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Adipocyte lipolysis

Dl-R ligand ( 10),D2-R ligand (>10) (PA-R, O-R, PKC, TOPII) [AI, blocks COX-2 iNOS induction] Dl-R ligand (<10)(alA-R, a2A-R, 5HT1-R, O-R) [inhibits Epinephrine-induced adipocyte lipolysis]... [Pg.192]

Dl-R ligand (> 10) (a2A-R, PA-R, GPT, SU-R, O-R) [inhibits Epinephrine-induced adipocyte lipolysis]... [Pg.192]

GN-R agonist [antihypoglycaemic, gluconeogenesis, glycogenolysis, adipocyte lipolysis catabolic hyperglycaemic]... [Pg.222]

Brookes, 1. Andersson, and P. Arner, Evidence for an important role of perilipin in the regulation of human adipocyte lipolysis, Diabetologia, 2003, 46, 789-797. [Pg.329]

J.T. Tansey, C. Sztalryd, and J. Gruia Gray, et ah, Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity, Proc. Natl. [Pg.329]

Ketone body production and utilization. Ketone bodies are produced in the liver from fatty acids derived from adipocyte lipolysis. They are released and used as fuel in peripheral tissues. The initial step in acetoacetate metabolism is activation to acetoacetyl-CoA by succinyl-CoA. HMG-CoA, /S-hydroxy-y3-methylglutaryl-CoA HB, /i-hydroxybutyrate. [Pg.507]

Although fatty acids are avidly utilized by skeletal muscle during exercise, their plasma concentrations do not differ significantly from those at rest. Their utilization is being balanced by production from adipocyte lipolysis, probably as a result of an elevated catecholamine level. [Pg.518]

Neural NE and plasma E are both stimulators of adipocyte lipolysis, an effect that is mediated by )8,- and 63-adrenergic receptors and involves cAMP-mediated phosphorylation of hormone-sensitive lipase (HSL). There are regional differences in 3-adrenergic receptor density (visceral fat has more than subcutaneous fat), which determines that catecholamine is physiologically important. Note that receptors are low-affinity receptors that require high concentrations of catecholamines. They respond better to neural stimulation because of the higher local concentration of NE at the fat tissue site. [Pg.766]

The process of triacylglycerol hydrolysis is a complex phenomenon that involves at least three lipases, lipid droplet associated proteins, and FABPs, although other adipocyte lipases (i.e., triacylglycerol hydrolase) may play a role in basal lipolysis. The data at this time support the model that three lipases are the major contributors to adipocyte lipolysis. Complete hydrolysis of triacylglycerol involves the hydrolysis of three ester bonds to liberate three fatty acids and a glycerol moiety. ATGL catalyzes hydrolysis of the first... [Pg.288]

Additional information <2, 6> (<6> enzyme functions as a metabolic sensor that monitors cellular AMP and ATP levels [31] <2> phosphory-lates key target proteins that control flux through metabolic pathways of hepatic ketogenesis, cholesterol synthesis, adipocyte lipolysis and skeletal muscle fatty acid oxidation [30] <4> regulates triacylglycerolsynthesis and fatty acid oxidation in liver and muscle reciprocally [29]) [29-31]... [Pg.469]

The hypertriglyceridemia of Type II diabetes, unlike that which is found with Type I diabetes, is not due to excessive adipocyte lipolysis. This is because only a small level of insulin action is required to suppress excessive adipose tissue hormone-sensitive lipase activity. In Type II diabetes, there is insufficient adipose tissue lipoprotein lipase and excessive hepatic triglyceride synthesis. Thus, inefficient VLDL triglyceride catabolism and excessive VLDL triglyceride secretion both contribute to the excess VLDL in Type II diabetes. [Pg.92]

We have previously shown that in addition to its genotoxic properties, B[a]P can inhibit adipocyte lipolysis and contribute to the hypertrophy/hyperplasia of adipose tissue [2], and have consequently hypothesized that in humans, B[a]P can generate both obesity and cancer... [Pg.454]


See other pages where Adipocyte lipolysis is mentioned: [Pg.164]    [Pg.49]    [Pg.146]    [Pg.165]    [Pg.143]    [Pg.143]    [Pg.161]    [Pg.181]    [Pg.181]    [Pg.184]    [Pg.184]    [Pg.185]    [Pg.187]    [Pg.192]    [Pg.206]    [Pg.206]    [Pg.206]    [Pg.220]    [Pg.280]    [Pg.299]    [Pg.233]    [Pg.395]    [Pg.469]    [Pg.496]    [Pg.505]    [Pg.506]    [Pg.508]    [Pg.212]    [Pg.300]    [Pg.156]    [Pg.705]   
See also in sourсe #XX -- [ Pg.469 ]




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