Metabolism and Regulation of Body temp Flashcards

1
Q

nutrient

A

gen = substance used to promote normal growth, maintenance and repair

essential = can’t make ourselves, need to obtain from diet

macro = carb, protein, lipid
micro = vitamins and minerals

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2
Q

energy value of food

A

in kcal, 1000 calories
amount of heat E required to raise the temp of 1kg go water by 1 deg C

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3
Q

carbs dietary sources

A

mostly plants, expect for lactose (dairy) and glycogen (meats)

sugars = fruits, cane sugar, honey,
starch = grains, legumes, veggies
insoluble fibres= cellulose in veggies
solute fibres = pectin in fruits (apples)

insol** = stay in lumen of GI, hold water, make poop water
sol** = no digestion, binds cholesterol, helps keep levels under control

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4
Q

carbs uses in body

A

glucose = major body fuel (other monos get converted to glucose)
neurons and RBC uses only glucose, other cells can use other fats
blood glucose must be monitors, if drops, feel it at CNS, brain not working properly
if too high, excess converted to glycogen in liver and muscles. if glycogen reserves fill up, to fat in adipose tissue
sugars found in nuclear acids, glycoproteins, glycolipids

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5
Q

carb = dietary requirements

A

focus on complex carbs = not simple sugars but starches that take longer to breakdown, prevent spike in glucose levels,

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6
Q

lipids dietary source

A

most abundant = triglycerides

sat = meat, dairy, coconut = only single bonds
eat in moderation, more rigid, can clog vessels

unset = seeds, nuts, vegetable oils = double bonds = bends, more fluid, more liquid, less solid

cholesterol (egg yolk, meats, dairy) + phospholipids.
85% of cholesterol in your body rn you made yourself, but sat fats stim body to make more,

omega 3 and 6, can’t make ourselves.

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7
Q

lipids luses in body

A

controlled by liver and adipose tissue
1. absorption of vitamins
2. TG = major fuel of liver nad muscles
3. phospholipids = myelin + plasma mb
4. fatty deposits = cushion to protect organs, insulate against heat loss, source of E fuel
5.cholestrol = mb, precursor for bile salt and steroid hormones

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8
Q

lipid dietary requirements

A

we usually intake higher than need, should be less than 30%
sat fats should be 10% of total fats,
so little cholestrol

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9
Q

protein dietary sourcees

A

animal products = biggest amount + best ratio of aa
= egg, milk, fish and meat
= complete = get enough of all aa bc source of protein is another animal (we need same aa)

plant = aa you get depends what type of plants you eat, so need to balance source to get a variety of aa

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10
Q

protein uses in body
storage + all or none

A

structural = keratin of skin, collagen, elastin of CT

functional = enzymes, Hb, protein/peptide hormones

energy = last resort, if running out of options for ATP prod, will sacrifice muscle tissue to get aa

can’t be stores = bc when making a protein, were getting specific instructions of DNA. RNA foes into cytoplasm and says make this protein bc needed,
there is no instruction to make storage proteins

if excess, stored as fats In adipose tissue

all or none = if even one aa is missing, no protein is made, why a full source is so important

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11
Q

vitamin

A

essential for use of protein and carbs

coenzymes in E related reactions
B vitamins

most not made in body (except for vit D, biome = some B and K, and carotene (substrate to carry out remaining steps in liver to make A)

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12
Q

classes of vitamins

A

fat soluble
A,D, E, K,, with dietary lipid, can be stored (except K), could have vitamin toxicity

water soluble= B complex and C
not much storage

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13
Q

antioxidants

A

ACE

help inactivate free radical, generated In metabolic reactions, have unpaired electrons, so very reactive molecules are trying to take an e from another molecule, that molecule becomes a free molecules goes looking else where, leads to cascades of reactions that can mess things up in the body.

they take the bullet and gives it another e pair
they are not as reactive is missing a pair, so calm things down

protect against tissue damage and chronic disease and cancer = if free radicals are chronically actve

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14
Q

minerals

A

moderate amounts of 7 minerals
= Ca P (bones), K, Na, Cl, (excitable cells, AP), Mg, S (useful but not talked about)

trace of Fe, I, Mn, Cu, Zn, Co, F, Se, Ce

Fe = Hb
I = thyroid hormone
Na, C; = osmolarity and water

critical balance bn intake and excretion

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15
Q

water

A

carries nutrient throughout body
cleanses blood from waste
solvent fro minerals, vitamins, aa, glucose
participate in chem rxns

lubricant around joint
shock absorber (SC, joints, amniotic fluid, eyes)
body temp reg

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16
Q

anabolic vs catabolic

A

a = synth reactions

c = breaking down
glycogen to glucose
glucose to ATP
in the cells of body

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17
Q

glycolysis

A

glucose to pyruvic acid

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18
Q

glycogenesis

A

polymerize glucose to glycogen

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19
Q

glycogenolysis

A

hydrolyze glycogen to glucose

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20
Q

gluconeogenesis

A

glucose from non carbs precursors

  • if running out of glycogen, we start hunting down other molecules to maintain blood sugars, like glycerol or aa . well sacrifice anything to maintain adequate levels
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21
Q

why is gluconeogenesis so imp

A

bc you can only store so much glucose in your body

  • if running out of glycogen, we start hunting down other molecules to maintain blood sugars, like glycerol or aa . well sacrifice anything to maintain adequate levels

if fasting, and emptied reserves, will sacrifice muscles, to protect CNS to not go into a coma and die.

