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Lipid Deposition (lipid + deposition)
Selected AbstractsInsulin resistance and endothelial dysfunction: the road map to cardiovascular diseasesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2006Eugenio Cersosimo Abstract Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined. Copyright © 2006 John Wiley & Sons, Ltd. [source] Is the Presence of Mitral Annular Calcification Associated with Poor Left Atrial Function?ECHOCARDIOGRAPHY, Issue 8 2009Vignendra Ariyarajah M.D. Introduction: Mitral annular calcification (MAC) is characterized by calcium and lipid deposition in the annular fibrosa of the mitral valve. MAC is associated with cardiovascular events but little is known of its association with left atrial (LA) function. Methods: We prospectively obtained 12-lead electrocardiograms (ECGs) and transthoracic echocardiograms (TTE) on patients scheduled for nonemergent echocardiographic assessment at a tertiary care hospital. MAC was graded as 0 = none, 1 = mild, 2 = moderate, 3 = severe. LA linear and volume measurements (stroke volume, LA passive emptying fraction, LA active emptying fraction and LA kinetic energy) were done specifically in addition to commonly measured TTE parameters. Results: From the 124 considered for the study, 72 patients remained (aged 68±18 years; 44% male) after excluding those with poor ECG tracings and/or poor TTE images. Eighteen patients had MAC; mild MAC = 14, moderate MAC = 3, severe MAC = 1. When patients with MAC were compared to those without MAC, no significant difference was noted, except for LA linear dimension index (2.1±0.4 vs. 1.9±0.3 cm/m2; P = 0.03). For those with mild and moderate MAC, a trend was noted toward lower LA function with increasing MAC severity. In addition, significant differences were noted between those with and without interatrial conduction delay, where those with such delay had significantly impaired LA stroke volume (9.8±3 vs. 19.93±4 ml; P < 0.0001), LA active emptying fraction (18.83±8 vs. 65.71±9%; P < 0.0001) and LA total/reservoir fraction (39.54±6 vs. 75.1±6%; P < 0.0001). Conclusions: MAC is associated with increase in LA linear dimension on TTE and may be equally represented with lower overall LA function. Further study in a much larger cohort is warranted to delineate these and other potential associations of MAC. [source] Combined loss of orphan receptors PXR and CAR heightens sensitivity to toxic bile acids in mice,HEPATOLOGY, Issue 1 2005Hirdesh Uppal Efficient detoxification of bile acids is necessary to avoid pathological conditions such as cholestatic liver damage and colon cancer. The orphan nuclear receptors PXR and CAR have been proposed to play an important role in the detoxification of xeno- and endo-biotics by regulating the expression of detoxifying enzymes and transporters. In this report, we showed that the combined loss of PXR and CAR resulted in a significantly heightened sensitivity to bile acid toxicity in a sex-sensitive manner. A regimen of lithocholic acid treatment, which was tolerated by wild-type and PXR null mice, caused a marked accumulation of serum bile acids and histological liver damage as well as an increased hepatic lipid deposition in double knockout males. The increased sensitivity in males was associated with genotype-specific suppression of bile acid transporters and loss of bile acid,mediated downregulation of small heterodimer partner, whereas the transporter suppression was modest or absent in females. The double knockout mice also exhibited gene- and tissue-specific dysregulation of PXR and CAR target genes in response to PXR and CAR agonists. In conclusion, although the cross-regulation of target genes by PXR and CAR has been proposed, the current study represents in vivo evidence of the combined loss of both receptors causing a unique pattern of gene regulation that can be translated into physiological events such as sensitivity to toxic bile acids. (HEPATOLOGY 2005;41:168,176.) [source] Ethanol Self-Administration and Alterations in the Livers of the Cynomolgus Monkey, Macaca fascicularisALCOHOLISM, Issue 1 2007Priscilla Ivester Background: Most of the studies of alcoholic liver disease use models in which animals undergo involuntary administration of high amounts of ethanol and consume diets that are often high in polyunsaturated fatty acids. The