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Animal nutrition fin

QuestionAnswer
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
Created by: Jeremee Charles Lewis Jeremee Charles Lewis on 2012-05-02



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