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22
Q

what are 2 main substrates for gluconeogeneiss

A

amino acids and glycerol

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23
Q

lipid metabolism steps/what actually is happening

A

stored fats in adipose tissue or dietary fats you’re consuming = TG

TG = split into glycerol (OCH) + FA (CH)

glycerol = 1 per TG
can join in the middle of glycolysis
so can reform glucose by going backwards or continue on (make pyruvate) enter the Krebs cycle and make ATP

FA = can’t be used to maintain blood sugars, can’t reform to glucose
3 per TG

FA = undergoes Beta-oxidation= chopped up into 2 C molecules, join citric acid cycle as acetyl CoA
can only continue to make ATP but can’t go backwards and form glucose

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24
Q

FAs can’t from glucose, but what happens when there’s really too little carbs……

A

they produce ketone bodies
through ketogenesis in the liver

ketone bodies = are acetic molecule produced by FA when they can’t run the citric acid cycle normally (not enough carbs)

25
fates for glycerol
depends on what body needs, can be used to make glucose or can be burned to make ATP
26
fates for FA chain
can't make glucose, can either joint the citric acid cycle to make ATP or make ketones.
27
amino acids , uses
used to build proteins needed in body or as last resort provide energy can also be stores as fats if in excess
28
how can aa be used for energy
when blood glucose levels drop significantly, aa are converted to keto acids and building blocks for glucose
29
keto acid vs ketone body
an acidic molecule, an aa without an amino group, left with ketone grp very imp made in liver when doing stuff w other aa, can be used to produce ATP or glucose molecules ketone body = what we can do with FA
30
transamination vs deanimation
trans = helps liver cells form nonessential aa as needed take amino grp from one aa to place on a keto acid **forms a new aa and a new keto acid** deanimation = an amino grp is removed, leaving behind a keto acid and ammonia, turn into urea, expelled as waste
31
pathway for proteins
proteins into aa transamination = an amino grp switched from an aa to a keto acid resulting keto acid is modified and enters the citric acid cycle the resulting aa undergoes deamination = amine group is removed (forms sure) expelled either make glucose or make ATP
32
how lipolysis produces glucose
TG = glycerol + 3 FA glycerol enters glycolysis and forms glucose bu going backwards
33
noncarbohydrate fates for glucose
lipogenesis = converted into fats (TG) stored in adipose tissue aa synthesis = produce non essential aa
34
2 possible nonprotein fates for aa
deanimaion => possible non-protein fates for amino acids are: Energy production: After deamination, the remaining carbon skeleton of the amino acid can enter the citric acid cycle and be used to produce ATP. Glucose or ketone body production: The carbon skeleton can be converted into glucose through gluconeogenesis (if the amino acid is glucogenic) or into ketone bodies through ketogenesis (if the amino acid is ketogenic).
35
absorptive state vs post absorpative state
absroptive state = time during and shortly after eating nutrients are entering the circulation and blood glucose levels are high either gonna burn glucose or store postabs. state = GI tract is empty we draw from reserves to meet E needs, and ot meet blood glucose levels
36
processes in absorptive state
anabolic exceed catabolic synth proteins you need from aa excess aa =keto acids, either to be used for ATP or store. store glucose as glycogen stre fats as TG in adipose, all = anabolic only catabolic = burning glucose for ATP
37
principle pathway of absorptive state
glucose is plentiful so used to make ATP glucose reserves in liver and muscles are synthesized needed proteins are amde everything left over to TG stored in adipose in muscles = glucose to glycogen aa to proteins in liver = glucose to glycogen (stored) glucose to glycerol to TG (stored) glucose to FA to TG (stored) aa to proteins aa to keto acids to fatty acids to TG (stored) aa to keto acids to ATP production in adipose tissue TG from diet = stored = glycerol or FA glucose t glycerol and FA = make TG stored.
38
insulin
small protein that directs everything that happens in absorptive state produced by beta cells of islets go pancreas if unable to produce insulin = won't be able to do imp reactions needed during abs state, can't use glucose effectively
39
stimulus and how it does it job
stimulis for secretion = rise in blood glucose or in aa levels activates carrier mediated facilitated diffusion for glucose into cells, (esp adipose and skeletal muscles) help not needed for brain, kidney, liver, intestinal epi.
40
structure of insulin
small protein (51 aa) w 2 aa chains connected by disulphide bonds initially is proinsulin = we make a larger molecule, then middle is removed to make active insulin, why? so we can have proper folding and so can hold things together better
41
diff cells have diff types of glucose trasnporters
glut-4 = insulin dependent in adipose and muscles glut-2 = not insulin dependent, low affinity for glucose liver cells, and pancreatic beta cells, beta = need to be informed of rise in glucose levels glut-1 = doesn't require insulin, most other cells (neurons) since insulin isnt always present, these need constant access all the time, can't depend on it
