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Lipogenic Enzymes (lipogenic + enzyme)
Selected AbstractsAntiadipogenic properties of retinol in primary cultured differentiating human adipocyte precursor cellsINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 2 2000Garcia Synopsis The aim of this study was to investigate the effect of retinol on the human adipose conversion process using primary cultured human adipocyte precursor cells. When these cells were seeded in a medium containing retinol (concentrations ranging from 3.5 nM to 3.5 ,M), cell proliferation was slightly inhibited by high concentrations of retinol, as demonstrated by cell counting and [3H]-thymidine incorporation. Moreover, the differentiation capacities of these cells were markedly and dose-dependently inhibited by retinol, as shown by the reduced expression of the lipogenic enzyme glycerol-3-phosphate dehydrogenase and by microscopic morphological analysis. These results strongly suggest that retinol, by inhibiting the ability of human preadipocytes to convert into mature adipocytes, could be of potential interest in the prevention of human adipose tissue development in general and of cellulitis in particular. Résumé Le but de ce travail est l'étude de l'effet du rétinol sur le processus d'adipoconversion chez l'homme en utilisant des cultures primaires de préadipocytes humains. Lorsque les cellules sont cultivées dans un milieu contenant du rétinol (de 3,5 nM à 3,5 ,M), la prolifération cellulaire est légèrement inhibée par de fortes concentrations de rétinol comme le démontrent le comptage cellulaire et l'incorporation de thymidine tritiée. De plus, les capacités de différenciation de ces cellules sont fortement diminuées par le rétinol de façon dose-dépendante comme le montrent l'analyse microscopique des cellules et l'expression réduite de la glycéro-3-phosphate déshydrogénase, enzyme lipogénique majeure. Ces résultats suggèrent que le rétinol, en inhibant la capacité d'adipoconversion des préadipocytes humains en adipocytes matures, pourrait avoir un intérêt potentiel dans la prévention du développement du tissu adipeux humain en général et de la cellulite en particulier. [source] Effect of Cogent db, a herbal drug, on serum and tissue lipid metabolism in experimental hyperglycaemic ratsDIABETES OBESITY & METABOLISM, Issue 3 2003G. Saravanan Aims:, We have previously reported the antidiabetic effect of Cogent db. The present study with alloxan-induced hyperglycaemic rats is focused on the mechanism of action, specifically on the activity of hepatic lipogenic enzymes, serum and tissue lipids. Methods:, Male Wistar rats body weight of 180,200 g (six normal and 18 diabetic rats) were used in this study. The rats were divided into four groups after the induction of alloxan diabetes: normal rats; diabetic control; diabetic rats given Cogent db (0.45 g/kg body weight); diabetic rats given glibenclamide (600 µg/kg body weight). After 40 days treatment, fasting blood glucose, plasma insulin, activities of hepatic lipogenic enzymes, serum and tissue lipids were determined in normal and experimental animals. Results:, Oral administration of Cogent db for 40 days resulted in significant reduction in blood glucose, serum and tissue (liver and kidney) lipids, whereas the level of plasma insulin and the activity of hepatic lipogenic enzymes were significantly increased in alloxan diabetic rats. Similar studies using glibenclamide have been conducted to compare the mode of action of these two drugs. Conclusions:, Thus our study shows that Cogent db exhibits a strong antihyperlipidaemic effect, which could exert a beneficial action against macrovascular complications (cardiovascular disease) associated with diabetes mellitus. [source] The influence of dietary linoleic and , -linolenic acid on body composition and the activities of key enzymes of hepatic lipogenesis and fatty acid oxidation in mice,JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 1-2 2007M. Javadi Summary We have recently suggested that feeding the C18 polyunsaturated fatty acid, , -linolenic acid (ALA), instead of linoleic acid (LA) reduced body fat in mice. However, the difference in body fat did not reach statistical significance, which prompted us to carry out this study using more animals and diets with higher contents of ALA and LA so that the contrast would be greater. The diets contained either 12% (w/w) LA and 3% ALA or 12% ALA and 4% LA. A low-fat diet was used as control. The diets were fed for 35 days. The proportion of body fat was not influenced by the type of dietary fatty acid. Plasma total cholesterol and phospholipids were significantly lower in ALA-fed mice than in mice fed LA. Activities of enzymes in the fatty acid oxidation pathway were significantly raised by these two diets when compared with the control diet. , -Linolenic acid vs. LA did not affect fatty acid oxidation enzymes. In mice fed the diet with LA activities of enzymes of de novo fatty acid synthesis were significantly decreased when compared with mice fed the control diet. , -Linolenic acid vs. LA feeding did not influence lipogenic enzymes. It is concluded that feeding mice for 35 days with diets either rich in LA or ALA did not significantly influence body composition. [source] S -Adenosylmethionine Attenuates Hepatic