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Metabolism 4 > Energy Balance > Flashcards

Energy Balance Flashcards

1
Q

what are the two types of fat? how are they functionally different?

A

brown and white

white- energy storage as triglyceride

brown- oxidizes FA for heat using mitochondrial uncoupling

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2
Q

how is fat energy stored?

A

triglycerides

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3
Q

how does white fat receive FAs?

A

VLDLs- liver
chylomicrons- intestines

uses lipoprotein lipase to break TGs into FAs that can be taken into cells

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4
Q

how does white fat make glycerol?

A

it needs glucose

glycolysis to DHAP

DHAP to glycerol-3-phosphate

glycerol 3 phosphate gets two acyl-CoAs esterified, forming phosphatidic acid

phosphatidic acid gets dephosphorylated to diacylglycerol

diacylglycerol is esterified w/ third acyl glycerol to TG

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5
Q

how does glucose get into adipose tissues?

A

GLUT4

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6
Q

how does TG leave the cell?

A

it gets broken down, first by adipocyte triglyceride lipase (ATGL), then Hormone sensitive lipase

both of which are regulated

finally, monoglyceride lipase frees the final FA

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7
Q

how does insulin affect adipocytes?

A

increases LPL
increases GLUT4
decreases ATGL and HSL
decreases perilipin, decreasing HSL activity

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8
Q

how is glucose uptake different in muscle and adipocytes relative to other tissues

A

in RBCs, CNS, etc., GLUT channels are always activated

muscle and fat have GLUT4, which is highly regulated by insulin

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9
Q

what property of GLUT4 does insulin regulate?

A

the amount of it expressed on the enzyme- does not regulate it affinity

causes the fusion of GLUT4 containing vesicles w/ plasma membrane

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10
Q

why do muscle cells uptake glucose?

A

to use as energy immediately or to store as glycogen

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11
Q

why do fat cells uptake glucose?

A

for fuel or to convert to glycerol for fat storage

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12
Q

describe brown fat

A

many small lipid droplets

lots of mitochondria (high oxidative capacity)

fatty acid oxidation can be uncoupled for heat (UCP)

mainly found in infants, but also in adults (cold adaptation, inverse w/ obesity)

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13
Q

describe white fat

A

one very large lipid droplet

low oxidative capacity

most FA returns to circulatoin

job is to store energy as TG

belly fat may be more dangerous than limb fat

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14
Q

what determines FA uptake one it has been removed from TG by LPL

A

concentration gradients.

  1. following a meal, the blood will have a lot of FA, and so it will push FA into cells
  2. at the same time, adipocytes will be internally creating TG, creating a low FA gradient

these two mechanisms work together

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15
Q

what hormones interact w/ perilipin and HSL?

A

perilipin and HSL are activated via phosphorylation in PKA dependent manner

PKA is caused by glucagon, catecholamines

PKA inhibited by insulin (phosphodiesterase)

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16
Q

what happens to the glycerol after it is broken down during lipolysis?

A

it leaves the cell and goes to the liver for gluconeogenesis

17
Q

describe the role of inflammation in diabetes?

A

adipocytes only make up 20-40% of cells in fat. immune cells, including macrophages, help make up the remaining cells.

when adipocytes get sufficiently enlarged, they become stressed, releasing signals that convert M2 macrophages to M1. These newly proinflammatory macrophages secrete cytokines that play a role in insulin resistance

18
Q

what mechanisms are used to regulate energy balance oh a

second to second basis

hour to hour basis

week to week basis

A
  1. phosphorylation/allostery
  2. transcription
  3. . transcription/neuronal
19
Q

describe your metabolic status prior to breakfast (healthy)

A

low insulin

low GLUT4 on membrane

low glucose uptake

increased HSL activity,
releasing FA to blood for muscle

low ACC activity- meaning

  1. low FA synthesis in liver
  2. low malonyl-CoA allows CAT allow FA oxidation

RESULT: FA oxidation is primary energy source

20
Q

describe your metabolic response to food intake (healthy)

A

high insulin

high GLUT4

high glucose uptake

low HSL and perilipin activity

high ACC activity-

  1. FA synthesis
  2. no FA oxidation

RESULT: glucose oxidation favored

21
Q

which is faster to get into circulation: glucose or FAs?

A

glucose

glucose is taken immediately to liver

FAs are taken through lymphatics to thoracic duct and hit the heart first

22
Q

how does insulin prepare the adipocytes based off the speed at which fat arrives?

A

insulin activates LPL on multiple levels: transcription, transport, processing

these take time. but FA is slow to get into the blood so the timing is apporpriate

23
Q

why are your primary uses of energy?

A

basal metabolic rate: energy to keep muscle, brain, liver, kidney, heart happy. adipose uses relatively little

physical activity

diet-induced- energy it takes to digest food

24
Q

where are the neurons responsible for appetite control found?

A

arcuate nucleus of hypothalamus 2 types

POMC- appetite suppressing
release MSH

NPY- appetite activating
1 inhibits downstream neurons that POMC neurons activate
2. inhibits POMC neurons

25
Q

how does MSH inhibit appetite

A

acitvates MC4 receptor

26
Q

what do NPY neurons respond to?

A

FAs

CAT1 is the key enzyme

low CAT1 activity decreases appetite (b/c it is caused by high malonyl-CoA levels, which exist when ACC has the resources to make fat- aka times of plenty)

high CAT1 activity increases appetite (b/c low malonyl-CoA indicates that there isn’t much excess resources to be made into fat)

27
Q

AMPK effects on appetite

A

AMPK can phosphorylate and inactivate ACC, raising the level of CAT, and thus raising appetite

28
Q

leptin

A

peptide secreted by and proportional to adipose

acts at arcuate nucleus of hypo to inhibit NPY and stimulate POMC

decreased appetite

29
Q

what are long term effects of leptin?

A

creates more POMC and less NPY synpases

30
Q

what happens when there is defective leptin?

A

morbid obesity

leptin injections can help

31
Q

what other mutations might cause phenotypes similar to leptin deficiency?

A

leptin receptor mutation

a-MSH deficiency

MC4R

32
Q

leptin as a set point and the rebounding effect

A

leptin is proportional to adipose tissue, so it acts to keep your adipose tissue in a certain range

as you diet, you lose adipose tissue, so the amount of satiation you experience after eating decreases by causing increased NPY and decreased POMC

also, the neural rewiring that occurs seems to favor weight gain over time

33
Q

ghrelin

A

peptide secreted from the stomach inversely related to stomach distension

stimulates NPY (appetite)

gastric bypass can help by reducing ghrelin levels

34
Q

endocannabinoids

A

derived from low-abundance phospholipids, acting as a paracrine factor

CB1R in hypothalamus has strong appetite inducing effect

35
Q

PPAR

A

heterodimer (RXR) transcription factors that bind FAs and exert medium to long term effects on metabolism

two types: alpha and gamma

36
Q

PPAR-a

A

expressed in liver, heart, muscle (fat burning tissues)

activates FA oxidation by increasing b-oxidation protein transcription and CAT 1 and 2

binds fibrate ligands

37
Q

fibrate

A

bind PPAR-a to increase FA utilization

38
Q

PPAR-y

A

expressed in adipocytes and activates adipogenesis and FA uptake

binds thiazolidinedione (TZD)

39
Q

TZD

A

binds PPAR-y- insulin sensitizer

side effect can be weight gain

Metabolism 4 (5 decks)

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