lipids, lipid membranes; lipid metabolism and transport Flashcards
(32 cards)
what are lipids?
Lipids are fats, waxes, and similar molecules that do not dissolve well in water.
what are fatty acids composed of
Fats are composed of glycerol and fatty acids. Glycerol always has three carbon atoms and three hydroxyl (OH) groups, but there are several dozen kinds of fatty acids, ranging in size from 4 carbon atoms to 24. On one end of a fatty acid we find a carbon atom with a double bond to an oxygen atom and a single bond to a hydroxyl group. This entire group of four atoms, often written as COOH, is called a carboxyl group and is able to ionize to release a hydrogen ion into solution, thus acting as an acid. (The ionized carboxyl group is symbolized as COO-.)
what are the acidic properties of fatty acids?
the carboxyl group at the end of a fatty acid is able to ionize and release a hydrogen ion into solution, thus acting as an acid. (The ionized carboxyl group is symbolized as COO-.). In any group of such molecules, only a few are ionized at any one time, so fatty acids are all weak acids. All the rest of a fatty acid molecule is pure hydro- carbon (hydrogen and carbon). Fatty acids are designated as saturated or unsaturated according to whether they are filled to capacity with hydrogen atoms or not.
how are the carbon atoms in saturated fatty acids bonded?
In a saturated fatty acid, all of the carbon atoms are joined to one another by single bonds, and each one (other than the carboxyl carbon) is bonded to at least two hydrogen atoms. (The one on the end has three.) In an unsaturated fatty acid, at least one pair of carbon atoms is joined by a double bond, so that each of those carbon atoms is bonded to only one hydrogen atom, leaving the fatty acid with at least two fewer hydrogen atoms than it would have if it were saturated. The double bond often throws a kink in the hydrocarbon chain as shown in the space-filling model here.
what is a triglyceride and what is its structure?
A fat–chemically known as a triglyceride–consists of a molecule of glycerol joined to three fatty acid molecules by the same kind of dehydration condensation we saw in the formation of disaccharides and polysaccha- rides. The three fatty acids may be all the same or any combination of different ones.
what is a monounsaturated fatty acid?
if two of the fatty acids are saturated and one is unsaturated. This would be called a monounsaturated fat, because it is unsaturated (has a carbon double bond) at only one point in the entire triglyceride molecule. If it were unsaturated at two or more points, it would be called a polyunsaturated fat.
why are triglycerides non-polar?
Since hydrocarbons are nonpolar the entire triglyceride molecule is nonpolar except for a slight polarity around the oxygen atoms. For this reason, triglycerides (fats) are not attracted much to water molecules. If you have ever tried to wash butter or other animal fat off of your hands with just water, you will have noticed that.
what are phospholipids?
In molecular structure phospholipids are like triglycerides except that in place of the third fatty acid they have a phosphate group and some other polar group. This results in a molecule with a dual nature. The hydrocarbon chains of the fatty acids are not attracted to water and are called hydrophobic (water-fearing”). The phosphate and the other group are attracted to water and are called hydrophilic (water-loving”). It is precisely this dual nature that allows phospholipids to form membranes.
what is the structure of a steroid nucleus?
The steroid nucleus consists of four interlocking rings of carbon atoms with numerous hydrogen atoms attached It forms the core of a wide variety of important molecules including many hormones, which differ in the groups of atoms substituted for the hydrogen atoms at various points on the rings
why are waxes important for plants?
Waxes provide protective coatings for various plant and animal tissues and for bees to make honeycombs. They are formed by the dehydration condensation of a long-chain alcohol (hydrocarbon with a hydroxyl group at one end) and a long-chain fatty acid. Other, less common lipids (not illustrated) combine) fatty acids with various other groups, such as sugars and amino acids.
