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Animal nutrition fin
| Question | Answer |
|---|---|
| Stockpile glucose for later, metabolic life -prominent in muscle and liver cells | Glycogen |
| Constant supply of ______________ is needed for the brain and red cells in animals | glucose |
| when glucose is readily available, __________ synthesis increases | glycogen |
| During Fasting most of the body's glucose needs are met by ___________ | gluconeogenesis |
| The 3 enzymes needed for glycogen breakdown: | glycogen phosphorylase,glycogen debranching enzyme, and phosphoglucomutase |
| bond cleavage by substitution of phosphate group | Phosphorolysis |
| removes branching: makes additional glucose residues accessible to glycogen phosphorylase | Glycogen debranching enzyme |
| converts G-1-P to G-6-P | phosphoglucomutase |
| synthesis of glycogen from G-1-P is thermodynamically _____________ without free energy | Unfavorable |
| Glycogen synthesis requires 3 enzymes: | UDP (glucose pyrophosphorylase), Glycogen synthase, Glycogen branching enzyme |
| exergonic step that drives the glycogen synthase | UDP |
| The 2 ways to control Glycogen Metabolism | Enzyme control, and hormone control |
| How does hormone control, effect glycogen metabolism | -Glucagon is synethesized by the pancreas in response to low levels of blood glucose -in the muscle,(insulin, epinephrine, and norepinephrine) response involves release of second messenger that then triggers either glycogen degradation, or glycogen syn |
| -When dietary sources of glucose are not available -When liver has exhausted its supply of glucose from glycogen | Stimulation of Gluconeogenesis |
| supplies glucose from non-CHO sources -provides a lot of glucose in between meals and during fasting | Gluconeogenesis |
| Lactate, pyruvate, TCA intermediates, carbon skeletons of amino acids | Non-CHO |
| FBP is hydrolyzed by ____________ to F-6-P | Fructose-1,6-bisphosphate |
| G-6-P is hydrolyzed by ___________ to glucose | glucose-6-phosphate |
| ATP cost of Gluconeogenesis | 6 total -2: pyruvate -2: PEPCK -2: Phosphoglycerate kinase |
| gluconeogenesis and __________ do not proceed simultaneously in vivo | glycolysis |
| -fructose-2,6-bisphosphate activates PFK, inhibits FBPase -Acetyl-CoA activates pyruvate carboxylase -Pyruvate kinase is inhibited in the liver by alane, a major gluconeogenic precursor | The controls of Gluconeogenesis |
| low level of insulin stimulates transcription of genes for: | PEPCK, FBPase, Glucose-6-phosphate |
| 90% of dietary lipids are | Triacylglycerol |
| Triacyglycerol are a major form of: | metabolic energy storage |
| detergent-like molecules act to solubilize fat globules | bile acids |
| bile acids are stored and secreted where? | Stored in the gall bladder, secreted in the small intesitine |
| Catalyzes hydrolysis at 1 and 3 positions forming 1,2-diacylglycerols and 2-acyglycerol | Pancreatic Lipase |
| Fatty acids, mono- and diacyglycerols are absorbed by: | Cells lining small intestine |
| Bile acids formL | Micelles |
| Bile acids allow for efficient absorption of: | Lipid-soluble vitamins A,D,E and K |
| Transported in lymph and blood vessels to be transported to various tissues | Chylomicrons |
| Within _________, triacyglycerols within chylomicrons are hydrolysed by lipoprotein lipase to mono acyglycerols and fatty acids | capillaries |
| A healthy person wants _____ HDL, _____ LDL, and ______ triacyglycerides | high, low, low |
| VLDL: synthesized in the liver | Very Low Density Lipoproteins |
| Carry _____________ and _____________ in capillaries where it is degraded by lipoprotein lipase to fatty acids (then to adipose, muscle) | triacyglycerols, cholesterol |
| oxidized for energy productions synthesized triacyglycerols | Free Fatty Acids |
| Transported to liver and converted to DHAP | Glycerols Backbone |
| IDL | intermediate density lipoproteins |
| LDL | Low density lipoproteins |
| HDL: removes cholesterol from the tissues | High Density lipoproteins |
| HDL assembled in the plasma from: | Degraded components of lipoproteins, and is extracted cholesterol from cell surface memebranes |
| HDL transfers ___________ to ____ | Cholesterol esters to VLDL |
| Stored as triacyglycerides in adipose tissues. is moblized when energy is needed by the body | Fatty acids |
| When Free Fatty Acids are released into the bloodstream, they bind to what? | Albumin |
| "Priming" fatty acids occurs in the | Cytosol |
| Oxidation of Fatty acids occurs in the | Mitochondria |
| Degradation of fatty acyl-CoA (shortening by 2-carbons) | beta oxidation |
| formation of double bond by dehydrogenation | Acyl-CoA dehydrogenase |
| hydration of double bonds | Enol-CoA hydratase |
| NAD+ dependent dehydrogenation | Hydroxyl-CoA |
| cleavage between alpa and beta-carbons | beta-ketoacyl-CoA Thiolase |
| double bonds begin between C9 and C10, additional double bonds occur at 3-carbon intercals | Unsaturated fatty acids |
| ATP gain from a 16C fatty acid | 131 -7 FADH2 -7 NADH -8 Acetyl CoA (goes through TCA cycle) |
| During severe starvation, brain can use _______ ________ if glucose is depleted | Ketone bodies |
