Physio 2 - Metabolism 2

drraythe's version from 2015-06-09 01:47


Question Answer
how many of the body's solids are proteins?75%
two types of AAs?essential and non-essential.
what IS an AA?carb with an acid group and an amino group
what are the fxns of proteins? (5)(1) structural (2) contractile elements (3) transporters (4) enzymes/hormones (5) hemostatic factors, antibodies
how are AA'S absorbed from circulation? where?facilitated diffusion or active transport, in particular liver and mm
what happens after the AAs are absorbed into the cell? (just eating, dont need anything)formed into peptides+proteins to make a Labile prot. pool (temporary storage form)
what is the temporary storage form of proteins in a cell?labile prot. pool
in what way does the cell allow a constant turnover between plasma aas and the labile protein pool?lysosomal enzymes allow rapid proteolysis
what performs proteolysis in the cell?lysosomal enzymes
what are FXNL proteins formed from?the labile pool
how does the body utilize aas (metabolize)?deaminize them into keto-analogues which are then able to enter path of carb metabolism (Krebs)
most aas are metabolized after (what do you do to them to metabolize them)after deamination to keto-analogues (remove amino group so it turns into its respective keto-analogue)
is deamination irreversible?no, you CAN reverse this process
ex of deamination of alanine?alanine <---> pyruvate
what part of proteins can enter the carbohydrate metabolism paths/krebs cycle?the keto-analogues
where does the keto-analogue enter the krebs?there are MANY places it can enter-- at pyruvate, acetyl CoA, alpha-keto glutarate, succinylCoA, fumarate, oxaloacetate
after keto-analogues are put into Krebs, they are pulled out as what? for what? (if glucose is needed)drawn out as malate/OAA for gluconeogenesis
after keto-analogues are put into Krebs, they are pulled out as what? for what? (if fat is needed)shunted via CITRATE for LIPOGENESIS (my fat is lemony fresh)
if there are keto-analogues made, and then there is too much acetyl CoA, what do they make?form ketone bodies
what happens to keto-analogues when the body needs prot?intermediates leave krebs cycle for amination to NONESSENTIAL aas
what is the problem with deaminatingaas into keto-analogues?it involves release of amino groups= NH3 (AMMONIA) which is potentially toxic
what are the two ways NH3 can be removed?Transamination and Urea formation
Transamination is akare-use of NH3 groups
how does transamination work? (specifics here)amino groups are transferred to (alpha-ketoglutarate to form glutamate), or to (pyruvate to form alanine) which is the "transport form" of NH3. gluta/alan then xfer NH3 to other compounds (eg for AA synth, involving various amino-transferases)
what are the xsport forms of NH3? What process is this part of?glutamate/alanine (transamination)
What is of diagnostic value in protein meta? exs?Amino-transferases (used for AA synth from glut/alan) (ALT= alanine a.t. and AST aspartate a.t.) are found in mm/liver esp. So increases of a.t.'s in PLASMA are of diagnostic value
urea formation akaexcretion of NH3 groups
where does urea formation take place?LIVER converts potentially toxic NH3 into UREA to be excreted in the KIDNEYS
What happens in regards to NH3 if there is liver failure? (interferes with what to lead to what)NH3 accumulates, the NH3 interferes with GABA a/o glutamate NTs --> neurotoxicity --> depression/neuro deficits/coma/ death = HEPATIC ENCEPHALOPATHY
what is hepatic encephalopathy?when NH3 accumulates, interferes with gaba and glutamate NTs, and eventually causes death

Key Points of Ruminant Metabolism

Question Answer
What happens to the ruminant's dietary carbs?they are all fermented to VFAs (acetate, butyrate, propionate) and so very little sugar reaches sm int for absorption= POTENTIAL HYPOGLYCEMIA
how would you describe the glucose demands of a rumi?just as high if not higher (lactation) than monogastric species
What are ruminants dependent on to prevent them from being hypoglycemic? HOW dependent are they?depend on GLUCONEOGENESIS (permanently switched on) for 90-100% of their blood glucose needs
what is the blood glucose level needed for a ruminant?40-80mg/dl (monogastrics is 80-120)
what are the main glc precursors, and what is the % they're used?(1) propionate (70%) (2) amino acids (20%) (3) lactate, pyruvate, glycerol
Proprionate is C_?C3 (3 is inapropionate)
what is propionate extracted by?the liver
once extracted by the liver, what happens to propionate? ( enters what process as what? )enters krebs as succinate (achieved via CARBOXYLATION) and so PROPRIONATE-->GLUCONEOGENESIS
what does a cobalt deficiency cause? Explain the pathogenesis (and locations)Propionate needs to be carboxilated into succinate to enter krebs. However, this carboxylation requires VitB12, which has/needs cobalt, and this is a common deficiency in Fl, Australia, and New Zealand)
--> summary of propionatePropionate --> gluconeogenesis (three is inapropionate because he's on a sugar high)
Acetate is C_?C2 (2 ass cheeks)
where is acetate absorbed?ALL TISSUES EXCEPT THE LIVER (liver will make its own damn energy)
once acetate is absorbed, what happens to it? (2)(1) enters Krebs as Acetyl CoA for energy gain (ETC) = MAJOR ENERGY SUPPLIER (2) enters lipogenesis as Acetyl CoA in mammary gland and fat tissue (I'm an ace at energizing fatties)
what is the major energy supplier for the ruminant?acetate (hustle that ass!)
--> summary of acetate(1) Acetate --> ATP. (2) Acetate --> lipogenesis
butyrate is C_?C4 (B=bi=doublebutt)
once produced in the rumen, what happens to butyrate? how is this done?partly converted in rumen epi. and after liver uptake to Beta-hydroxybutyrate, acetoacetate, and acetone= KETONE BODIES
once the butyrate is turned into ketone bodies, what happens? (2)(1) ketone bodies used in peripheral tissues for energy gain after entering Krebs cycle as Acetyl CoA (2) ketone bodies contribute to lipogenesis via acetyl CoA in fat tissue/ mammary gland
--> summary of butyrate?(1) butyrate --> **ketone bodies --> ATP OR LIPOGENESIS (your butt is part of your bodies, it can be fat or energetic)