how are Body fats divided into fuel & what are their differing structural types
Fuel fats are stored in fat depots of the adipose tissue, which consists of fat cells with large cytoplasmic stores of fat. Adipose tissue is active, continuously forming and degrading fats, It occurs in the abdominal cavity, within or around organs (muscle, heart), and under the skin. The subcutaneous fat helps in thermal insulation. Brown fat is a form of subcutaneous fat with many mitochondria that liberate mainly heat (not ATP) upon oxidation, to protect the body against cold temperatures. Brown fat location, structure, and physiology are discussed in plates 140 and 141. Structural fats (phospholipids, cholesterol) are not utilized for energy; phospholipids occur in cell membranes, and cholesterol functions in synthesis of steroid hormones, vitamin D and neural myelin tissue
basic chemistry of fats
Triglycerides (TG, triacylglycerols, neutral fats) are the storage fats (fat depots). They are esters of glycerol and three fatty acids (FA). FA are long hydrocarbon chains with a single carboxylic acid group at one end. The longer the chain and the smaller the number of double bonds, the lower the fluidity state of the FA and the associated TG. The most commonly occurring body FA are palmitic, stearic, and oleic acids with chains between 14 and 16 carbon atoms long. TG are broken down either completely to glycerol and FA or incompletely to FA and mono- or diglycerides. The breakdown of TG (lipolysis) is catalyzed by various lipase enzymes in the intestine, liver, and adipose tissue.
fats as an energy source
Fats take small space & liberate much energy- Fats are ideal for fuel storage because per unit weight they occupy less volume and produce more energy (ATP) than carbohydrates or proteins. When oxidated, 1 g of fat produces 9.3 kcalories- 2.3 times more than 1 g of carbohydrate or protein. Some tissues easily utilize FA for energy; 60% of the heart’s basal energy requirement is derived from fats, chiefly FA. Skeletal muscle also utilizes FA to obtain energy –especially during recovery from strenuous exercise – to replenish the exhausted supply of ATP, creatine phosphate, and glycogen (plate 27).
FA undergo ß-oxidation to form ATP or for conversion to amino acids –To liberate their energy, the FA are degraded to acetate (acetyl CoA) by a process called ß-oxidation. The acetyl CoA is then oxidized to CO2 and H20 in the mitochondria to produce ATP
Glycerol can be oxidized through glycolysis or used to form glucose–Both of the products of triglyceride lipolysis- glycerol and FA–can be utilized for energy production. Glycerol can be converted to intermediates of glycolysis and then to pyruvate, which then enters the Krebs cycle to form ATP (plate 6). Alternatively, glycerol can be converted to glucose in the liver (gluconeogenesis); glucose is used by tissues such as the brain for fuel
fat metabolism in adipose tissue
Glycerol and FA are esterified to make storage fats (lipogenesis)- After a carbohydrate meal, the adipose tissue fat cells, stimulated by insulin, take up the abundant plasma glucose and convert it to glycerol and FA. The glycerol (alcohol) and FA (acids) are then esterified to form TG (lipogenesis). Fatty meals increase the blood chylomicrons -very large size lipoprotein particles transporting the absorbed TG and cholesterol in the blood. Within the capillaries of adipose tissue and liver, an enzyme called lipoprotein lipase hydrolyzes the glycerides, freeing glycerol and FA. These are taken up by fat cells and re-esterified to form storage TG. TG with
sufficiently long chains tend to solidify and are therefore easily stored. Increased storage of solid fats in the cytoplasm increases the size of fat cells, which accumulate in the thick fat pads of the adipose tissue. If excessive, this condition leads to obesity
Lipase enzymes degrade stored fats to glycerol and FA (lipolysis)
When stimulated by catecholamines and other hormones, the TG are lipolyzed by lipase enzymes, mobilizing the glycerol and FA into the blood. The mobilized FA are then used by the heart, muscles, and liver for energy. Glycerol is usually taken up by the liver to make new glucose.
FAT METABOLISM IN THE LIVER
Liver can convert fats into proteins & glucose and vice versa
The liver, like the adipose tissue, is capable of forming, degrading, and storing fats, although the fat granules in the liver hepatocytes are not intended for long-term storage. The particular importance of the liver lies in its capability for metabolic interconversion between fats, carbohydrates, and proteins. The liver hepatocytes contain all the enzymes required for these chemical transformations. For example, excess glucose can be metabolized into fatty acids, which are then either incorporated into TG or mobilized for consumption by tissues. Glycerol can be converted to glucose by reverse glycolysis and then to glycogen, FA can be converted to some amino acids and vice versa. These amino acids can then make proteins. The only reaction that the liver, and animal cells in general, cannot do in this regard is convert FA into glucose.
