQ, on the ischemic gerbil hippocampus. Both TSQ fluorescence dye and AMG staining, which are widely employed to demonstrate loosely bound or chelatable zinc ions, were employed to assess the effects of CQ on chelatable zinc pools in the gerbil brain. Consistent with a previous report, our data showed that CQ reduced the density of TSQ fluorescence and AMG staining in the mossy fibers, suggesting that intraperitoneal treatment of CQ rapidly targets chelatable zinc pools in the hippocampus of the gerbil brain. Most importantly, we showed for the first time that CQ attenuates ischemia-induced zinc accumulation, accompanied by less delayed neuronal death in the CA1 field revealed by Nissl and TUNEL staining. These findings indicate that CQ can target a reduction in delayed zinc accumulation, and is a potential therapeutic FTY720 approach to preventing neuronal death after transient global ischemia. Though overfeeding increases body weight, do lean individuals necessarily have to eat less than obesity-prone people to remain lean? To answer this question, we first investigated voluntary caloric intake in lean and obese rats. The process of Tag-induced islet hyperplasia is accompanied by apoptosis, but b cells generated by proliferation outnumber the apoptotic cells. As major organs for energy conversion and storage, both the liver and white adipose tissue play crucial roles in metabolic homeostasis by responding to body’s nutritional and energy states. In this study, we show that in an adaptive response to overnutrition, the early onset of hyperleptinemia most likely contributes to the suppression of the lipogenic program in the liver and white adipose tissue; leptin exerts crucial liporegulatory functions via its metabolic control of the peripheral lipogenic pathway. Taking a proteomic approach, we attempted to characterize the global protein expression profiles in the WAT of mice when challenged with HFD feeding, leading to the identification of lipogenic enzymes, including ACL and FAS, which exhibited most predominantly decreased expression patterns. Importantly, the islet hyperplasia is reversible upon de-induction of Tag in RIP7-rtTA; tet-o-Tag bitransgenic mice, and the islets are gradually restored to their normal sizes through apoptosis within 4- 8 weeks after doxycycline removal, an outcome different from our observation in PyMT-induced b-cell hyperplasia.