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Biochem 385 Unit 2 > Lecture 26: Metabolic Integration: Physiology > Flashcards

Lecture 26: Metabolic Integration: Physiology Flashcards

1
Q

metabolic homeostasis

A

metabolite levles maintained by reg system

LIVER

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2
Q

Addipose tissue

A

endocrine organ: controlls fatty acid homeostasis

nrg storage

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3
Q

metabolic adaptations to starvation:

A

inc in gluconeogensis

switch to dependency of fatty acids as major nrg source

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4
Q

what’s so special about the liver?

A

it can preform all synth and degredation reactions

metabolic control of carbohydrate, lipid, amino acid metabolism, control of oxidative phosphorylation

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5
Q

other cells (not in liver)

A

mostly limited to catabolizing glucose and FA to make ATP throuh oxidative phosphorylation

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6
Q

What does the liver do?

A

processes fats, carbs, proteins (dietary)
synth and distribute lipids, ketone bodies, glucose
converts nitrogen to urea

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7
Q

glucose-6-phosphate

A 
central metabolite!!!
used in glycolytic pathway
makes lipids, OAA, ketones
makes glycogen
used in PPP

can ALL HAPPEN IN THE LIVER

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8
Q

what biochemical mechanisms determine glucose-6P flux through these pathways?

A

enzyme activity

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9
Q

what can glucose-6P be converted to?

A

glucose 1P (glyc synth)
glucose (go to blood)
fructose 6P: (glycolysis)
6-phosphogluconate (PPP)

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10
Q

Metabolic functions of skeletal muscles: resting

A

uses fatty acid release from adipose tissue as nrg

b/c ATP needs to be used during contraction

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11
Q

Metabolic functions of skeletal muscles: contracting

A

use intracellular ATP pool

ATP hydrolysis for myosin/actin interactions

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12
Q

replinishing ATP pool for skeletal muscle

A

replinished by phosphoryl transfer: use creatine kinase to make
PHOSPHOCREATINE

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13
Q

PHOSPHOCREATINE

A

can replinish ATP pools for a few seconds of intense activity
directly converts ADP to ATP

pool of PHOSPHOCREATINE gets rebuilt during rest

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14
Q

Adipose tissue

A 
endocrine organ
secretes adipokines (peptide hormone)
regulate fatty acid secretion and circulation
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15
Q

visceral fat

A

belly region
surrounds and cushions organs
very metabolically active: Releases lots of adipokines
high CVD risk

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16
Q

subcutaneous fat

A

less metabolically active
more distance from organs
stored beneath skin

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17
Q

BMI

A

weight/height^2

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18
Q

waist/hip ration (WHR)

A

may be better predictor of CVD than BMI
may not be

maybe we just can’t really tell well whose at risk for CVD

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19
Q

Metabolic functions of adipose tissue

A

regulates triacylglycerol cycle (circulates FAs between adipose and liver)
this is done by adipokines im pretty sure

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20
Q

triacylglycerol cycle

A

circulates fatty acids and glycerols between adipose tissue and liver
so that they can circulate through the blood (liver so they can be remade into triacylglycerols)

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21
Q

What is the metabolic logic of maintaining circulating fatty acids even though 75% of it is returned to adipose tissue and stored?

A

when you need it, its available!

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22
Q

what’s the primary nrg source for brain?

A

glucose
half of it is used by sodium potassium ion transporter
FATTY ACIDS ARE NOT USED IN THE BRAIN

23
Q

what can/can’t cross blood brain barrier

A

glucose and ketone bodies can

fatty acids can’t

24
Q

what are the two metabolic fuels exported by the liver

A

glucose

triacylglycerol

25
Q

metabolic homeostasis

A

maintain balance in the body
requires:
neuronal signaling from brain
release of small molecules into blood (ligands for cell signaling)

26
Q

why are glucagon and insulin call the ying and yang of homeostasis?

A

they balance each other

complementary and opposing actions

27
Q

what causes type 1 diabetes

A

may lack beta cells

28
Q

where are glucagon and insulin made

A

pancreas, islets of Langerhans
alpha cells: glucagon
beta cells: insulin
delta cells: somatostatin

29
Q

effects of Insulin and Glugacgon signaling on Liver

A

G: stim glucose export
I: Stim glucose uptake (glycolysis, glyc synth, FA sytn)

30
Q

effects of Insulin and Glugacgon signaling on skeletal muscle

A

G: No effect
I: stim glucose uptake by inc glucose transporters, glycolysis, glyc synth

31
Q

effects of Insulin and Glugacgon signaling on adipose

A

G: stim fatty acid export
I: stim glucose uptake (transporter levels), inc FA synth, activate FA uptake

32
Q

effects of Insulin and Glugacgon signaling on brain

A

G: No effect
I: stim nueronal signaling to DECREASE eating, INCREASE nrg expendature

33
Q

Glucagon circulates through the body, why does it have no effect in muscle and brain tissue?