Liver can form cholesterol & ketone bodies
A major liver role in fat metabolism is to make cholesterol and ketone bodies. Cholesterol metabolism is detailed in plate 135. When carbohydrates are low in the diet or in cells (as in diabetes), the liver degrades FA to acetate (acety] CoA). When the available pool of acetyl CoA exceeds the loading capacity of the mitochondria, the acetate molecules are instead condensed together to form compounds such as acetoacetic acıd, acetone, and other keto acids, collectively called ketone bodies. Ketone bodies leak out from the liver into the blood, where they are excreted ìn the kidneys. Excessive amounts of ketone bodies in blood lead to ketosis and metabolic acidosis, conditions that may be fatal, such as untreated insulin-deficiency diabetes (Type I).
Ketones are normally excreted but may be used as fuel in certain conditions
In normal adults, ketone bodies are little utilized for energy. However, in newborns, pregnant women, and individuals subjected to prolonged starvation, many tissues, particularly the brain, undergo metabolic adaptation, increasing their rate of uptake and utilization of the ketone bodies for energy. This ability accounts not only for the continued function of the brain (an organ that usually uses only glucose) in starvation, but also for the lack of ketone toxicity in children and starved individuals.
Cholesterol has many functions but is not a fuel
CholesteroÌ is a structural fat of animal origin. It is a sterol syn- thesized from acetate, mainly in the liver; the adrenal cortex and gonads also synthesize cholesterol. In the liver it is used to make bile salts to facilitate intestinal fat digestion. It is the precursor for gonadal and adrenocortical steroids and vitamin Da formation in the skin. Cholesterol is a component of the neural-tissue myelin sheath and in the corneum of the skin (the outer keratinized layer), which helps make the skin waterproof and prevents water evaporation. In the membranes of cells and some cellular organelles, cholesterol helps stabilize the movement of phospholipid chains.
Dietary vs. endogenous cholesterol
In the body, choles- terol may be exogenous (dietary) or endogenous –i.e., synthe- sized in the tissues, chiefly the liver. Dietary cholesterol comes solely from foods of animal origin (egg yolk, liver, fatty meats, cheese). Cholesterol is absorbed in the intestine with other fats inside chylomicrons, large lipoprotein particles (LPPs). Chylomicrons are digested by the enzyme lipoprotein lipase in the capillaries of liver and adipose tissue. Triglycerides are delivered to the adipose tissue, and the remaining cholesterol and phospholipids are delivered to the liver
Cholesterol can be made in the liver from acetate
To make cholesterol, liver acetate (acetyl-CoA) undergoes several reactions to form mevalonic acid, which is converted first to squalane and then to cholesterol. Cholesterol regulates its own synthesis by substrate inhibition of the enzyme that forms mevalonic acid. Dietary cholesterol inhibits the liver’s synthesis of cholesterol in the same manner. Most of the liver cholesterol is used to form bile salts (e.g. cholate) that help digest fat by emulsification
Liver cholesterol is exported to tissues packed in lipo-protein particles
The liver supplies cholesterol to most tis- sues through the blood. Cholesterol is packed in LPPs that resemble chylomicrons. LPPs have different fat and protein composition and are of different size and density. The higher the fat content of the LPPs, the lower their density. Each LPP has a core of hydrophobic fats (triglycerides and cholesterol as cholesteryl esters) engulfed in a coat of hydrophilic proteins and phospholipids. The protein in the coat is called apoprotein (apolipoprotein), a very important protein since it binds with the tissue receptors that bind LDL.
Lipoprotein particles vary in size, density, & lipid content
LPPs vary in size between 10 to 80 um. Cholesterol for export is transported in the largest of plasma LPPs-very low density lipoproteins (VLDL). In the plasma, these are transformed to smaller lipoproteins –low density lipoproteins (LDL) and intermediate density lipoproteins (IDL)-by the actions of enzymes. Cholesterol delivered directly to tissues is in LDL particles. Once inside the tissue cells, cholesterol is utilized for the variety of functions named above. The excess cholesterol is packed in the smallest of LPP- high density lipoproteins (HDL)–and transported back to the liver for processing.
Thyroid & sex hormones influence cholesterol levels
Thyroid hormones, decrease plasma cholesterol by increasing its uptake by the liver and tissues. Estrogen, the female sex steroid hormone, decreases cholesterol level, while androgen, the male sex steroid hormone, increases it. These sex steroid effects may relate to the higher incidence of atherosclerosis (see below) in men
