Since apoD is often upregulated under stress conditions or disease states, mice were fed an atherogenic Western diet. We tested the hypothesis that apoD affects circulating plasma HDL-cholesterol levels by altering the lipid and protein content of HDL and the catalytic activities of associated enzymes. This study investigated apoD as a candidate regulator of plasma HDL-C metabolism. ApoD occurs predominantly on HDL and several studies suggest that plasma apoD levels are associated with those of HDL or apoAI levels. This is the first study to provide evidence that apoD deficiency modulates plasma HDL-C and LDL-C levels. We observed a profound increase in circulating plasma HDL-cholesterol levels and particle size in the apoD2/2 mice on an atherogenic diet. These observations were confirmed by size-exclusion chromatography, as well as lipoprotein-lipid and -protein analyses. PLTP but not LCAT activity was modestly changed by apoD deficiency in male apoD2/2 mice only. Despite being,5% of HDL-protein in WT mice, apoD deficiency altered the distribution of the major HDL protein and HDL particle size, which were associated with higher circulating plasma HDL-C levels. More importantly, in female apoD2/2 mice there was substantial decrease in plasma 3 H-CE-HDL metabolism, which coincided with a decrease in the expression of the hepatic HDL receptor, SR-BI. These data suggest that reduction of plasma apoD levels plays a role in plasma cholesterol homeostasis. Ovarian cancer is one of the leading causes of mortality in malignant gynecological tumors. There were approximately 22,240 new cases and 14,030 deaths associated with ovarian diseases in the United States in 2013. One reason for this high mortality rate is that ovarian cancer is often diagnosed at latestage. Surgical resection and subsequent chemotherapy are still the major therapeutic strategies, with limitation for controlling cancer growth and metastases. Furthermore, drug resistance and cancer recurrence are major clinical challenges. The tricarboxylic acid cycle regulates energy generation in mitochondrial respiration and plays a central role in carbohydrate metabolism. Citrate synthase catalyzes the first reaction of the TCA cycle and is generally assumed to be the rate-limiting enzyme of the cycle. Increasing evidence suggests that CS activity is closely associated with various kinds of cancers. The activity of citrate synthase was measured using tissue extract prepared from specimens obtained from 24 patients with ductal carcinoma who underwent pancreatoduodenectomy or total pancreatomy, enhanced CS activity was observed in pancreatic cancer. It is likely that enhanced citrate synthase activity contributes to the conversion of glucose to lipids in pancreatic cancer providing substrate for membrane lipids synthesis. In an KRX-0401 in-vitro model, Ramos cells were exposed to varying concentrations of doxorubicin and vincristine for 1 hr; and allowing for recovery in culture over a 7- day period, recovering or residual cells from chemotoxicity exhibited an increase in citrate synthase. All these suggested CS play an essential role in tumors.