objectives of this study were (1) to evaluate whether cynomolgus monkeys (Macaca fascicularis) drinking ethanol voluntarily and consuming a diet with moderate amounts of lipid would demonstrate any indices of alcoholic liver disease past the fatty liver stage and (2) to determine whether these alterations were accompanied by oxidative stress. Methods: Six adult male and 6 adult female cynomolgus monkeys were allowed to consume ethanol voluntarily for 18 to 19 months. Additional monkeys were maintained on the same consumption protocol, but were not provided with ethanol. During the course of the study, liver biopsy samples were monitored for lipid deposition and inflammation, serum for levels of liver enzymes, and urine for concentrations of the isoprostane (IsoP) metabolite, 2,3-dinor-5,6-dihydro-15-F2t -IsoP, a biomarker for oxidative stress. Liver mitochondria were monitored for respiratory control and liver for concentrations of neutral lipids, adenine nucleotides, esterified F2 isoprostanes, oxidized proteins, 4-hydroxynonenal (HNE)-protein adducts, and protein levels of cytochrome P-450 2E1 and 3A4. Results: Ethanol consumption ranged from 0.9 to 4.05 g/kg/d over the period of the study. Serum levels of aspartate amino transferase were elevated in heavy-consuming animals compared with those in ethanol-naïve or moderate drinkers. Many of the ethanol consumers developed fatty liver and most showed loci of inflammation. Both hepatic energy charge and phosphorylation potential were decreased and NADH-linked respiration was slightly, but significantly depressed in coupled mitochondria as a result of heavy ethanol consumption. The urinary concentrations of 2,3-dinor-5,6-dihydro-15-F2t -IsoP increased as high as 33-fold over that observed in ethanol-abstinent animals. Liver cytochrome P-450 2E1 concentrations increased in ethanol consumers, but there were no ethanol-elicited increases in hepatic concentrations of the esterified F2 isoprostanes, oxidized proteins, or HNE-protein adducts. Conclusion: Our studies show that cynomolgus monkeys undergoing voluntary ethanol consumption for 1.5 years exhibit many of the features observed in the early stages of human alcoholic liver disease. Ethanol-elicited fatty liver, inflammation, and elevated serum aspartate amino transferase were evident with a diet that contained modest amounts of polyunsaturated lipids. The dramatic increases in urinary IsoP demonstrated that the animals were being subjected to significant oxidative stress that correlated with their level of ethanol consumption. [source] Dietary energy requirement of piracanjuba fingerlings, Brycon orbignyanus, and relative utilization of dietary carbohydrate and lipidAQUACULTURE NUTRITION, Issue 3 2006M.R. BORBA Abstract Ten isonitrogenous casein,gelatin-based diets were formulated to contain five estimated metabolizable energy concentrations (10.92, 12.29, 13.63, 14.82 and 16.16 kJ g,1) at two carbohydrate-to-lipid ratios (CHO : L, 5.3 and 12.8, g : g) in a 5 × 2 factorial arrangement. Each diet was assigned to triplicate groups of 11 piracanjuba fingerlings (5.25 ± 0.14 g) and fed to apparent satiation twice a day for 90 days. Higher daily weight gain was obtained by fish fed the 13.63 kJ g,1 diets for both CHO : L ratios. There was a significant reduction of feed consumption when dietary energy concentration increased above 13.63 kJ g,1. Feed conversion ratio and apparent net energy retention improved as dietary energy increased. Apparent net protein retention tended to be lower in the highest and lowest dietary energy concentrations. The results suggest that dietary lipid energy was more efficiently utilized by piracanjuba fingerlings than carbohydrate energy. Body composition and hepatosomatic index (HSI) were not influenced by dietary CHO : L ratio. However, an increase in dietary energy concentration beyond 13.63 kJ g,1 resulted in a significant increment in lipid deposition, while body moisture and HSI decreased. Our findings indicate that at 300 g kg,1 dietary crude protein, a CHO : L ratio of 5.3 is recommended for piracanjuba, and the required energy is either 13.63 kJ g,1 if raised for aquaculture or 14.82 kJ g,1 if destined to stock enhancement. [source] Evaluation of carbohydrate rich diets through common carp culture in manured tanksAQUACULTURE NUTRITION, Issue 3 2002P. KESHAVANATH Four diets (T0,T3) were