| A | B |
|---|
| fats are (water loving or not?) | hydrophobic |
| where does most fat end up? | in the duodenum as small globules |
| what is used to aid in the digestion of fat in the duodenum | biles |
| bile is produced where and stored where | produced in the liver, stored in the gallbladder |
| where does bile enter? | the GI tract at the small intestine |
| what is the puropse of bile | to break down fat globules into smaller ones, |
| what is a micelle | a group of molecules with polar and non polar ends |
| what end is on the outside of the system? | polar ends |
| what is pancreatic lipase | an enzyme used in the hydrolysis of fats |
| pancreatic lipas produces what two things? | glycerine and monoglycerides |
| colipase | a protein that binds to the surface of the lipid droplet |
| after hydrolyisiems.. where do fatty acids and monoglycerides pass through? | the wall of the small intestine |
| after the monoglycerides and fatty acids pass through the wall what are they reassembled into? | triglycerides |
| what is added to the triglycerides after hydrolysis? | protein is added so that chylomicrons are produced |
| chyomicrons are passed via what system in the blood | the lymph system |
| what are the 4 main classes of complex lipids/ | chylomicrons, very low density lypoporteins, lowdensity lypoproteins, and high density lypoproteins |
| what is the function of chylomicrons | transport tryglycerides form intestines to other tissues (except kindey) |
| chylomicrons transport what kind of products | exogenic products |
| VLDL | bind triglycerides in liver and released to the blood |
| LDL | carry fat and chlorestorol to peripheral tissues. produced from VLDL in blood ( conversion also relesases chloestorol into blood vessels |
| HDL | bound to plasma chloestorol, transport it and fat to liver, |
| receptor mediated endocytosis | receptors on cell membrane sense LDL, invagination, forms endosome, endosome fuses with lysosome, digest LDL releasing chloestorol |
| invagination | pocket forms in the membrane of cell |
| when a cell takes in LDL it forms a | endosome |
| presence of chlestorol in a cell | reduces synthesis of more cholestorol, inhibits production of LDL receptors |
| large number of receptors in live cause what? | rapid removal from liver |
| LDL defect coding is what? | allows too much cholestorol to accumulate in the plasma |
| atherosclerosis | excess chloresterol is deposisted into walls |
| fatty acids are stored as what in the what of an adipocyte | triglycerides in the cytoplasm |
| glycogen vs. fat supply | g- one day fat-one month |
| glycogen vs. fat energy per gram | g-less that fat- more no water! |
| fat is releases after... | glycogen is gone |
| glycerol hydrolyzed from fat can be used as... | an energy source |
| beta oxidation | fatty acids are recycled through the same process |
| how many carbons are removed each time fatty acid degradtion occurs | 2 |
| what is produced? | a fatty acid CoA |
| Acetyl COA goes onto what? | the citric acid cycly |
| during Beta oxidation what happens | the beta carbon of the fatty acid is oxidized to a carbonyl |
| what is the first phase of beta oxidation | the fatty acid is converted into acetyl COA |
| conversion of a fatty acid into acetyl COA requires.... | 2 ATP |
| acetyl COA can enter where | the mitochondria |
| beta oxidation is the net reaction for what? | stearic acid |
| The FADH and NADH are converted to what from the acetyl COA | converted to ATP via the electron transport chain and oxidative phosphorylation |
| if too much acetyl COA is produced from beta oxidation, what will it be converted to? | ketone bodies |
| acetyl COA + oxaloacetate | citrate |
| acetone, acetoacetate, and beta hydroxybuterate are all produced from an excess of what? | ACETYL coa |
| ketosis | abnormal rise of ketone bodies in the blood |
| ketosis causes? | starvation, low carb diet, and diabeties mellitus |
| ketoacidosis | two of the ketone bodies are acids which causes lowering of blood pH |
| ketogenesis | pathway for production of ketone bodies |
| ketogenesis starts with... | the reversal of the last step of Beta oxdation |
| acetone breath | spontaneous loss of Co2 by acetoacetate to form acetone |
| acetone breath is a sympton of what is is it enzymatic | its a nonenzymatic process, and its a symptom of untreated diabetis metlitus or stavation |
| acetoacetate and beta hydroxybutyrate | produced in liver, diffuse in blood to other tissues, can be reconverted to acetyl COA in mitochondria, transported to muscles and brain for use as energy sources |
| acetone is produced in and is eliaintaed by | small amounts, and emilnated in urine and breath |
| in humans acetyl COA is converted into what | fatty acid esters |
| fatty acid synthesis vs. degradiation where they occur | synthesis cytoplasm, degradtion in the mitochondria |
| fatty acid synthase | when all synthesis occurs in a multienzyme complex |
| the liver plays a huge role in what? | cotrolling fat usage and production |
| what does the liver supply to other systems? | glucose |
| the liver regulates glucose levels by what? | conversion to and from glycogen |
| what can produce glucose from materials like lactate | liver |
| the liver will make fatty acids if there is excess what? | glucose and glycogen |
| the liver makes what that are useful to other organs | ketone bodies |
| adipse tissue stores what? | fatty acids as triglycerides |
| fatty acids are transported form the liver to it as | VLDL complexes |
| what is required to make triglycerides | glycerol-3-phosphate |
| we cannot store fat unless we have excess what? | glucose! |
| muscle tissue at rest is supplied by | beta oxidation of fatty acids |
| muscle tissue at work is supplied by | internal supply of glucagon |
| alanine and lactate are sent to liver to produce glucose during what | muscle tissue at work |
| this is the primary energy source for the brain and 60% of this in the body is in the brain | glucose |
| if glucose levels drop what will be used | ketone bodies |
| what cannot pass the blood brain barrier | fatty acids |
| amino acids serve as a source of nitrogen for what compounds> | nitrogen bases of DNA, and RNA, heme structures, phosphoipids, homrmones etc. |
| can amino acids be stored by the body? | no |
| what does the body use amino acids for | energy only if there is an excess of them, or if their is a lack of resources |
| amino acids require the removal of what to be useful | amino group |
| removing the amino group is a two step process between whar | transmation and oxidative deamination |
| transmation | aminetransferase moves the amin to alpha ketoglutarate producing glutamate or to ocaloacetate prodcuing asparate |
| oxdative demation | removal of the amine from glutamate producing an ammonium ion |
| the urea cycle does what | elimates ammonium |
| excess amino acids need to be | deaminated |
| THE UREA CYCLE TAKES PLACE WHERE | in the liver |
| a complete block of A STEP in the urea cycle does what | incompatibale with life |
| genetic disorders with problems in the urea cycle | arginase, carbonyl phosphate synthase, and ornthine transcarbamolyase |
| biosynthestic intermediates | divert excess material to the production of glycerol and lipids for fat production |
| production of ribose | nuclotide backbone |
| biosynthetic intermediates can produce | heme for porphyrin for hemoglobin |
| biosynthetic intermediates acan be used to make what kind of amino acids | non essential ones! |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
| x | x |