Lipid Synthesis in Micropigs Fed Ethanol With a Folate-Deficient DietALCOHOLISM, Issue 7 2007Farah Esfandiari Background: To demonstrate a causative role of abnormal methionine metabolism in the pathogenesis of alcoholic steatosis, we measured the effects on hepatic lipid synthesis of supplementing ethanol and folate-deficient diets with S -adenosylmethionine (SAM), a metabolite that regulates methionine metabolism. Methods: Yucatan micropigs were fed folate-deficient diets as control, with ethanol at 40% of kcal, and with ethanol supplemented with SAM at 0.4 g/1,000 kcal for 14 weeks. Histopathology, triglyceride levels and transcripts, and protein levels of the regulatory signals of hepatic lipid synthesis were measured in terminal omental adipose and liver samples. Results: Feeding ethanol at 40% of kcal with folate-deficient diets for 14 weeks increased and supplemental SAM maintained control levels of liver and plasma triglyceride. Serum adiponectin, liver transcripts of adiponectin receptor-1 (AdipoR1), and phosphorylated adenosine monophosphate kinase- , (p-AMPK,) were each reduced by ethanol feeding and were sustained at normal levels by SAM supplementation of the ethanol diets. Ethanol feeding activated and SAM supplementation maintained control levels of ER stress-induced transcription factor sterol regulatory element-binding protein-1c (SREBP-1c) and its targeted transcripts of lipid synthesizing enzymes acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and glycerol-3-phosphate acyltransferase (GPAT). Conclusions: Ethanol feeding with a folate-deficient diet stimulates hepatic lipid synthesis by down-regulating adiponectin-mediated pathways of p-AMPK to increase the expression of nSREBP-1c and its targeted lipogenic enzymes. Preventing abnormal hepatic methionine metabolism by supplementing ethanol diets with SAM reduces liver triglyceride levels by up-regulation of adiponectin-mediated pathways to decrease fatty acid and triglyceride synthesis. This study demonstrates that ethanol-induced hepatic lipid synthesis is mediated in part by abnormal methionine metabolism, and strengthens the concept that altered methionine metabolism plays an integral role in the pathogenesis of steatosis. [source] EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cellsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 9 2009Chi-Hung Huang Abstract In the previous studies, (,)-epigallocatechin-3-gallate (EGCG) has been shown to have anticarcinogenic effects via modulation in protein expression of p53. Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation. Caloric restriction (CR) reduces the incidence and progression of spontaneous and induced tumors in laboratory rodents. EGCG has multiple beneficial activities similar to those associated with CR. One key enzyme thought to be activated during CR is AMP-activated kinase (AMPK), a sensor of cellular energy levels. Here, we showed that EGCG activated AMPK in both p53 positive and negative human hepatoma cells. The activation of AMPK suppressed downstream substrates, such as mammalian target of rapamycin (mTOR) and eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) and a general decrease in mRNA translation. Moreover, EGCG activated AMPK decreases the activity and/or expression of lipogenic enzymes, such as fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC). Interestingly, the decision between apoptosis and growth arrest following AMPK activation is greatly influenced by p53 status. In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression. However, EGCG inducted apoptosis in p53 negative Hep 3B cells. Based on these results, we have demonstrated that EGCG has a potential to be a chemoprevention and anti-lipogenesis agent for human hepatoma cells. [source] Activities of glucose phosphorylation, glucose-6-phosphatase and lipogenic enzymes in the liver of perch, Perca fluviatilis, after different dietary treatmentAQUACULTURE RESEARCH, Issue 2001B Borrebaek Abstract Glucose phosphorylation was increased and the activity of glucose-6-phosphatase was decreased in the liver of perch Perca fluviatilis after feeding previously fasted fish with a high protein/low carbohydrate diet as well as with a diet containing 23% carbohydrate. Activity of the low affinity hexokinase IV (or D), also called glucokinase (GK), was not observed in the liver of perch on the natural diet, fasted perch or perch after feeding with the high protein/low-carbohydrate diet (< 0.2% CHO). How ever, hepatic GK-activity appeared after feeding with the carbohydrate containing diet. By contrast, the activity of hepatic high affinity hexokinase (HK), which was very low in fasted fish, was strongly increased after feeding with the low-carbohydrate as well as the carbohydrate-containing diet. Apparently, HK rather than GK is the hexokinase isoenzyme that is consistently regulated inversely to glucose-6-phosphatase. Activities of the lipogenic enzymes glucose-6-phosphate dehydrogenase, ATP-citrate lyase and malic enzyme were increased by feeding, particularly with the high protein/low carbohydrate diet. Very high levels of hepatic glycogen were observed after both diets. The results are in accordance with the hypothesis that the hepatic high affinity isoenzyme (HK) has a particular anabolic role. [source] | |||||||||||||