formulated reducing the fishmeal (Indian) component by 100 g kg,1 from 300 to 0 g kg,1 and including proportionately increasing quantities of maize. Diets were fed for 120 days at 50 g kg,1 body weight to triplicate groups of common carp (av. wt. 2.11,2.18 g) stocked at 1 m,2 in mud bottomed cement tanks (18 m2), fertilized with poultry manure. Fish growth, SGR and FCR in the different treatments were statistically not significantly different (P > 0.05). PER was lowest for the 300 g fishmeal kg,1 diet treatment (diet T0), increasing with decrease in dietary fishmeal content (diets T1,T3). Fish survival ranged from 96.29 to 100%. Diets influenced carcass composition and digestive enzyme activity. A significant increase in lipid deposition was recorded with increasing dietary carbohydrate content. Amylase, protease and lipase activities were higher in fish fed with diets T2 and T3. The protein sparing effect of dietary carbohydrate and the economic implication of eliminating fishmeal from the diet are discussed. [source] Effects of feeding levels on growth performance, feed utilization, body composition and apparent digestibility coefficients of nutrients for juvenile Chinese sucker, Myxocyprinus asiaticusAQUACULTURE RESEARCH, Issue 7 2010Yong-Chao Yuan Abstract An experiment was conducted to determine effects of feeding levels on growth performance, feed utilization, nutrient deposition, body composition and apparent digestibility coefficients (ADCs) of nutrients for juvenile Chinese sucker (initial weight, 11.77±0.22 g). Chinese sucker were fed a practical diet from 0% (starvation) to 4.0% (at 0.5% increments) body weight (bw) day,1 for 8 weeks. The results showed that growth performance, feed utilization, nutrient deposition, body composition and ADCs of dry matter, protein and energy were significantly (P<0.05) affected by feeding levels. Survival was the lowest for the starvation group. Final mean body weight, growth rate, thermal-unit growth coefficient (TGC) increased with feeding rate from 0% to 3.0% bw day,1 (P<0.05) and showed no significant differences above the level (P>0.05). Feed conversion rate was significantly lower at a feeding level of 2.5% bw day,1 than above and below the level (P<0.05). Protein efficiency ratio was markedly highest at the 2.5% bw day,1 ration level (P<0.05). Fish fed at the feeding level (1.0% bw day,1), which represented a maintenance ration (energy gain was less than 2.27 kJ fish,1 day,1), showed positive protein deposition but negative lipid deposition. This indicates that fish fed a maintenance ration mobilize body lipid reserve to support protein deposition. Lipid contents of whole body, muscle and liver increased with increasing feeding rates from 0.5% to 3.0% bw day,1 and showed no significant differences above the level (P>0.05). Protein contents of whole-body composition increased with feeding rate from 0.5 to 3.0% bw day,1 (P<0.05) and showed no significant differences above the level (P>0.05), whereas muscle and liver remained relatively stable with the different ration amount with the exception of fish fed a ration of 0.5% bw day,1, at which Chinese sucker possessed significantly lower body protein concentration (P<0.05). The ADCs of dry matter, protein and energy decreased with increasing feeding levels from 0.5% to 3.0% bw day,1 and then remained relatively constant over the level. Based on the broken-line regression analysis using WG data, the optimum and maintenance feeding levels for Chinese sucker were 3.10% bw day,1 and 0.45% bw day,1 respectively. [source] Weight gain and lipid deposition in Atlantic salmon, Salmo salar, during compensatory growth: evidence for lipostatic regulation?AQUACULTURE RESEARCH, Issue 12 2001S J S Johansen Abstract Feed-restricted fish gain less body mass and storage reserves than well-fed fish, and reduced rates of gain often trigger compensatory responses, characterized by increased appetite (hyperphagia) and growth rate. The results of previous investigations have introduced a hypothesis in which adipose tissue (fat stores) had a regulatory role in governing appetite. An extension of this suggests that hyperphagia may relate to the severity of the feed restriction, and that the compensatory responses will cease once fat reserves are restored relative to body size. This was tested in two trials in which feed-restricted or -deprived