Tissue specific metabolism Flashcards

1
Q

Hepatocytes metabolize what nutrients

A

CHO, AA, lipids

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2
Q

What are the functions of liver

A

Provides energy precursors to all tissues

Maintains balance between nutrient supply and precursor demand

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3
Q

Nutrient supply and precursor requirement varies

A

Nutrient: varies with diet and feeding

Precursors: varies with level of activity and health

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4
Q

enzymes in liver are sensitive to

A

Various hormones

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5
Q

Liver has a flexibility in

A

Enzymatic machinery

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6
Q

White Adipose tissue (WAT) are situated

A

Under skin, around major blood vessels and abdomen

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7
Q

What are adipocytes

A

One lipid droplet

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8
Q

Energy source for WAT

A

glucose

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9
Q

WAt can do what

A

Capable of FAs synthesis from glucose- insulin sensitive

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10
Q

WAT is the major storage of

A

TAG

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11
Q

How do get TAG from WAT

A

Hydrolysis to NEFA (epinephrine sensitive)

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12
Q

where BAT are

A

Under skin (chest and back)

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13
Q

Who has BAT

A

Only in children ,not adults, but new studies have shown can be found in adult also

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14
Q

Why BAT are brown

A

Many mitochondria and high blood supply

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15
Q

How many droplets BAT has

A

Many

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16
Q

What is the energy source for BAT

A

Fatty acid through beta-oxidation

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17
Q

Major role of BAt

A

Non-shivering thermogenesis- thermogenin (UPC1)-> maintain body temperature

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18
Q

How can we get BAT

A

Preadipocytes can differentiate into BAT in adults during chronic cold exposure

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19
Q

Muscles can use what fuel

A

Resting state: FA from adipose and ketone bodies from liver

Moderate: Blood glucose(aerobic glycolysis) in addition to FA and ketone bodies

Vigorous: stored glycogen gives glucose

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20
Q

Each glycogen origin glucose give how many ATPs

A

3

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21
Q

The result of anaerobic glucose metabolism is

A

Lactic acid

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22
Q

What is the additional pathway in muscles for ATP

A

Phosphocreatine

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23
Q

How can we synthesize creatine

A

Dietary
OR
De novo (glycine, arginine, methionine)

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24
Q

What hormone helps in using glucose from blood and glycogen

A

Epinephrine

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25
Q

Muscles can maintain temperature through

A

Vigorous contraction->shivering thermogenesis

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26
Q

What happens in muscles during recovery through activity

A

Lactate is converted to glucose in liver (kori cycle)

Creatine ->phosphocreatine

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27
Q

What metabolism is carried by cardiac muscles

A

Aerobic

Mainly FAs, but can also use ketone bodies and glucose

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28
Q

What cellular structure is abundant in cardiac muscles

A

Mitochondria

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29
Q

Comparing to skeletal muscles, cardiac muscles have less

A

Stored glycogen

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30
Q

Cardiac muscles are sensitive to

A

O2 deprivation

31
Q

Neurons are highly dependent on

A

Glucose energy

32
Q

How many grams of glucose neurons use every day

A

130 grams

33
Q

Atp is used fr what in neuron

A

To maintain membrane potential (Na+ K+ATPase)

34
Q

Apart form glucose, neurons can use

A

Beta-hydroxybutyrate

35
Q

What are astrocytes and what so they use

A

star-shaped glial cells in the brain and spinal cord.

They use FA

36
Q

Does brain store glycogen?

A

No

37
Q

What metabolism is performed by FAs

A

Aerobic

38
Q

What fuel is used by neurons during fasting/starvation

A
Ketone bodies (from FA)
Glucose (from muscle protein)
39
Q

What happens immediately after meal

A

Glucose level rise

Glycolysis and glucogenesis rise ( insulin levels rise)

40
Q

What happens 2 hours post-prandial

A

Glucose begins to drop

Liver glycogen releases glucose (glucagon)

41
Q

What happens 4 hours post-prandial

A

More glucagon

More TAG hydrolysis, FA become major fuel

42
Q

Metabolism in prolonged fasting

A

Glucose is at the minimal levels

FAs are depleting fast

Non-essential AAs are deaminoated and the carbon backbone can enter TCA cycle and lead to oxaloacetate-> glucoenogenesis->glucose dependent cells

beta-oxidation pathway->accumulation of acetyl-CoA->ketogenic pathway, because oxaloacetate is depleted-> no TCA

43
Q

Does fat accumulation lead to more energy source during starvation?

