Effect of lipase specificity on triglyceride synthesis

1991 ◽  
Vol 13 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Fran�oise Ergan ◽  
Michael Trani
Keyword(s):  
Triglyceride Synthesis ◽  
Lipase Specificity

Pengaruh Pemberian Ekstrak Jambu Biji (Psidium Guajava) Terhadap Kadar Trigliserida Darah Tikus Putih (Rattus Norvegicus) Jantan Galur Wistar Yang Diinduksi Deksametason

2018 ◽  
Vol 16 (1) ◽  
pp. 81
Author(s):  
MARIA EVANE NAVY CAHAYA PUTRI ◽  
NITA PRANITASARI
Keyword(s):  
Plasma Level ◽  
Triglyceride Level ◽  
Rattus Norvegicus ◽  
Food Group ◽  
Psidium Guajava ◽  
Triglyceride Synthesis ◽  
Flavonoid Quercetin

<p><strong>Abstract</strong></p><p> </p><p>Dexamethasone induction may result in increased of both triglyceride synthesis and VLDL plasma level, which contribute to the increase in triglyceride level. Guava (<em>Psidium guajava)</em> consists flavonoid (quercetin) compounds that can inhibit triglyceride synthesis and decrease blood triglyceride level.</p><p><strong>Methode</strong></p><p>This research used 24 rats divided into 3 groups: group of rats fed with standard food, group of rats induced by 0.13 mg/kgBW dexamethasone for 14 days starting from day 8, and group of rats induced by 0.13 mg/kgBW dexamethasone for 14 days starting from day 8 and received 3 gr/kgBW guava extract for 21 days. On day 22, blood triglyceride level was measured with glycerol blanking method.</p><p><strong>Result</strong></p><p>The result of <em>Mann-Whitney U</em> showed that blood triglyceride level of group of rats induced by dexamethasone (=198.25±55.296 mg/dl) was significantly higher (p=0.001) than group of rats fed with standard food (=68.50±16.062 mg/dl). Blood triglyceride level of group of rats induced by dexamethasone and received guava extract (=98.75±26.778 mg/dl) did not significantly decreased (p=0.487) compared to group of rats induced by dexamethasone (=198.25±55.296 mg/dl).</p><p><strong>C</strong><strong>onclusion</strong></p><p>The conclusion of this research showed that dexamethasone significantly increased blood triglyceride level and guava extract tend to decrease blood triglyceride level because guava consists flavonoid (quercetin) compounds.</p><p><strong> </strong></p><p><strong>Keywords</strong>: <em>Psidium guajava, triglyceride</em>, <em>dexamethasone</em><em></em></p>

scholarly journals Large increases in adipose triacylglycerol flux in Cushingoid CRH-Tg mice are explained by futile cycling

2013 ◽  
Vol 304 (3) ◽  
pp. E282-E293 ◽  
Author(s):  
Charles Harris ◽  
Donald J. Roohk ◽  
Mark Fitch ◽  
Benjamin M. Boudignon ◽  
Bernard P. Halloran ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Collagen Synthesis ◽  
Muscle Protein ◽  
Subcutaneous Fat ◽  
Skin Thickness ◽  
Breakdown Rate ◽  
Triglyceride Synthesis ◽  
Fat Depots ◽  
Breakdown Rates ◽  
Skin Collagen

Glucocorticoids are extremely effective anti-inflammatory therapies, but their clinical use is limited due to severe side effects, including osteoporosis, muscle wasting, fat redistribution, and skin thinning. Here we use heavy water labeling and mass spectrometry to measure fluxes through metabolic pathways impacted by glucocorticoids. We combine these methods with measurements of body composition in corticotropin-releasing hormone (CRH)-transgenic (Tg)+ mice that have chronically elevated, endogenously produced corticosterone and a phenotype that closely mimics Cushing's disease in humans. CRH-Tg+ mice had increased adipose mass, adipose triglyceride synthesis, and greatly increased triglyceride/fatty acid cycling in subcutaneous and abdominal fat depots and increased de novo lipogenesis in the abdominal depot. In bone, CRH-Tg+ mice had decreased bone mass, absolute collagen synthesis rates, and collagen breakdown rate. In skin, CRH-Tg+ mice had decreased skin thickness and absolute collagen synthesis rates but no decrease in the collagen breakdown rate. In muscle, CRH-Tg+ mice had decreased muscle mass and absolute protein synthesis but no decrease in the protein breakdown rate. We conclude that chronic exposure to endogenous glucocorticoid excess in mice is associated with ongoing decreases in bone collagen, skin collagen, and muscle protein synthesis without compensatory reduction (coupling) of breakdown rates in skin and muscle. Both of these actions contribute to reduced protein pool sizes. We also conclude that increased cycling between triglycerides and free fatty acids occurs in both abdominal and subcutaneous fat depots in CRH-Tg+ mice. CRH-Tg mice have both increased lipolysis and increased triglyceride synthesis in adipose tissue.

