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Cellular Biochemistry > Chapter 19 > Flashcards

Chapter 19 Flashcards

(50 cards)

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1
Q

What organ is specialized for Gluconeogenesis
Ketogenesis
Urea Production

A

Liver

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2
Q

Where is glycogen stored

A

Liver/muscle, when fed

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3
Q

Kidney:

A

Glutamine –> alpha-ketoglutarate –> glucose

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4
Q

Fasting/Starving: How does liver make ketone bodies?

A

Triacylglycerols –> acetyl-CoA –> Ketone Bodies

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5
Q

Cori Cycle

A

Cori cycle transfers free energy from liver to muscles

Waste disposal
Lactate dehydrogenase, reversible

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6
Q

Glucose-Alanine Cycle

A

transport nitrogen from muscles to liver.

Pyruvate –> Alanine

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7
Q

Why is insulin released?

A

In response to glucose

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8
Q

Insulin receptor is an

A

RTK, not a lot of questions, that would be chapter 10 review

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9
Q

Unique about glucokinase (insulin) Glucose –> G6P?

A

sigmodial curve, yet 1 active site

substrate-induced conformational change: at end of catalytic cycle, enzyme briefly maintains high affinity for next glucose molecule.

Increase glc uptake > insulin release
High Km, sensitive to glc
Glucokinase- pancreatic glucose sensor

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10
Q

Is glucokinase only pancreatic glucose sensor?

A

Yes → mutations in gene causes rare form of diabetes

No → Other cellular factors:
Mitochondria of beta cells
Mitochondrial NAD+/NADH or ADP/ATP ratios

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11
Q

Insulin action in muscle

A

+: glucose uptake and glycogen synthesis

-: glycogen breakdown

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12
Q

Insulin action in Adipose tissue

A

+: extracellular lipoprotein lipase/acetyl-CoA carboxylase
+: triacylglycerol synthesis
-: lipolysis

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13
Q

Insulin in liver

A

+: glycogen/triacylglycerol synthesis

-: gluconeogenesis

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14
Q

Insulin =

A

fuel abundance, decreases metabolism of stored fuel, promotes fuel storage

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15
Q

Insulin’s Vmax for glucose increases because…

A

insulin increases number of transporters at cell surface.

Increase GLUT4 passive receptors

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16
Q

Insulin activates extracellular

A

lipases, hydrolyze triacylglycerols so fatty acids can be taken up and stored

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17
Q

Glycogen synthase

A

Homodimer
+: G6P
Phosphorylation deactivates
Dephosphorylation activates

UDP-glucose + glycogen (n residues) → UDP + glycogen (n+1 residues)

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18
Q

Glycogen Phosphorylase: Phosphorolysis

A

Heterodimer
+: AMP
-: ATP

Phosphorylation activates
Dephosphorylation deactivates

Glycogen (n residues) + Pi → glycogen (n-1 residues) + G1P
(G1P ←PHOSPHOGLUCOMUTASE→ G6P, 1st glycolysis intermediate)

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19
Q

Primary mechanism for regulating glycogen synthase/phosphorylase is through ______________________ (phosphorylation/dephosphorylation) under HORMONE CONTROL. Both enzymes undergo reversible phosphorylation at specific _______

A

Covalent modification

Serine residues

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20
Q

Insulin activates phosphatases

A

Dephosphorylation
Activate- glycogen synthase
deactivate- glycogen phosphorylation

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21
Q

`What does liver use to opposed insulin and trigger fuel metabolism?

Study These Flashcards
A

Norepinephrine/Epinephrine and Glucagon

22
Q

Glucagon/Epinephrine/Norepinephrine bind to receptors with

Study These Flashcards
A

7 membrane-spanning segments.