postsmolt Atlantic salmon, Salmo salar, became hyperphagic after transfer to excess feeding. At the end of the first trial, previously feed-restricted fish had fully compensated for their lost weight gain compared to continuously fed control fish, but had a leaner body composition (i.e. reduced energy stores) and were still showing signs of compensatory growth. In the second trial, feed deprivation drained body lipids and caused a stronger hyperphagic response than restrictive feeding, although it took longer to develop. Feed intake became coincident when fish had a similar body composition for size, but this occurred at different times. Hence, the fish that had been deprived of feed were smaller than the restricted fish at the end of the trial. The results of the present study demonstrate a link between the magnitude of lipid stores, feed intake and weight gain, and provide some evidence for lipostatic appetite regulation in fish. [source] Effects of dietary lipid level on liver and muscle lipid deposition in juvenile haddock, Melanogrammus aeglefinus L.AQUACULTURE RESEARCH, Issue 2001D A Nanton Abstract The effects of dietary lipid levels on growth, feed utilization, hepatosomatic index (HSI), liver lipid deposition and tissue fatty acid composition in haddock were investigated. Triplicate tanks of juvenile haddock (6.9 g) were fed graded levels of herring oil to supply 14, 16, 19 and 22% lipid (DM, dry matter) in fish meal-based, isonitrogenous diets. Growth and feed conversion ratio of juvenile haddock was not significantly (P < 0.05) affected by increasing the lipid content of the diet. A significant increase in HSI (9.8,12.1%), total liver lipid (63.2,69.0%) and whole body gross energy content (6.03,6.39 kcal g,1 DM) were observed in haddock fed 14% vs. 22% lipid. Although the HSI of these cultured haddock was high in comparison to wild gadoids, histological analyses of these haddock livers did not reveal any overt pathology. Muscle lipid levels (1.0%) did not increase significantly with dietary lipid. Liver fatty acid levels mirrored dietary fatty acid (FA) composition. The muscle consisted mainly of polar lipid (84.3 ± 2.5% of total lipid) and a large proportion (52.6 ± 0.8%) of polyunsaturated FA. A dietary lipid level of 14% DM or less is recommended for juvenile haddock. [source] Combined intravitreal anti-vascular endothelial growth factor (Avastin®) and photodynamic therapy to treat retinal juxtapapillary capillary haemangiomaACTA OPHTHALMOLOGICA, Issue 5 2010Stefan Mennel Abstract. Objective:, Retinal capillary haemangioma complications are characterized by progressive exudation with consecutive intraretinal and subretinal leakage. A successful therapy without side-effects has not been found. We report a case of retinal juxtapapillary capillary haemangioma causing consecutive leakage with macular involvement. The tumour was treated with a combination of anti-vascular endothelial growth factor (VEGF) and photodynamic therapy (PDT) and was followed for 1 year. Methods:, A 44-year-old woman with retinal juxtapapillary capillary haemangioma in the right eye experienced a decrease of visual acuity from 20/20 to 20/60 because of a severe leakage from the tumour involving the macula with lipid depositions. Two sessions of PDT (sparing the part of the haemangioma located within the optic disc) and five injections of bevacizumab were applied in a period of 5 months. Visual acuity, visual field testing, retinal thickness measurements, fundus photography and fluorescein angiography were performed to evaluate the treatment effect. Results:, One year after the last injection, visual acuity increased to 20/40. All lipid exudates at the posterior pole resolved. Retinal thickness decreased from 490 to 150 ,m with the restoration of normal central macular architecture. Leakage in fluorescence angiography reduced significantly, but hyperfluorescence of the tumour was still evident. Visual field testing and angiography did not show any treatment-related vaso-occlusive side-effects. Conclusion:, In this single case, the combination of anti-VEGF and PDT appeared to be an effective strategy for the treatment of retinal juxtapapillary capillary haemangioma without side-effects. Further studies with a greater number of eyes and adequate follow-up are necessary to support these first clinical results. [source] | |||||||||||||