Metabolism Flashcards
1
Q
fuel metabolism
A
- reactions involving degration, synthesis and transformation of 3 fuels
protein
carbs
fat
2
Q
two complications
A
- need energy released during periods of fasting
- brain needs continour energy but only ever use glucose
3
Q
control of glucose
A
- vertebrate brain relies solely on glucose as energy
- tightly regulated so it doesnt fall below a critical level
- liver glycogen: main source of glucose for short term balance
- during fasting
- tissues except brain shift from glucose to fatty acids as energy source
- when glycogen storage is depleted glucose source = protein breakdown and aa glucose
- vertebrate brain relies solely on glucose as energy
- tightly regulated so it doesnt excreed a critical level
- high concentrations of glucose: long term consequences
glucose homeostasis: prevents short term hypoglycemia and prevents long term hyperglycemia
4
Q
alternate anergy sources
A
- some intermediates may be used as alternate energy sources
- glycerol (backbone of trglycerides ) can be converted to glucose in the lvier
- lactate ( from incomplete catabolism of glucose in muscle ) can be converted to glucose in the liver
- ketones produced by the liver during glucose sparing
5
Q
hormonal regulation
A
- pancreas: endocrine and exocrine tissues
- endocrine cells:
- beta cells and alpha cells
- delta cells ( released when [glucose] and [AA] high in the blood
- decrease nutrient absorption by digestion
6
Q
insulin regulation
A
- decrease blood glucose and fatty acid conc in blood and promoting their storage
7
Q
effect of insulin on carbohydrates
A
- facilitate glucose transport into most cells
- stimulates glycogenesis in muscle and liver
- inhibi glycogenolysis
- inhibits gluconeogensis in the liver
8
Q
GLUT 1/3
A
1= mores through glucose in the blood through bbb
3= transport glucose into neurons
9
Q
GLUT 4
A
- the only insulin independent GLUT
- stored in vesicles inside the cells
- when insulin is detected by the cell - release glut 4 on the cell membrane via exocytosis
- 10-30 fold increase in glucose absorbtion
- common in fat cells, strirated muscle cells
10
Q
skeletal muscles and glut 4
A
- at rest skeletal muscles are insulin independent
- muscle contrations - release glut 4 on the cell membrane promotes absorption of glucose from the blood
- implications for managing diabetes
11
Q
effects of insulin on fat
A
- increase transport of glucose into fatty tissues (GLUT4)
- activate enzymes that turn nutrients into fatty acids
- promote uptake of fatty acids into fatty acids
- inhibits fat breakdown
12
Q
effects of insulin on protein
A
- promote transport of AA into muscles and other tissue
- enhance protein synthesis by activating cell machinery
- inhibits protein breakdown
13
Q
main control
A
increase blood glucose - activates beta cells - release insulin
- decrease blood glucose - inhibits beta cells - no insulin secretion
- other controls = increased blood aa - activates beta cells - release insulin
14
Q
glucagon
A
- when insulin released is inhibited glucagon released is stimulated
- has opposite effect to insulin
- act primarily on liver (increase glucose, ketone, production and protein degradation)
- also promote fat breakdown in fatty tissue
- increase blood AA - stimulates beta cells - insulin secreation
15
Q
diabetes mellitus
A
- elevated blood glucose levels
- high volume of urine production (water attraction to high glucose levels in urine)
- vision problems
type 1: insulin dependent - beta cells are damaged and do not produce insulin
type 2: non insulin dependent - insulin secretion but cells dont listen
16
Q
long term failed glucose homeostasis
A
- blindness (from cataracts, glaucoma, from retinopathy)
- leg pain - increase inflammation, increased plaque and decreased vascularization
17
Q
prevention
A
- avoid sugar spike
- work out regularly
- loss wait
18
Q
calcium homeostasis short term
A
- neuromuscular excitability: decrease Ca increased excitability by increasing Na permeability (depolarizes nerve and muscle cells)
- decrease muscle contraction in cariac and smooth muscle
- cause vesicle exocytosis (synaptic neurotransmitters, peptide hormones)
- blood clotting cascade
- 2nd messanger cascades
- enzyme co-factos
19
Q
calcium homeostasis long term
A
- structural support in bones, teeth
- calcium/phosphate complex = hyroxyapatite
- milk production, egg laying (medullary bone - low calcium = takes it out of bone, weakening the bone)
- egg shell: hen mobilizes 47% of her body calcium to make an egg shell
