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Biochemistry 2 > Tissue specific metabolism > Flashcards

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
Muscles can maintain temperature through
Vigorous contraction->shivering thermogenesis
26
What happens in muscles during recovery through activity
Lactate is converted to glucose in liver (kori cycle) Creatine ->phosphocreatine
27
What metabolism is carried by cardiac muscles
Aerobic Mainly FAs, but can also use ketone bodies and glucose
28
What cellular structure is abundant in cardiac muscles
Mitochondria
29
Comparing to skeletal muscles, cardiac muscles have less
Stored glycogen
30
Cardiac muscles are sensitive to
O2 deprivation
31
Neurons are highly dependent on
Glucose energy
32
How many grams of glucose neurons use every day
130 grams
33
Atp is used fr what in neuron
To maintain membrane potential (Na+ K+ATPase)
34
Apart form glucose, neurons can use
Beta-hydroxybutyrate
35
What are astrocytes and what so they use
star-shaped glial cells in the brain and spinal cord. They use FA
36
Does brain store glycogen?
No
37
What metabolism is performed by FAs
Aerobic
38
What fuel is used by neurons during fasting/starvation
``` Ketone bodies (from FA) Glucose (from muscle protein) ```
39
What happens immediately after meal
Glucose level rise | Glycolysis and glucogenesis rise ( insulin levels rise)
40
What happens 2 hours post-prandial
Glucose begins to drop | Liver glycogen releases glucose (glucagon)
41
What happens 4 hours post-prandial
More glucagon | More TAG hydrolysis, FA become major fuel
42
Metabolism in prolonged fasting
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
Does fat accumulation lead to more energy source during starvation?
Ketone bodies accumulation-> toxic-> fat people will not starve longer
44
T1DM are due to and develops when
Due to autoimmune destruction of Beta-cells->insufficient production of insulin Develops early in life
45
T2DM are due to and develops when
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
What is the purpose of INSR signalling
Usually regulate gene expression that is needed for inflammation, stimulated of cytokines
47
Cytokines influence what mechanism
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
Inflammatory cytokines are coming from
Adipose tissue
49
How Inflammatory cytokines pathway can influence RTK
SOC 1 and 3 can inhibit phosphorylation of IRS by insulin receptor-> insulin resistance-> no GLUT 4 brought
50
In both types of diabetes what are the consequences to metabolism
Blood glucose is high Increased osmolarity-excessive urination and thirst Proteins get glycosylated-> inhibits protein activity
51
In T1DM, fat breakdown accelerated, because there is not enough glucose for energy-> high ketone bodies. What is the effect
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
Untreated T1DM leads to
Dramatic weight loss
53
Adipose tissue is ___ organ
Endocrine
54
Adipose tissue release
Adipokines- one of the main leptin hormones, another one is adiponectin
55
Adipokines: role
Carry info about fuel stores to brain
56
The difference between anorexigenic neurons and orexigenic neurons
Anorexigenic- less eating, more burning Orexigenic neurons- less energy expenditure, more eating
57
What are stimulators and inhibitors for anorexigenic protons
Leptin No inhibitor
58
What are stimulators and inhibitors for orexigenic protons
Inhibitor:leptin, insulin, hormone from gut (satiety signals) Stimulator:ghrelin(stomach) hunger signals
59
Leptin ___ appetite
Reduces
60
What were the mice that had ob/ob-obesity gene
Ate continually, obese, elevated cortisol, shivered, infertile, insulin resistance, died early
61
What happened to mice with leptin injected into obese mice
The mice lost weight, temperature returned to normal
62
Did leptin injection helped obese people?
No, they have higher leptin levels ( not deficiency)-> leptin resistance
63
Leptin resistance ultimately leads to
Diabetes
64
What does db gene encodes
Leptin receptor in brain, expressed mostly in hypothalamus ( functions in food intake and fertility)
65
There are ghrelin receptors are in
Brain, heart, adipose tissue
66
Ghrelin works through what mechanism
GPCR to increase sensation of hunger
67
PYY is
An appetite-suppressing hormone
68
Why PYY peptide is called like that
36 AA with two Tyr (Y) residues in the end
69
PYY secreted from
The small intestine and colon
70
PYY results in
Reduced hunger Inhibits release of NPY - stops oroxigenic neurons
71
Obese and lean people have
Microbiota
72
How microbiota can affect adipose tissue
Most bacterial products are short chain FAs Propionate acts through GPCR 43 and 41-> stimulates adipocyte differentiation and inhibits lipolysis
73
Lipid burden hypothesis link between Obesity and T2DM
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

Biochemistry 2 (17 decks)

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