The Hyplip2 locus causes hypertriglyceridemia by decreased clearance of triglycerides

The Hyplip2 congenic mouse strain contains part of chromosome 15 from MRL/MpJ on the BALB/cJ background. Hyplip2 mice show increased plasma levels of cholesterol and predominantly triglycerides (TGs) and are susceptible to diet-induced atherosclerosis. This study aimed at elucidation of the mechanism(s) explaining the hypertriglyceridemia. Hypertriglyceridemia can result from increased intestinal or hepatic TG production and/or by decreased LPL-mediated TG clearance. The intestinal TG absorption and chylomicron formation were studied after intravenous injection of Triton WR1339 and an intragastric load of olive oil containing glycerol tri[(3)H]oleate. No difference was found in intestinal TG absorption. Moreover, the hepatic VLDL-TG production rate and VLDL particle production, after injection of Triton WR1339, were also not affected. To investigate the LPL-mediated TG clearance, mice were injected intravenously with glycerol tri[(3)H]oleate-labeled VLDL-like emulsion particles. In Hyplip2 mice, the particles were cleared at a decreased rate (half-life of 25 +/- 6 vs. 11 +/- 2 min; P < 0.05) concomitant with a decreased uptake of emulsion TG-derived (3)H-labeled fatty acids by the liver and white adipose tissue. The increased plasma TG levels in Hyplip2 mice do not result from an enhanced intestinal absorption or increased hepatic VLDL production but are caused by decreased LPL-mediated TG clearance.     

Apolipoprotein C-I binds free fatty acids and reduces their intracellular esterification

Mice that overexpress human apolipoprotein C-I (apoC-I) homozygously (APOC1(+/+) mice) are protected against obesity and show cutaneous abnormalities. Although these effects can result from our previous observation that apoC-I inhibits FFA generation by LPL, we have also found that apoC-I impairs the uptake of a FFA analog in adipose tissue. In this study, we tested the hypothesis that apoC-I interferes with cellular FFA uptake independent of LPL activity. The cutaneous abnormalities of APOC1(+/+) mice were not affected after transplantation to wild-type mice, indicating that locally produced apoC-I prevents lipid entry into the skin. Subsequent in vitro studies with apoC-I-deficient versus wild-type macrophages revealed that apoC-I reduced the cell association and subsequent esterification of [(3)H]oleic acid by approximately 35% (P < 0.05). We speculated that apoC-I binds FFA extracellularly, thereby preventing cell association of FFA. We showed that apoC-I was indeed able to mediate the binding of oleic acid to otherwise protein-free VLDL-like emulsion particles involving electrostatic interaction. We conclude that apoC-I binds FFA in the circulation, thereby reducing the availability of FFA for uptake by cells. This mechanism can serve as an additional mechanism behind the resistance to obesity and the cutaneous abnormalities of APOC1(+/+) mice.     

Time sequence of the damage to the acceptor and donor sides of photosystem II by UV-B radiation as evaluated by chlorophyll a fluorescence

The effects of ultraviolet-B (UV-B) radiation on photosystem II (PS II) were studied in leaves of Chenopodium album. After the treatment with UV-B the damage was estimated using chlorophyll a fluorescence techniques. Measurements of modulated fluorescence using a pulse amplitude modulated fluorometer revealed that the efficiency of photosystem II decreased both with increasing time of UV-B radiation and with increasing intensity of the UV-B. Fluorescence induction rise curves were analyzed using a mechanistic model of energy trapping. It appears that the damage by UV-B radiation occurs first at the acceptor side of photosystem II, and only later at the donor side.     