Metabolic Disorders Overview

Question Answer
3 causes of metabolic disorders?(1) endocrine disorders (2) nutritional deficiencies (3) genetic defects
3 examples of endocrine disorders which cause a metabolic disorder?diabetes mellitus, cushings, thyroids... (etc)
some examples of nutritional deficiencies which might cause a metabolic disorder?minerals, trace elements, vitamins, lack of fuels, lack of essential amino acids
genetic defects in what two things lead to metabolic disorders?enzymes and transport proteins
what are the three forms of a glycogen storage disease/polysaccharide storage myopathy (PSSM)?(1) glycogen formed, but not broken down/released (2) abnormal glycogen type is formed/stored (3) too much glycogen is formed and released too fast
if glycogen is formed but cannot be broken down/released, what is the problem with? (PSSM)enzyme defect with DEBRANCHING ENZYME if not broken down, if not released it's enzyme deficiency of glu-6-phosphatase
what is the problem if an abnormal glycogen type is formed and stored?it's wrong thing, so can't be mobilized
what is the problem if too much glycogen is formed and released too fast?it's a hypersensitivity to insulin
clinical signs of PSSM depend on cause, but some of the major ones areenergy deficiency in mm. hepato/cardiomegaly. Hypoglycemia. Lactic acidosis. Exertional rhabdomyolysis (mm necrosis)

