1. - Storage of energy - Building blocks are fatty acids and glycerol
2. Main Type of Lipids
2.1. Triglycerides
2.1.1. are fats from the food we eat that are carried in the blood. Most of the fats we eat are in triglyceride form. Extra calories, alcohol and sugar in the body turn into triglycerides and are stored in fat cells throughout the body.
2.2. Phospholipids
2.2.1. amphiphilic molecules with hydrophobic fatty acid chains and hydrophilic moieties. They occur naturally in all living organisms as the major components of cell membranes. Various phospholipid classes with different polar moieties are found in nature.
2.3. Steroids and waxes
2.3.1. •mixtures of fatty acid (long chain of alcohol esters) • the acids usually have an even number of carbons from 16 through 36, while the alcohols have an even number of carbons from 24 to 36
2.3.2. • Beeswax • Waxy protective coatings on most fruits, berries, leaves and animal furs
3. Energy
3.1. Fats are an important source of calories. Typically 30-40% of calories in diet are from fat. Fat is the major form of energy storage.
3.2. Body fuel reserves: - fat: 100,000 kcal. - protein: 25,000 kcal. - carbohydrate: 650 kcal. - ATP: 7,300kcal
4. Ketone Bodies
4.1. ALTERNATE FUEL FOR CELLS
4.1.1. • During a fast, the liver is flooded with fatty acids mobilized from adipose tissue.
4.1.2. • The resulting elevated hepatic acetyl CoA produced primarily by fatty acid degradation inhibits pyruvate dehydrogenase and activates pyruvate carboxylase.
4.1.3. • The OAA thus produced is used by the liver for gluconeogenesis rather than for the TCA cycle. Therefore, acetyl CoA is channeled into. ketone body synthesis.
4.2. • Ketone bodies are produced by the liver and used peripherally as an energy source when glucose is not readily available.
4.3. • The two main ketone bodies are acetoacetate (AcAc) and 3-beta-hydroxybutyrate (3HB), while acetone is the third, and least abundant, ketone body.
4.4. • Ketones are always present in the blood and their levels increase during fasting and prolonged exercise.
4.5. • They are also found in the blood of neonates and pregnant women.
4.6. • Diabetes is the most common pathological cause of elevated blood ketones.
5. Classification of Lipids
5.1. Fats
5.1.1. • Solid at room temperature • Found in animals (cow and goat) • Melting point is more than 20˚C
5.1.2. Hydrogenated fats
5.1.2.1. • Hydrogenation leads to either saturated fats and or trans fatty acids • The purpose of hydrogenation is to make the oil/fat more stable to oxygen and temperature variation (increase shelf life)
5.1.2.2. example of hydrogenated fats: Crisco, margarine
5.2. Oils
5.2.1. • Oil at room temperature • Found in plants (olive, palm, peanuts) • Melting point is less than 20˚C
5.3. Fats are solids or semi solids • Oils are liquids • Melting points and boiling points are not usually sharp (most fats/oils are mixtures) • When shaken with water, oils tend to emulsify • Pure fats and oils are colorless and odorless (color and odor is always a result of contaminants) – i.e. butter (microbes give flavor, carotene gives color)
6. - large and diverse group of naturally occurring organic compounds - solubility in non-polar organic solvents - general insolubility in water
7. Composed of carbon, hydrogen and oxygen with definite ratio, the number of oxygen atoms is very much less compared to hydrogen atoms
8. Digestion and absorption
8.1. Digestion in the Mouth: enzymes are aqueous -little effect on lipids
8.1.1. Digestion of fat begins in the mouth where lingual lipase breaks down the short chain lipids in to diglycerides
8.2. Digestion in the Stomach: causes a large physical change: -Churned into droplets: “Chyme”
8.2.1. Fats are mainly broken down in the small intestine , when fat is presented there the intestines produce hormone that stimulate the release of pancreatic lipase from the pancreas and ( bile acid from the liver
9. TYPES
9.1. Simple Lipids
9.1.1. Ester of fatty acids
9.1.1.1. Fats
9.1.1.1.1. Esters of fatty acids and glycerol
9.1.1.2. Waxes
9.1.1.2.1. Esters of long chain fatty acids and long chain alcohols
9.2. Compound Lipids
9.2.1. Ester of fatty acids and alcohol contain other groups also
9.2.2. SPHINGOLIPIDS
9.2.2.1. substances that yield an unsaturated amino alcohol (spingosine), a long fatty acid, and either a carbohydrate or phosphate and a nitrogen base
9.2.3. GLYCOLIPIDS
9.2.3.1. substances that yield spingosine, a fatty acid and a carbohydrate upon hydrolysis
9.3. Derived Lipids
9.3.1. Composed of hydrocarbon rings and a long hydrocarbon side chain
9.3.2. STERIODS
9.3.2.1. • Substances that possess the steriod nucleus, which is a 17-carbon structure consisting of four fused carbocyclic rings
9.3.2.2. • Cholesterol and Hormones like Estrogen, Progesterone
9.3.3. MISCELLANEOUS LIPIDS
9.3.3.1. • Substances that do not fit into the preceding classifications
9.3.3.2. • Includes: fat – soluble vitamins A, D, E, and K and lipoproteins
10. Lipid Storage Diseases
10.1. • Tay Sachs disease
10.1.1. • a fatal disease which is due to the deficiency of hexosaminidase activity
10.1.2. • accumulation of ganglioside GM2 in the brain of infants
10.1.3. • Rapid and progressive neurodegeneration, blindness, inability to swallow, muscular weakness
10.1.4. • a “cherry red “ spot develops on the macula (back of the the eyes) and seizures
10.1.5. • Tay-Sachs children usually die by age 5 and often sooner
10.2. • Gaucher’s disease
10.2.1. • Also known as globoid cell leukodystrophy
10.2.2. • Increased amount of galactocerebroside (glycolipid – laden macrophages) in the white matter of the brain
10.2.3. • Mental and motor deterioration, blindness and deafness, near-total loss of myelin
10.2.4. • Caused by a deficiency in the lysosomal enzyme galactocerebrosidase
10.3. • Niemann-Pick disease
10.3.1. • principal storage substance: sphingomyelin which accumulates in reticuloendothelial cells
10.3.2. • enzyme deficiency: sphingomyelinase
10.3.3. • liver and spleen enlargement, neurodegenerative course (mental retardation)
10.4. • Fabry’s disease
10.4.1. Accumulation of ceramide trihexoside in kidneys of patients who are deficient in lysosomal agalactosidase A
10.4.2. Now treated with enzyme replacement therapy: agalsidase beta (Fabrazyme)
10.4.3. • sometimes referred to as ceramide trihexosidase
10.4.4. • Globosides accumulate in the vascular endothelial lysosomes of the brain, heart, kidneys and skin
10.4.5. • Reddish-purple skin rash, kidney and heart failure, burning pains in the lower extremities