Physiological and cytological mechanisms of silicon-induced resistance in rice against blast disease

Rice (Oryza sativa L.) blast disease caused by Magnaporthe grisea is one of the most destructive diseases in the rice-growing areas of the world. Silicon is an important nutritional element especially for rice. Two near-isogenic lines of rice with different resistance to blast disease, i.e. CO39 (susceptible) and C101LAC (Pi-1) (resistant), were selected to determine the effects of Si amendment on the severity and incidence of rice blast disease. The physiological and cytological mechanisms involved in the induced disease resistance by silicon were investigated. Exogenous Si application at a concentration of 2 mM reduced the disease index by 45% for CO39 and 56% for C101LAC (Pi-1). Si application alone did not change lignin content and the activities of defense-related enzymes including peroxidase (POD), polyphenol oxidase (PPO) and phenylalanine ammonia-lyase (PAL) in rice leaves of both isogenic lines. However, after inoculation with M. grisea, Si-treated rice plants significantly increased the activities of POD, PPO and PAL in leaves of both isogenic lines. Si and lignin content were also significantly increased in Si-treated inoculated seedlings. Environmental scanning electron microscope observations revealed that Si amendment resulted in higher Si deposit on dumbbell bodies in the rice leaves and silicon papilla accumulation on the guard cell of stoma. These results suggest that silicon-induced defense response and cell silicification of rice leaves altogether contribute to the silicon-induced rice resistance to blast disease.     

CETP expression reverses the reconstituted HDL-induced increase in VLDL

Human data suggest that reconstituted HDL (rHDL) infusion can induce atherosclerosis regression. Studies in mice indicated that rHDL infusion adversely affects VLDL levels, but this effect is less apparent in humans. This discrepancy may be explained by the fact that humans, in contrast to mice, express cholesteryl ester transfer protein (CETP). The aim of this study was to investigate the role of CETP in the effects of rHDL on VLDL metabolism by using APOE*3-Leiden (E3L) mice, a well-established model for human-like lipoprotein metabolism. At 1 h after injection, rHDL increased plasma VLDL-C and TG in E3L mice, but not in E3L mice cross-bred onto a human CETP background (E3L.CETP mice). This initial raise in VLDL, caused by competition between rHDL and VLDL for LPL-mediated TG hydrolysis, was thus prevented by CETP. At 24 h after injection, rHDL caused a second increase in VLDL-C and TG in E3L mice, whereas rHDL had even decreased VLDL in E3L.CETP mice. This secondary raise in VLDL was due to increased hepatic VLDL-TG production. Collectively, we conclude that CETP protects against the rHDL-induced increase in VLDL. We anticipate that studies evaluating the anti-atherosclerotic efficacy of rHDL in mice that are naturally deficient for CETP should be interpreted with caution, and that treatment of atherogenic dyslipidemia by rHDL should not be combined with agents that aggressively reduce CETP activity.     

Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice

Insulin signaling in the central nervous system (CNS) is required for the inhibitory effect of insulin on glucose production. Our aim was to determine whether the CNS is also involved in the stimulatory effect of circulating insulin on the tissue-specific retention of fatty acid (FA) from plasma. In wild-type mice, hyperinsulinemic-euglycemic clamp conditions stimulated the retention of both plasma triglyceride-derived FA and plasma albumin-bound FA in the various white adipose tissues (WAT) but not in other tissues, including brown adipose tissue (BAT). Intracerebroventricular (ICV) administration of insulin induced a similar pattern of tissue-specific FA partitioning. This effect of ICV insulin administration was not associated with activation of the insulin signaling pathway in adipose tissue. ICV administration of tolbutamide, a K(ATP) channel blocker, considerably reduced (during hyperinsulinemic-euglycemic clamp conditions) and even completely blocked (during ICV administration of insulin) WAT-specific retention of FA from plasma. This central effect of insulin was absent in CD36-deficient mice, indicating that CD36 is the predominant FA transporter in insulin-stimulated FA retention by WAT. In diet-induced insulin-resistant mice, these stimulating effects of insulin (circulating or ICV administered) on FA retention in WAT were lost. In conclusion, in insulin-sensitive mice, circulating insulin stimulates tissue-specific partitioning of plasma-derived FA in WAT in part through activation of K(ATP) channels in the CNS. Apparently, circulating insulin stimulates fatty acid uptake in WAT but not in BAT, directly and indirectly through the CNS.     