20
Q
calcium in the body
A
- 99% of Ca in the body found in the bones and teeth
- 98% is crystallized (bone and teeth) stable pool of Ca and P
- 1% is in the bone fluid (labile pool of Ca2)
-the other 1% - 0.9% intracellular within soft tissues
<0.1% extracellular fluid. Of that: - 50% free Ca - biologically active pool
- 41% protein - bound
- 9% complexed anion (with P)
21
Q
2 timescales of regulation
A
- short term: immediate adjustment to maintain constant free plasma Ca (minute to minute adjustment) primary: rapid exchange between bone EFC (bone resorption), modifiation of urine excretion of Ca (reabsorbtion from renal tubules)
long term: maintain the constant total amount of Ca in the body - dietary Ca absorption from the intestine
- modification in urine excretion of Ca (reabsorbtion of renal tubules
22
Q
bone remodelling
A
- Osteoclasts attach to the matrix, dump HCL + enzymes, dig itself in a city
- Either move on to make another hole or dies from apoptosis (based on signals it is getting)
- osteoblast moves in the cavity, secretes osteroid to fill in the hole
23
Q
PTH and kidneys
A
- PTH promotes Ca2 conservation and elimination of PO34
- Increased reabsorption of calcium from renal tubules ( lose less calcium in the urine)
- decreased reabsorption of phosphorus (lose more phosphorus in the urine)
- activates vitamin D
24
Q
what happens if phosphate gets higher
A
- Ca and PO34, form insoluble calcium phosphate crystals (precipitate out of solution
- is plasma Po34 rises, calcium phosphate forms, taking away CA
- deposited in bone - lowers plasma Ca in the process
- so phosphate goes up, plasma calcium goes down
- hypocalcemia: try to lower plasma phosphate and increase calcium concentrations
25
Q
calcitonin
A
- produced by c cells in the thyroid
- in non-mammals, CT is produced by its own glands (ultimobranchial body - in neck and heart)
- function: decreased [Ca+]plamsa (opposite of PTH) - acting on bones
- short term: decrease calcium movement from bone fluid into plasma (calcium pumps get blocked)
- long term: decreased bone resorption by inhibiting osteoclasts (decrease both [po34] and [Ca]
- no effect on kidneys of instestine
- limited role in humans, and many mammals (ie, excess CT doesnt effect [Ca])
- regulation [ca2] Plasma
26
Q
vitamin D
A
- produced in the skin, activated by UV radiation, released into the blood and acts on intestinal target cells (hormone)
- not usually produced in sufficient quantities, so also conisdered essential nutrients
needs to be activated: sunlight, liver, kidney and controlled by PTH
27
Q
vitamin D functions
A
- increased calcium absorption from intestine (increased synthesis of protein calbindin) calcium: absorbtion from the intestines is regulated (unlike other nutrients)
- increased phosphate absorption from the intestine
- increased bone responsivemness to PTH
- overall function: for long term calcium balance (not short term regulation)
28
Q
hyperparathyroidism
A
- excess secretion of PTH
- causes: low ca or vit d or high p in diet (renal disease) tumour of parathyroid gland
- symptoms: decreased nervous / muscle excitability, weakened bones or fractures, increased kidney stones (calcium oxalate)
29
Q
vitamin d deficiency
A
- not enough sun exposure, low diet supplementation
- decrease intestinal absorption of Ca, increase PTH to compensate
- Ca taken from bones leads to long term softening (rickets (vit D deciciency in younger animasl ), osteomalacia (vit d decifiency in older animals
- reptiles and amphibians very susceptible to vit d deficiency
30
Q
rickets
A
llamas and sheep are the most common
- cattle and horeses rare
- pig - nutritional and inherited forms
- dogs and cats: rare (lots of P in diets) but high p and low ca diets can cause rickets
31
Q
milk fever
A
- hypocalcemia shortly after calving in high producing dairy cows
- initial signs: increased neural excitability/ restlessness
- progreses to recumbency (unable to stand), cardiac arrythmias and depression
- intravenous and subcutaneous calcium
32
Q
why feed a low calcium diet before calving
A
- high calcium diets: calcitonin predominates immediatly prior to calving (not PTH)
- when milk production starts, blood calcium drops and pth is released
- but calcitonin inhibits calcium resorption from bone - PTHs main method of increasing plasma calcium
anionic acid diets: - cause minor metabolic acidosis
- increase bone resorption and intestinal calcium uptake (via vit D activation)
