Kristin Miller Caleb Conrad 13.9 What Are Steroids.

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Presentation transcript:

Kristin Miller Caleb Conrad 13.9 What Are Steroids

Steroids 3 rd major class of lipids Contains the following ring system:

Cholesterol The most abundant steroid in the human body Purpose Plasma membrane component Red blood cells Raw material for synthesis of other steroids Sex, adrenocorticoid hormones and bile salts Exists free form and esterified fatty acids Gall stones contain free cholesterol Many think it’s a bad thing Correlation with high serum cholesterol levels Necessary to human life Liver manufactures enough for our daily needs

Constantly circulates in blood It’s hydrophobic Needs water soluble carrier to circulate in aqueous medium of blood

Lipoproteins: Carriers of cholesterol Contain core of hydrophobic lipid molecules surrounded by a shell of hydrophobic molecules Four kinds of lipid proteins High- density (“good cholesterol”) 33% protein 30% cholesterol Low- density (“bad cholesterol”) 25% protein 50% cholesterol Very-low-density Comes from triglycerides synthesized by the liver Chylomicrons Carry dietary lipids synthesized in intestines

Transport of cholesterol To liver Starts as large VLDL particles (55 nanometers in diameter) Core contains triglycerides and cholesteryl esters Surrounded by polar coat phospholipids and proteins Reaches muscle or fat tissue Triglycerides and proteins are removed from VLDL (aPOB-100 isn’t) Lipoprotein shrinks 22 nanometers Contains only cholesteryl esters Fat is removed, becomes more dense, turns into LDL LDL Stays in plasma for about 2.5 days

LDL Carries cholesterol to cells Concentrated areas called coated pits aPOB- 100 protein Binds to LDL receptor molecules LDL taken inside of cell Enzymes break down into lipoproteins During the process Free cholesterol liberated from cholesteryl esters Cell can then tell if it’s a component of a membrane No enough LDL receptors? Cholesterol accumulates in blood

Transport of cholesterol in HDL Cholesterol from peripheral tissues to liver Transfer cholesterol to LDL In serum, free cholesterol in HDL convert to cholestryl esters Delivered to liver for synthesis of bile, acids, and steroid hormones Does not involve endocytosis & degradation of lipoproteins Selective lipid uptake HCL binds to liver cell surface & transfers cholestryl ester to cell HDL depleted from lipid content Reenters circulation Bodies with high HDL Remove cholesterol from blood stream

Levels of LDL and HDL Cholesterol = insoluble in water If elevated in blood stream Plaque deposits form in arteries Decreases blood flow Leads to high blood pressure which leads to Heart attack, stroke, kidney failure Clot arteries = less oxygen Mayocardio infraction

Most cholesterol is transferred by LDL’s A lot of LDL receptors = cholesterol easily removed from body Synthesis of LDL’s goes up, LDL receptors are surpressed Causes LDL concentration in plasma to rise Not enough LDL receptors Familial hypercholesterolemia Plasma is 680 mg/100 mL compared to 175 mg/100 mL Can cause atherosclerosis and heart attack High LDL = low HDL Results in atherosclerosis

High serum cholesterol Synthesis is low Synthesis inhibitors Diets low in cholesterol and saturated fatty acids Prescription drugs Zocor, Lipitor, Block biocatalysts in cholesterol synthesis What do you want in your body? High HDL Carry plaque out of arteries to liver Increased with exercise and weight loss Low LDL