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