Liver X receptor α participates in LPS-induced reduction of triglyceride synthesis in bovine mammary epithelial cells

2020 ◽  
pp. 1-7
Author(s):  
Jianfa Wang ◽  
Shuai Lian ◽  
Jun Song ◽  
Hai Wang ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Dairy Cow ◽  
Milk Fat ◽  
Mammary Epithelial Cells ◽  
Liver X Receptor ◽  
Mammary Epithelial ◽  
Triglyceride Synthesis ◽  
Milk Fat Depression ◽  
Liver X Receptor Α

Abstract Lipopolysaccharides (LPS) could induce milk fat depression via regulating the body and blood fat metabolism. However, it is not completely clear how LPS might regulate triglyceride synthesis in dairy cow mammary epithelial cells (DCMECs). DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS. The level of triglyceride synthesis, the expression and activity of the liver X receptor α (LXRα), enzymes related to de novo fatty acid synthesis, and the expression of the fatty acid transporters were investigated. We found that LPS decreased the level of triglyceride synthesis via a down-regulation of the transcription, translation, and nuclear translocation level of the LXRα. The results also indicated that the transcription level of the LXRα target genes, sterol regulatory element binding protein 1 (SREBP1), fatty acid synthetase (FAS), acetyl-CoA carboxylase-1 (ACC1), were significantly down-regulated in DCMECs after LPS treatment. Our data may provide new insight into the mechanisms of milk fat depression caused by LPS.

scholarly journals Insulin-independent regulation of hepatic triglyceride synthesis by fatty acids

2015 ◽  
Vol 112 (4) ◽  
pp. 1143-1148 ◽  
Author(s):  
Daniel F. Vatner ◽  
Sachin K. Majumdar ◽  
Naoki Kumashiro ◽  
Max C. Petersen ◽  
Yasmeen Rahimi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Insulin Signaling ◽  
Plasma Fatty Acid ◽  
Hepatic Triglyceride ◽  
Triglyceride Synthesis ◽  
Hepatic Glucose ◽  
Acid Esterification ◽  
Fatty Acid Esterification

A central paradox in type 2 diabetes is the apparent selective nature of hepatic insulin resistance—wherein insulin fails to suppress hepatic glucose production yet continues to stimulate lipogenesis, resulting in hyperglycemia, hyperlipidemia, and hepatic steatosis. Although efforts to explain this have focused on finding a branch point in insulin signaling where hepatic glucose and lipid metabolism diverge, we hypothesized that hepatic triglyceride synthesis could be driven by substrate, independent of changes in hepatic insulin signaling. We tested this hypothesis in rats by infusing [U-13C] palmitate to measure rates of fatty acid esterification into hepatic triglyceride while varying plasma fatty acid and insulin concentrations independently. These experiments were performed in normal rats, high fat-fed insulin-resistant rats, and insulin receptor 2′-O-methoxyethyl chimeric antisense oligonucleotide-treated rats. Rates of fatty acid esterification into hepatic triglyceride were found to be dependent on plasma fatty acid infusion rates, independent of changes in plasma insulin concentrations and independent of hepatocellular insulin signaling. Taken together, these results obviate a paradox of selective insulin resistance, because the major source of hepatic lipid synthesis, esterification of preformed fatty acids, is primarily dependent on substrate delivery and largely independent of hepatic insulin action.

Reassessing triglyceride synthesis in adipose tissue

2008 ◽  
Vol 19 (10) ◽  
pp. 356-361 ◽  
Author(s):  
Colleen Nye ◽  
Jaeyeon Kim ◽  
Satish C. Kalhan ◽  
Richard W. Hanson
Keyword(s):  
Adipose Tissue ◽  
Triglyceride Synthesis

Effect of carbohydrate intake on de novo lipogenesis in human adipose tissue

1987 ◽  
Vol 253 (6) ◽  
pp. E664-E669 ◽  
Author(s):  
C. Chascione ◽  
D. H. Elwyn ◽  
M. Davila ◽  
K. M. Gil ◽  
J. Askanazi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
De Novo ◽  
Acid Synthesis ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
High Intake ◽  
Carbohydrate Diet ◽  
Triglyceride Synthesis ◽  
High Carbohydrate

Rates of synthesis, from [14C]glucose, of fatty acids (de novo lipogenesis) and glycerol (triglyceride synthesis) were measured in biopsies of adipose tissue from nutritionally depleted patients given low- or high-carbohydrate intravenous nutrition. Simultaneously, energy expenditure and whole-body lipogenesis were measured by indirect calorimetry. Rates of whole-body lipogenesis were zero on the low-carbohydrate diet and averaged 1.6 g.kg-1.day-1 on the high-carbohydrate diet. In vitro rates of triglyceride synthesis increased 3-fold going from the low to the high intake; rates of fatty acid synthesis increased approximately 80-fold. In vitro, lipogenesis accounted for less than 0.1% of triglyceride synthesis on the low intake and 4% on the high intake. On the high-carbohydrate intake, in vitro rates of triglyceride synthesis accounted for 61% of the rates of unidirectional triglyceride synthesis measured by indirect calorimetry. In vitro rates of lipogenesis accounted for 7% of whole-body lipogenesis. Discrepancies between in vitro rates of fatty acid synthesis from glucose, compared with acetate and citrate, as reported by others, suggest that in depleted patients on hypercaloric high-carbohydrate diets, adipose tissue may account for up to 40% of whole-body lipogenesis.

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