42
what happens to glucose levels if insulin is not present
not gonna be able to take up in muscles and adipose so gonna stay in blood stream, inc significantly
43
what insulin downs during abs state
inc glucose usage for E, since plentiful synth activities to store glucose as glycogen and fats in adipose synth proteins as needed, inc uptake of aa stops liver enzymes that help glucose formation from non carb subunits, stop breaking down glycogen into glucose
44
insulin is anabolic and hypoglycemic
anabolic = encourages synthesizing reactions to store glucose in other forms hypoglycaemic = lowers blood glucose levels by stimulating cells to use it
45
post absorptive state
maintain blood glucose w/in homeostatic range when no food being eaten imp bc brain only uses glucose fro E all we do is to make sure = to spare glucose for brain cells = make more glucose available to the circ system
46
making glucose available to the blood sources and methods
sources = stored glycogen fats (only glycerol) and proteins 1. glycogenolysis in liver glycogen reserves are first source from glycogen to glucose enough for 4 hours. 2. glycogenolysis in skeletal muscles 2nd option a little more complicated bc indirect source of blood glucose when broken down from glycogen to glucose, glucose doesn't leave the muscles, they're greedy. so need to keep going and break down to pyruvate or lactic acid which will be released into the blood, to the liver and remade into glucose, which enters circ system 3. lipolysis in adipose and in liver lipolysis = breakdown fats into glycerol and FA in adipose and liver glycerol to glucose = gluconeogenesis FFA feed into Krebs 4. catabolism of cellular proteins last resort, only if fasting for longggg times. run out go glycogen reserves and breaking up fats its enough can deanimate aa to use as building blocks to make glucose molecules
47
principle pathway of post absorptive state
in muscles = glucose to pyruvate or lactic acid (to liver to glucose) proteins to aa to liver in adipose tissue = TG to liver FA and glycerol make ATP in other tissues in liver =pyruvate/lactic acid from muscles to glucose to circ = stored glycogen = glucose, out = aa from muscles to keto acids to glucose, out = stored TG = FA and glycerol = glycerol from adipose + own supply to glucose = FA from adipose + own supply to ketone bodies to ATP in other tissues or in liver
48
glucose sparing
inc use of noncarbs fuel molecules to conserve glucose tp save for brain FFA to tissue cells to tissues FFA to ketone bodies to tissues eventually brain uses ketone bodies, after days
49
hormonal and neural control
interaction of sympathetic NS w hormones to regulate post abs state, glucagon = released when blood glucose decreases made by Alpha islets there are other hormones, depending on what you're doing during this state,
50
major target of glucagon and effect
is liver and adipose tissue breaking down glycogen to glucose making glucose from non carb subunits in adipose = lipolysis = release of FFA and glycerol into blood
51
Sympathetic NS
responses to sudden drop In blood glucose other stimulis = injury, anxiety, anger, F/F response effect = stimulates lipolysis and fat mobilization glycogenolysis
52
adrenal glands
epinephrine from medulla = stimulates glycogenolysis lipolysis and fat mobilization gluconeogenesis cortisol from cortex = stimulates lipolysis and fat mobilization gluconeogenesis **protein catabolism*
53
diabetes
lack/absence of insulin, insulin resistance or both glucose isn't used properly
54
types of diabetes
type 1. insulin dependent diabetes = autoimmune destruction of beta cells either receptor don't have perfect structures, or insulin iteslef type 2. body tissues stop responding to insulin, pancreas pushes more and more out until it eventually starts to tire and starts releasing less
55
liver
most metabolic organ process nearly every class of nutrients + reg plasma cholesterol levels
56
functions of the liver
packages FFA into forms they can be stored or transported makes plasma proteins formes nonessential aa, deamination of aa, converts ammonia to urea stores glucose as glycogen site of gluconeogenesis (bc of its enzymes) stores certain vitamins (ADB12) stores iron as ferritin from dead RBC metabolizes toxic substances (alcohol and drugs) degrades hormones so they can be secreted
57
lipoproteins
TG and cholesterol are transported in blood as lipoproteins all contain TGs, phospholipids and cholesterol and protein but fat/protein ratios vary high lipid % = lower its density
58
types of lipoproteins
chylomicron = transorts absorbed lipids from GI tract VLDLs = very low density lipoproteins = high lipids more oily = TG from liver to tissues ** as VLDL's unload TF to tissues = becomes LDL = become more dense as losing lipids (more % proteins) LDL's = cholesterol to tissues = bad = excessive LDL's = deposition of cholesterol in blood vessel walls HDL'S = cholesterol from tissues to liver = good = transports cholesterol destined for degradation in liver (into bile)
59
cholesterol management
good goal is 200mg/dl of blood restricting dietary intake = minor effect more imp = ratio of sat to unsat fats sat = stimulates cholesterol synth and inh its secretion unsat= FA enhance secretion of cholesterol vis bile salts trans fats = even worse then sat fats, bc are oils that have been hydrogenated, promote production of LDLs + elevate blood cholesterol levels