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Ds, and cholesterol levels compared with LFD+VEH and LFD +NDEA treated groups. In addition, the serum free fatty acid level was significantly lower in the LFD+NDEA compared with LFD+VEH treated rats, whereas the triglyceride and cholesterol levels were similar in the two groups. Therefore, hyperglycemia, hyper-insulinemia, and hyper-leptinemia were features of chronic HFD feeding, and worsened by
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F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
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Ysiol Cell Physiol. 2012;302(2):C383?91. 68. Sachdev U, Cui X, Hong G, Namkoong S, Karlsson JM, Baty CJ, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg. 2012;55(1):180?1.Yang et al. Cell Bioscience (2015) 5:Page 10 of69. Kang R, Livesey KM, Zeh HJ, Loze MT, Tang D. HMGB1: a
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F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
1
F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
1
Fects is clearly warranted. In this regard, guidance may be obtained from what is already known about STZ-induced diseases. STZ, like other N-nitroso compounds, causes cellular injury and disease by functioning as: 1) an alkylating agent and potent mutagen [14]; 2) an inducer of DNA adducts leading to increased apoptosis [23]; 3) a mediator of unscheduled DNA synthesis, triggering cell death [14];
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Sulin receptor substrate gene expression, and reduced expression of tau and choline acetyltransferase (ChAT), which are regulated by insulin and IGF-1. In addition, increased levels of 4-hydroxynonenal and nitrotyrosine were measured in cerebella of HFD ?NDEA treated rats, and overall, NDEA+HFD treatment reduced brain levels of Tau, phospho-GSK-3b (reflecting increased GSK-3b activity), glial fibr
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Ld lower than the cumulative doses needed to produce cancer in experimental animals [93-96], and beginning in early adolescence, we pair-fed the rats with either high (60 ) or low (5 ) fat containing diets. The NDEA doses were selected to be far below those needed for carcinogenesis and were based on empirical studies demonstrating absence of acute toxic effects in the rats.Longer durations of NDE