Hormone binds → conformation changes that activates G protein → adenylate cyclase → cAMP → PKA

23
Q

Glucagon functions

Study These Flashcards
A

Stimulates liver to generate glucose by glycogenolysis and gluconeogenesis
Stimulates lipolysis in adipose tissue

24
Q

Muscle cells don’t have glucagon

Study These Flashcards
A

They do, however, response to catecholamines, which have same overall effects as glucagon.
Epinephrine/Norepinephrine stimulation of muscle cells: activates glycogenolysis, which makes more glucose available to power muscle contraction

25
PKA phosphorylates hormone-sensitive lipase
Catalyzes rate limited step of lipolysis (triacylglycerols → diacylglycerols → monoacylglycerols → fatty acids) Hormone stimulation not only increases the lipase catalytic activity, also relocates the lipase from cytosol to the fat droplet of the adipocyte. Co-localization with substrate (possibly by interactions w/lipid-binding protein) boosts fatty acid mobilization rate.
26
Adiopectin
Adipose Tissue Activates AMPK (promotes fuel catabolism)
27
Resistin
Adipose Tissue | Blocks insulin activity
28
Leptin
Adipose Tissue | Signals fullness
29
Amylin
Pancrease | Signals fullness
30
Neuropeptide Y
Hypothalamus | +Stimulates Appetite
31
Ghrelin
Stomach | +: Stimulates Appetite
32
Cholecystokinin/PYY
Intestine | -: Suppresses appetite
33
Incretin
Intestine | Promotes insulin release, inhibits glucagon release
34
What do AMP-dependent protein kinases do?
Act as fuel sensor
35
AMP-dependent protein kinase
REgulated by thronine phosphorylation If fuel levels insufficient, ATP binds to regulatory component, blocks phosphorylation. Blocks activity ADP-prevents dephosphorylation ATP inhibits it. If no ATP, switches on ATP producing pathways
36
AMP PK effects
hypothalamus- increase food intake Liver: glycolysis and fatty acid oxidation No glycogen/gluconeogenesis Muscle: Fatty acid oxidation/mitochondrial biogenesis Adipose Tissue: Increase lipolysis Decrease fatty acid synthesis
37
Why does insulin secretion cease with the drop in circulating glucose?
Glucose will be available for brain
38
How do liver and kidneys respond to continued demand for glucose?
increasing the rate of gluconeogenesis, using noncarbohydrate precursors such as amino acids (derived from protein degradation) and glycerol (from fatty acid breakdown)
39
Fasting burns more...
Fatty acids
40
body weight that remains constant and independent of energy intake/expenditure even over many decades.
Set point Regulated by leptin
41
named for its high mitochondrial content, is specialized for generating heat to maintain body temperature.
Brown adipose tissue Norepinephrine- binds to receptors on brown adipocytes, signal transduction to PKA activates lipase that frees f.a. From triacylglycerols. UCP in brown adipose tissue allows fuel oxidation w/out ATP More brown=less obese
42
Type 1 (juvenile or insulin-dependent): Type 2 (adult or non-insulin-dependent):
Immune system destroys pancreatic beta cells Insulin resistance- failure of body to respond to normal or even elevated concentrations of the hormone
43
high levels of glucose in blood. Loss of responsiveness of tissues to insulin = cells fail to take up glucose
Hyperglycemia Insulin insensitivity
44
Glucose + NADPH + H⁺ ---ALDOSE REDUCTASE→ Sorbitol + NADP⁺
Sorbitol accumulation and disruption of osmotic balance; renal stress; protein precipitation leads to cataracts
45
Diabetic Ketoacidosis:
Uncontrolled diabetics also metabolics fatty acids instead of carbs, resulting in over production of ketone bodies.
46
Metabolic syndrome
set of symptoms, including obesity and insulin resistance, that appear to be related. High proportion of visceral fat (decreased leptin and adiponectin, increased resistin) TNFa promotes inflammation, insulin insensitivity B cell exhaustion from overstimulation impaired GLUT4 translocation increase in liver gluconeogenesis
47
Warburg effect
aerobic glycolysis Cancer cells have oxidative phosphorylation, but consume glucose and waste is lactate. Why? Make precuors for cell growth
48
How does glutamine support cancer growth?
Provides the nitrogen Converts to other stuff CAC flux increases
49
What is a control point for cancer metabolism?
Glutamate dehydrogenase Activated by ADP/Leucine Inhibited by GTP/Palmitoyl-CoA
50
Extreme loss of weight/muscle in cancer patients, only cure is food. White fat to brown
Cachexia

Cellular Biochemistry (15 decks)

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