| ______ releases ketones into bloodstream to ________ __________ | Liver, peripheral tissues |
| -Acetoacetate is produced faster than it can be metabolized -Build-up of ketones within the tissues -acetone breath -ketones released into urin-testing | Ketosis |
| The reversal of beta-oxidation, and occurs in the cytoplasm | Fatty Acids Biosynthesis |
| Production od NADH-use in fatty acid biosynthesis | Pentose Phosphate Pathway |
| When ATP demand is low, __________ can be stored as fat | Acetyl CoA |
| -Rate determing step -involes biotin and CO2 -enzymes stimulated by citrate and insulin | Conversion of acetyl CoA(2C) to Malonyl CoA(3C) |
| synthesis of __________ from acetyl CoA and malonyl CoA involves _ reactions | palmitate, 7 |
| Growing fatty acid is anchored to: | Acyl-carrier protein (ACP) |
| C16 FA converted to longer chain FA | Elongates |
| C16 sat. FA converted to Unsat. FA | Desaturase |
| 4 teminal desaturases | C9, C6, C5, C4 fatty acyl-CoA desaturases |
| 3 fatty acyl-CoA esters + GAP/DHAP will yield | Triacyglycerol |
| __________, ___________, and ____________ increase adipose tissue cAMP levels | Glucagon, Epinephrine, Norepinephrine |
| an increase in adipose tissue cAMP levels results in | Phosphorylation |
| Phosphorylation activates | Hormone-sensitive Lipase (HSL) |
| Stimulation of lipolysis in adipose tissue, increase in fatty acid levels in blood, Beta-oxidation in liver and muscle, production of ketone bodies in liver | HSL |
| -stimulates formation of glycogen and triacylglycerols -Decreases cAMP levels, dephosphorylation, inactivation of HSL -Activates acetyl-CoA carboxylase | Insulin |
| Use of lipids | For energy, Structure: membrane lipid, and Cholesterol metabolism |
| -Degradation of protein -Deamination -incorporation of nitrogen into urea for excretion | Catbolism |
| alpha amino goup removal of component amino acid | Deamination |
| synthesis of amino acids and proteins | Anabolism |
| -Store nutrients in form of protein and break down during metabolic need -eliminate abnormal proteins -regulate cellular metabolism by eliminating enzymes and regulatory proteins | Functions of Protein Degradation |
| Contain enzymes including proteases | Lysosomes |
| -Proteins are marked for degradation by linking themselves to equilibrium | Ubiquitin |
| 3 enzymes needed for Ubiquitin | Ubiquitin-activating enzyme Ubiquitin-conjugation enzyme Ubiquitin-protein ligase |
| degrade ubiquitinated proteins | Proteasomes |
| Urea is synthesized in the: | Liver |
| Urea is secreted into the bloodstream and taken up by the ___________ for excretion in urine | Kidneys |
| Degradation to compounds metabolized to CO2 and H2O or used in gluconeogenesis | Amino Acid Breakdown |
| degraded to pyruvate, alpha-ketoglutarate, succinyl-CoA, fumarate, oxaloacetate | Glucogenic amino acids |
| Degraded to acetyl-CoA, acetoacetate | Ketogenic amino aicds |
| synthesis by manmmals from common intermediates | Non-essential amino acids |
| The feeling of being full | Satiety |
| Control of food intake | hunger, temp, disease/injury, palability,distention of GI tract, photoperiod (pineal gland), hormones |
| bigger meals, more frequent meals, or combination | Level of production |
| increase in day length increase feed intake | photoperiod |
| increase in N increase feed intake | N status |
| temerature and humidity | Environmental |
| partitioning of nutrients to support requirments specific for each physiological state | Homeorhesis |
| Level of production Photoperiod N status Environmental Phsiological state | Long term control of feed intake |
| factors that begin and end each meal. (for a high roughage diet) | 1. Distention of rumen/reticulum 2. Passage rate 3. size of stomach compartments 4. Saliva 5. Motility of reticulo-rumen 6. Digestibility and particle size 7. osmolarity 8. Acetic acid in digesta 9.Propionic acid in ruminal veins or in liver 10. |
| factors that begin and end each meal. (for a high concentrate diet) | 1.VFA content 2.Endocrine |
| response of an animal to its food | Palatability |
| 4 responses the animal will have towards their food | taste, smell, flavor, texture |
| What will cause a negative response to food from animals | Dust, rancidity, moldy, bitter, and sudden changes in diet |
| CCK | Cholecystokinin |
| CCK activates: | pancreas |
| CCK inhabited: | gastric acid secretion |
| CCK is synthesized: | small intestines |
| stimulates gastric acid release by parietal cells in stomach | Gastrin |
| Gastrin is inhibited by the presence of _________ in the stomach | HCL |
| a neurotransmitter-secreted by the hypothalamus | Neuropeptide Y |
| How does Neuropeptide Y regulates energy balance | increase food intake, decrease physical activity, increase ability of body to store excess energy as fat |
| Neuropeptide Y is inhibited by | Leptin |
| -stimulates appetite and feed intake -stimulates release of GH from anterior pituitary -activates neropeptide Y neurons | Ghrelin |
| Ob is the gene for: | Leptin |
| a mutation in leptine results in an _______ mouse | obese |
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