Hormones Signal fromAdipose TissueAdipose celludemhlaCAMIThe hormone molecules bind to receptors on theplasma membrane of adipose cells and lead to theactivation of adenylyl cyclase to cAMPTriagtghueraTriacytchyeerolipase(active)MC
Hormones Signal from Adipose Tissue The hormone molecules bind to receptors on the plasma membrane of adipose cells and lead to the activation of adenylyl cyclase to cAMP
Hormones Signal from Adipose Tissue cAMP activates protein kinase A, whichphosphorylates and activates a triacylglycerollipase (TAG lipase). The TAG lipase hydrolyzes a fatty acid from C-1 orC-3 of triacylglycerols.Traleher Subsequent actions of diacylglycerol lipase andmonoacylglycerol lipase yield fatty acids andglycerol. The cell then releases the fatty acids into the blood,where they are bound to serum albumin. Serumalbumin transports free fatty acids to sites ofutilization
Hormones Signal from Adipose Tissue cAMP activates protein kinase A, which phosphorylates and activates a triacylglycerol lipase (TAG lipase). The TAG lipase hydrolyzes a fatty acid from C-1 or C-3 of triacylglycerols. Subsequent actions of diacylglycerol lipase and monoacylglycerol lipase yield fatty acids and glycerol. The cell then releases the fatty acids into the blood, where they are bound to serum albumin. Serum albumin transports free fatty acids to sites of utilization
DegradationofDietaryFattyAcids Dietary TAGs are degraded by stomach lipasespancreatic lipase and nonspecific esterases instomachand duodenum respectively The FAs pass into the epithelial cells, wherethey are condensed with glycerol to form newTAGs. These TAGs aggregate with lipoproteins toform particles and are then transported to theother organs. At these sites, the TAGs arehydrolyzed to release FAs, which can beoxidized in a highly exergonic metabolicpathway./eksa'gpnrk/放能的
Degradation of Dietary Fatty Acids Dietary TAGs are degraded by stomach lipases, pancreatic lipase and nonspecific esterases in stomach and duodenum respectively. The FAs pass into the epithelial cells, where they are condensed with glycerol to form new TAGs. These TAGs aggregate with lipoproteins to form particles and are then transported to the other organs. At these sites, the TAGs are hydrolyzed to release FAs, which can be oxidized in a highly exergonic metabolic pathway. /ˌeksəˈgɒnɪk/放能的
Disease of Lipid metabolismAtherosclertosisAthero =pasteSclerosis=hardness A slow progressive disease Characterized by hardening of thearteries due to lipid accumulation inblood vessel wallsFIGURE17.1Anatheroscleroticplaquein an artery.Note thethickening of thevessel wall. [James Cavallini/BSIP/Phototake.]
Disease of Lipid metabolism Atherosclertosis Athero = paste Sclerosis = hardness A slow progressive disease Characterized by hardening of the arteries due to lipid accumulation in blood vessel walls
口Atherosclertosis50% of all deaths in U.S. linked to this vascular disease Inflammation initiated and perpetuated by leukocytes (white blood cells) Plaque forms, containing cholesterol, dead macrophages, and calcifiedmuscle. Rupture of plaque releases blood clot Heart attack - disruption of circulation to heart Stroke-disruption of circulation to brainLipids deposited bylipoproteins
Atherosclertosis 50% of all deaths in U.S. linked to this vascular disease Inflammation initiated and perpetuated by leukocytes (white blood cells) Plaque forms, containing cholesterol, dead macrophages, and calcified muscle. Rupture of plaque releases blood clot Heart attack – disruption of circulation to heart Stroke – disruption of circulation to brain Lipids deposited by lipoproteins