Whole body metabolism

Question Answer
What is essential to maintain basal metabolism?constant energy supply (GLC levels must be constant)
what are the 2 (3) major stages of whole body metabolism?(1) Absorptive phase (2) post absorptive phase ( (3) fasting phase )
what are metabolic regulators, and how are they triggered?avail/unavail of fuels (glc) stim release of regulators= HORMONES!! which control flow/direction of metabolic paths
what is the absorptive phase also known as?post-prandial phase
How long does the absorptive phase last?3-5hrs
what does the hyperglycemia of the absorptive phase cause to be released? to be inhibited? What is the ratio caused?release INSULIN, which inhibits GLUCAGON which= HIGH INSULIN/GLUCAGON RATIO
what pathways does insulin stim in the liver? (3)(1) glycogenesis (2) AA uptake, temp. storage, plasma protein synth. (3) lipogenesis out of excess glc and AAs and release of VLDLs
what pathways does insulin stim in the mm? (2)(1) glycogenesis (2) AA uptake, temp. protein pool, synth of mm proteins
what does insulin stim in the fat tissue? (2)(1) stim endothelial LPL ONLY IN FAT CELLS (2) lipogenesis
Excess nutrients from absorptive phase are stored as?(3)glycogen, protein pool, fat
How does a carnivorous diet work during the absorptive phase? (VERY little glc) (what is absorbed? what does this cause?)AAs and Chylomicrons absorbed (but v. little glc) --> AAs stim insulin release --> stim uptake of AAs into cells. Then the hypoglycemia stim glucagon release --> stim gluconeogenesis using absorbed AAs as precursors
So what are carnivores essentially living off of?live off of fat/protein and gluconeogenesis
what organs does a carnivore target, and why?heart mm, liver, fetus b/c high in glycogen!
what is declining during the post-ab phase? why?blood glc, AAs, chylomicrons. B/c they are being taken up by the tissues.
hypoglycemia of post-ab stims what hormone? which inhibits what hormone? which leads to what ratio?glucagon is stim, which inhibits insulin, which means there's a LOW insulin/glucagon ratio
in post-ab phase, aside from glucagon, what else is released? from where?cortisol and epi from the adrenal gland
what does glucagon, cortisol, and epi do? (do _________ by 2 ways)they maintain basic blood glc levels via GLYCOGENOLYSIS (gluc and epi) and GLUCONEOGENESIS (gluc and cortisol)(new cortisol cream)
which two hormones are responsible for glycogenolysis?glucagon and epi (g and e are next to each other in the middle)
which two hormones are responsible for gluconeogenesis?glucagon and cortisol
in post ab, glc-independent tissues largely use _________ for energy gain, provided by the action of _________?(hormones not process)LIPIDS, by action of EPI AND CORTISOL
post ab phase- Fat tissue responds to what? (4)Epi, cortisol, glucagon, LACK OF insulin (b/c fat is greedy)
what does the stimulated fat path in post ab phase do? (action, enzyme, product)lipolysis via HSL (hormone sensitive lipase) with release of fatty acids as NEFAs and glycerol
how is HSL activated?HSL is INHIBITED by insulin, so a NO insulin will ACTIVATE HSL
post ab phase- liver tissue responds to what?glucagon, epi, cortisol
what does stimulated liver path in post ab do? (3)(1) glycogenolysis (2) gluconeogenesis (3) FFA uptake from NEFAs
(post ab phase) what does liver glycogenolysis involve? (precursor, hormones involved within liver, outside stim hormones)Glc-6-P with glycolysis being inhibited by glucagon (so liver doesn't use the energy), glucose accumulates --> diffuses out of hepatocytes as free Glc (glucagon + epi)
(post ab phase) what does liver gluconeogenesis involve? (what stims, made from what?)from AAs and glycerol (stim by glucagon and cortisol)
(post ab phase) why does FFA uptake from NEFAs happen in the liver?for energy gain and some release of ketone bodies and VLDLs
post ab phase- what does the muscle path respond to? (2)cortisol and epi
post ab phase- what happens in the mm path? (2)(need to keep moving) (1) glycogenolysis for energy gain (no release of glc) (2) FFAs uptake from NEFAs and VLDLs and Ketone bodies for energy gain
Define fasting/starvingstate of neg energy balance lasting more than a few days/weeks
how long do full liver glycogen stores last?a few hours
during fasting, how is blood glc levels maintained?depend on gluconeogenesis from AAs (proteolysis) and glycerol (lipolysis)
in fasting, what provides fuel for all glc-independent tissues?lipolysis
starving/fasting is charaterized by longstanding ____longstanding dominance of glucagon, cortisol, and epi while insulin is low
what happens in MM/ other TISSUES during fasting?proteolysis increases to provide AAs for gluconeogenesis (for glc dependent tissues)
what happens to fat tissue during fasting? what situation can this cause?(1) lipolysis inc to provide NEFAs for energy and glycerol for gluconeogenesis (2)**release of NEFAs soon EXCEEDS bodies demand for energy, but continues b/c hypoglycemia forces a hormonal situation which accelerates HSL action (dec insulin with inc cortisol, epi, and glucagon)
why, in fasting, does the fat tissue continue to release NEFAs way beyond the needed amount?EXCEEDS bodies demand for energy, but continues b/c hypoglycemia forces a hormonal situation which accelerates HSL action (dec insulin with inc cortisol, epi, and glucagon)
How does fasting cause hyperlipidemia? (organ responsible, mechanisms responsible)fat tissue is already releasing excess NEFAs. The LIVER then takes up many more NEFAs (fat sponge) than it needs for energy, then many of those FFAs are repackaged/exported as VLDLs, there are more VLDLs than the tissue can use, and they accumulate in the blood= HYPERLIPIDEMIA
what happens that causes hepatic lipidosis in fasting?after releasing so many VLDLs (which caused hyperlipidemia), the liver runs out of lipotropic factors to MAKE the VLDLs and the FFAs/TGs (which the fat keeps releasing due to its hormone situation, and the liver keeps sponging up) ACCUMULATE in the liver=> HEPATIC LIPIDOSIS => fatty liver
who is most at risk for fatty liver?Cats, Cows, horses (ESP OBESE CATS!!!)
aside from the hyperlipidemia and the hepatic lipidosis as problems caused by the liver in fasting, what else can happen/be caused?more ketone bodies are produced and released than can be utilized by peripheral tissues=> KETOACIDOSIS and ketonuria
The three major consequences of fasting/starvation (path)(1)mm wasting and organ wasting / malfunctions (2) hepatic lipidosis leading to hepatic damage (3) metabolic ketoacidosis
what should you be worrying about with hepatic lipidosis liver failure?Liver loses ability to detoxify, AMMONIA builds up, HEPATIC ENCEPHALOPATHY is what will kill them
cause of ketosis/hepatic lipidosis is the lack or unavail of ___, which is usually seen during (4)glc, during (1) fasting/starving/anorexia (2) times of high glc demands (ponies and sm rumi during preg and cows during milk) (3) hormonal imbalances (daibetes mellitus) (4) dietary imbalances (high protein, low carb)
what do you give to a lipidosis/ketoacidosis cat?NOT GLC (the body will just turn them into fat if you give glc+insulin) so feed them AAs to utilize the gluconeogenesis path

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