A

Ketone bodies accumulation-> toxic-> fat people will not starve longer

44
Q

T1DM are due to and develops when

A

Due to autoimmune destruction of Beta-cells->insufficient production of insulin

Develops early in life

45
Q

T2DM are due to and develops when

A

Usually develops in late adulthood

Cells do not respond appropriately to insulin

Typically INSR signaling is affected ->IRS proteins are dephosphorylated

GLUT4 is trapped inside of the cells in cytoplasm

46
Q

What is the purpose of INSR signalling

A

Usually regulate gene expression that is needed for inflammation, stimulated of cytokines

47
Q

Cytokines influence what mechanism

A

JAK-STAT mechanism

JAK-protein
STAT-TF
This mechanism influence SOC 1 and 3 and they help to regulate the pathway of inflammatory cytokines

48
Q

Inflammatory cytokines are coming from

A

Adipose tissue

49
Q

How Inflammatory cytokines pathway can influence RTK

A

SOC 1 and 3 can inhibit phosphorylation of IRS by insulin receptor-> insulin resistance-> no GLUT 4 brought

50
Q

In both types of diabetes what are the consequences to metabolism

A

Blood glucose is high

Increased osmolarity-excessive urination and thirst

Proteins get glycosylated-> inhibits protein activity

51
Q

In T1DM, fat breakdown accelerated, because there is not enough glucose for energy-> high ketone bodies. What is the effect

A

Raise in blood H+, leads to ketoacidosis

Bicarbonate buffering system (RBCs) is activated, leads to altered breathing pattern-> accelerated breathing

Acetone breathe, because of break down of acetoacetate to acetone

52
Q

Untreated T1DM leads to

A

Dramatic weight loss

53
Q

Adipose tissue is ___ organ

A

Endocrine

54
Q

Adipose tissue release

A

Adipokines- one of the main leptin hormones, another one is adiponectin

55
Q

Adipokines: role

A

Carry info about fuel stores to brain

56
Q

The difference between anorexigenic neurons and orexigenic neurons

A

Anorexigenic- less eating, more burning

Orexigenic neurons- less energy expenditure, more eating

57
Q

What are stimulators and inhibitors for anorexigenic protons

A

Leptin

No inhibitor

58
Q

What are stimulators and inhibitors for orexigenic protons

A

Inhibitor:leptin, insulin, hormone from gut (satiety signals)
Stimulator:ghrelin(stomach) hunger signals

59
Q

Leptin ___ appetite

A

Reduces

60
Q

What were the mice that had ob/ob-obesity gene

A

Ate continually, obese, elevated cortisol, shivered, infertile, insulin resistance, died early

61
Q

What happened to mice with leptin injected into obese mice

A

The mice lost weight, temperature returned to normal

62
Q

Did leptin injection helped obese people?

A

No, they have higher leptin levels ( not deficiency)-> leptin resistance

63
Q

Leptin resistance ultimately leads to

A

Diabetes

64
Q

What does db gene encodes

A

Leptin receptor in brain, expressed mostly in hypothalamus ( functions in food intake and fertility)

65
Q

There are ghrelin receptors are in

A

Brain, heart, adipose tissue

66
Q

Ghrelin works through what mechanism

A

GPCR to increase sensation of hunger

67
Q

PYY is

A

An appetite-suppressing hormone

68
Q

Why PYY peptide is called like that

A

36 AA with two Tyr (Y) residues in the end

69
Q

PYY secreted from

A

The small intestine and colon

70
Q

PYY results in

A

Reduced hunger

Inhibits release of NPY - stops oroxigenic neurons

71
Q

Obese and lean people have

A

Microbiota

72
Q

How microbiota can affect adipose tissue

A

Most bacterial products are short chain FAs

Propionate acts through GPCR 43 and 41-> stimulates adipocyte differentiation and inhibits lipolysis

73
Q

Lipid burden hypothesis link between Obesity and T2DM

A

Obesity leads to diabetes

As a person starts accumulating fat->MCP-1 is secreted acts as a trigger for macrophages-> accumulation of macrophages in adipose tissue->proinflammatory hormones (TNF)-> increased release of FAs-> accumulation of FAs in circulation->ectopic lipid interference with GLUT4->inhibit the signaling of bringing GLUT 4 to the surface