Apolipoprotein CI causes hypertriglyceridemia independent of the very-low-density lipoprotein receptor and apolipoprotein CIII in mice

We have recently shown that the predominant hypertriglyceridemia in human apolipoprotein C1 (APOC1) transgenic mice is mainly explained by apoCI-mediated inhibition of the lipoprotein lipase (LPL)-dependent triglyceride (TG)-hydrolysis pathway. Since the very-low-density lipoprotein receptor (VLDLr) and apoCIII are potent modifiers of LPL activity, our current aim was to study whether the lipolysis-inhibiting action of apoCI would be dependent on the presence of the VLDLr and apoCIII in vivo. Hereto, we employed liver-specific expression of human apoCI by using a novel recombinant adenovirus (AdAPOC1). In wild-type mice, moderate apoCI expression leading to plasma human apoCI levels of 12-33 mg/dl dose-dependently and specifically increased plasma TG (up to 6.6-fold, P < 0.001), yielding the same hypertriglyceridemic phenotype as observed in human APOC1 transgenic mice. AdAPOC1 still increased plasma TG in vldlr(-/-) mice (4.1-fold, P < 0.001) and in apoc3(-/-) mice (6.8-fold, P < 0.001) that were also deficient for the low-density lipoprotein receptor (LDLr) and LDLr-related protein (LRP) or apoE, respectively. Thus, irrespective of receptor-mediated remnant clearance by the liver, liver-specific expression of human apoCI causes hypertriglyceridemia in the absence of the VLDLr and apoCIII. We conclude that apoCI is a powerful and direct inhibitor of LPL activity independent of the VLDLr and apoCIII.     

Regulation of photosynthetic electron transport by bicarbonate formate and herbicides in isolated broken and intact chloroplasts

In this paper, we have presented a minireview on the interaction of bicarbonate, formate and herbicides with the thylakoid membranes.The regulation of photosynthetic electron transport by bicarbonate, formate and herbicides is described. Bicarbonate, formate, and many herbicides act between the primary quinone electron acceptor Q_A and the plastoquinone pool. Many herbicides like the ureas, triazines and the phenol-type herbicides act, probably, by the displacement of the secondary quinone electron acceptor Q_B from its binding site on a Q_B-binding protein located at the acceptor side of Photosystem II. Formate appears to be an inhibitor of electron transport; this inhibition can be removed by the addition of bicarbonate. There appears to be an interaction of the herbicides with bicarbonate and/or It has been suggested that both the binding of a herbicide and the absence of bicarbonate may cause a conformational alteration of the environment of the Q_B-binding site. The alteration brought about by a herbicide decreases the affinity for another herbicide or for bicarbonate; the change caused by the absence of bicarbonate decreases the affinity for herbicides. Moreover, this change in conformation causes an inhibition of electron transport. A bicarbonate-effect in isolated intact chloroplasts is demonstrated.Paper presented at the FESPP meeting (Strasbourg, 1984)     

华南农区典型植物的他感作用研究

研究华南农业区典型植物的他感作用,结果表明,用萝卜作生测受体时地上部水浸出物表明有他感作用的植物有拧檬按、隆缘按、赤按、木麻黄、茶、蟛蜞菊、胜红蓟、三叶鬼针草、香芳、马唐、马占相思、马尾松、蕃茄等,但无明显他感作用的有白茅、铺地木兰、凤尾竹、大叶桉、糖蜜草。研究表明柠檬桉、蟛蜞菊、胜红蓟的地上部挥发物和地部分泌物都有他感作用。木麻黄、茶、蟛蜞菊地上部水浸出物有自毒作用,花生、大豆、绿豆发芽中分泌出的物质也有自毒作用。三叶鬼针革、胜红蓟、香芳、蟛蜞菊、柠蒙桉和木麻黄地上部水浸物他感作用强度一般随着浓度而加剧,但低浓度下常表现有促进作用。三叶鬼针草水提物及柠檬桉地上部挥发物的他感效应强度与采集前一个月降雨量呈显著负相关。木麻黄小枝他感作用物浓度与温度有交互效应。柠檬桉的水浸提物在土壤中易随水流失而挥发物却易被土壤吸附。在土壤中柠檬棕叶的他感作用效应随时间成负指数减少,蟛蜞菊在土壤分解后的残留率与残留物的他感效应指数绝对值显著正相关。他感成份的分离鉴定结果表明,茶叶他感作用的主要成份为茶多酚与咖啡因,木麻黄小枝他感物中分离出五种黄酮类化合物和一种阿魏酸,胜红蓟地上部分离出胜红蓟素和一种豆甾醇。