A

skeletal and brain tissues need to use glucose themselves! no need for export!

liver and adipose export glucose and fatty acid for use by rest of body

glucagon still signals in these tissues, they just don’t respond

34
Q

PPAR proteins

A 
transcriptional regulators
in cell nucleuses
respond to fatty acids and ecosinods
maintain homeostasis
Lipid activated
35
Q

PPAR alpha

A

Fatty acid ox proteins stimulated
in muscle and liver
fasting response in liver

36
Q

PPAR delta

A

fatty acid ox in fat and muscle

produces UPC

37
Q

PPAR Gamma

A

activity in adipose, liver, and muscle
whole body insulin sensitivity
lipogenesis and storage
adipogenesis

38
Q

PPAR activations

A

Lipid activated!
if fatty acid derived molecs around and bind, they can go to nucleus
PPARs regulate gene expression
get enzymes in to respond to the lipid appropriately

39
Q

Why is PPAR imporant to us?

A

drug target for diabetes

try to control adipocyte differntiation and lipid synth in adipose tissue (PPAR gamma)

40
Q

TZDs

A

improve insulin sensitivity in type 2 diabetics

activate PPAR gamma target genes involved in lipid synth

41
Q

side effects of TZDs

A

water retention

liver damage

42
Q

why do diabetics who are treated with TZDs see a drop in blood glucose levels but also weight gain

A

stimulate lipogenesis and adipogenesis

the glucose is being used, but its being used to make fat for storage

43
Q

Metabolic adaptation to starvation

A

alter flux of metabolites between various tissues
provide glucose to brain (most important)
RBCs also need glucose–they have no mitochodria and can’t generate ATP

44
Q

why can’t RBCs utilize fatty acids as an energy source?

A

no mitochondria to break down fats!

45
Q

Short term starvation (24 hrs) vs. long term

A

24 hrs: glycogen and glucose levels drop like crazy, FA and ketone bodies inc
DAYs: glucose levels stabilize, FA and ketone bodies inc

46
Q

2 major adaptations to short term starvation

A
  1. inc gluconeogenesis so we have enough glucose

2. switch to fatty acids as fuel

47
Q

Why is ketogenesis stimulated?

A

we have lots of acetyl-CoA and not much OAA

acetyl CoA: b/c its released during fatty acid oxidation

48
Q

Why store nrg as fat rather than just glycogen?

A

fat has a lot more nrg, longer survival time, weighs less

49
Q

What is the stored nrg potential in kJ/g of glycogen and tiracylglycerols based on dry weight data (1cal=2.18 kJ)

A

TAGs=141,000 Cal/15,000g= 9.4 Cal/g=39.3 kJ/g

Glycogen=900Cal/220 g= 4.1 Cal/g= 17.1 kJ/g

50
Q

Which is more reduced: 1 mole of Palmitate (C18) or 3 moles of C6 glucose (C18)

A

palmitate

because of beta ox reactions

51
Q

If the nrg equivalent of 15 kg of fat in a 70 kg man were stored as glycogen: what is is total mass?

A

nrg ratio: 39.9/17.1= 2.3X more/g
15 kg fat * 2.3= 34.5 kg glycogen
REMEMBER GLYCOGEN HAS 2g water/1 g glycogen!!!!!!
so 34.5 kg + (2*34.5 kg)= 103.5 kg stored glycogen and water (almost 7X more mass required to store nrg as glycogen in this case)

so 70kg + 103.5 kg= 158.8 kg

52
Q

study slide 25!!!!!!!!!!!!!!!

A

study slide 25!!!!!!!!!!!!!!!

53
Q

Long term starvation (4 things happen)

A

only need major functions. 4 things happen
1. triacylglycerol hydrolysis from adipose tissue goes up (Release FA to fuel tissues)
2. Liver gluconeogenesis (and kidney) INC to supply body with glucose (to fuel brain)
3. ketone bodies–produced by liver: INC ketogensis in liver
ketone bodies go to heart and brain
4. protein degredation in muscle tissues: we need the carbon for the metabolites to make nrg (lose muscle mass)

Biochem 385 Unit 2 (13 decks)

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