Lecture 4 Flashcards

1
Q

Where is lipoprotein lipase absent

A

brain and liver

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2
Q

Where is LPL attached to?

A

sulfate proteoglycan on surface of capillary endotheliium

which chylomicrons bind to as they pass

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3
Q

When chylomicrons bind to LPL as they pass through sulfate proteoglycan on surface of capillary endothelium; the TG are hydrolyzed to what?

what happens to them?

A

FFA and 2-Monoacylglycerols

They diffuse freely into tissues

Each tissue has its own isoenzyme of LPL

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4
Q

Does LPL activity increase or decrease in fasting state?

A

Decrease

Except in skeletal muscle and myocardium; they stay moderate in either state

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5
Q

Following a fatty meal TG’s enter where?

A

adipocytes

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6
Q

In the transition period between meal and fasting TG’s are sent where?

A

Skeletal muscle and myocardium

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7
Q

What solubilizes LPL when injectedin skin?

A

Heparin, increasing LPL activity

The assessment is based on serumlipase activity level pre/and post heparin injection

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8
Q

When TAG is hydrolyzed and a glycerol is released, it does what?

A

Provides substrate for gluconeogenesis

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9
Q

What’s the primary regulation of gluconeogenesis

A

Availibility of substrates (glycerol)

Circulating level of glucagon

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10
Q

What’s the secondary regulation of gluconeogenesis?

A

Adaptive changes in the rate of enzyme synthesis, degradation or both

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11
Q

How many amino acids in glucagon?

Is it alpha or beta?

It’s made as a large precursor and converted to glucagon how?

A

29

alpha

By series of proteolytic enzyme cleavage

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12
Q

What’s the role of glucagon?

A

maintain normal blood glucose level

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13
Q

Epinephrine and Norepinephrine is made where?

A

Adrenal medulla which is mediated by autonomic nervous system

and triggered by Hypothalamic glucoreceptors

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14
Q

Cortisol is made where?

A

Adrenal Zona Fasciculata and Reticularis

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15
Q

What triggers growth hormone

A

adrenal corti co tropic hormone & anterior pituitary glands stored in somatotroph cells

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16
Q

What secretes norepinephrine?

A

Pancreatic symppathetic innervations in adrenal medulla

17
Q

What stimulates glucagon?

A

Low blood glucose (rises at night due to overnight fast)

AA in meals (stimulates insulin too)

IMplication in diabetes therapy (Byetta=exenatide

EPI/NorEPI

18
Q

During severe exercise what happens?

A

EPI overrides inhibitory effects of substrates and glucagon will remain high

19
Q

What inhibits glucagon?

A

elevated glucose

elevated insulin

20
Q

What does glucagon do to lipids?

A

stimulate liver oxidation of FA and the product of ketones via acetyl-CoA

minimal effect on adipocytes

21
Q

What does GLucagon do to carbs?

A

Increases blood glucose via mobilization of liver glycogen and increase gluconeogenesis (not muscle stored glycogen)

22
Q

Free glycerol from adipocytes ends up where? What happens to it?

A

LIver

Glycerol kinase turns glycerol into glycerol phophate (GPO4) where it is oxidized by dehydrogenase to turn to dehydroxyacetone phosphate

23
Q

What can’t adipocytes metabolize glycerol?

A

They lack glycerol kinase thus not being able to phosphorylate glycerol

24
Q

WHat are irreversible steps of gluconeogenesis?

A

Glucose 6 phophatase

Fructose 1,6 Bisphophatase

Pyruvate carboxylase

Phosphoenolpyruvate carboxykinase

25
Q

In gluconeogensis What is the irreversible step of phosphofructokinase-1 in glycolysis?

A

D-Fructose 1,6bisphophate is hydroylyzed in the next step by fructose 1,6 bisphophatase

26
Q

Because adipocytes lack glycerol kinase they cannot phosphorylate and sent to liver where what happens?

A

Glycerol is phophorylated making Glycerol 3 P which; forms TAG or convert to DHAP by G3P dehydrogenase

27
Q

What signals low energy state?

A

High AMP/ADP

28
Q

AMP/ADP inhibit what?

A

Fructose 1,6 bisphosphatase but activates 1,6 phophofructokinase

29
Q

What activates fructose 1,6 bisphosphatase?

A

HIgh citrate

30
Q

What stimulates GLuconeogenesis?

A

High ATP and citrate levels and low amp