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Cellular Biochemistry > Chapter 19 > Flashcards

Chapter 19 Flashcards

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?

A

Norepinephrine/Epinephrine and Glucagon

22
Q

Glucagon/Epinephrine/Norepinephrine bind to receptors with

A

7 membrane-spanning segments.

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

23
Q

Glucagon functions

A

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

24
Q

Muscle cells don’t have glucagon

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
Q

PKA phosphorylates hormone-sensitive lipase

A

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
Q

Adiopectin

A

Adipose Tissue

Activates AMPK (promotes fuel catabolism)

27
Q

Resistin

A

Adipose Tissue

Blocks insulin activity

28
Q

Leptin

A

Adipose Tissue

Signals fullness

29
Q

Amylin

A

Pancrease

Signals fullness

30
Q

Neuropeptide Y

A

Hypothalamus

+Stimulates Appetite

31
Q

Ghrelin

A

Stomach

+: Stimulates Appetite

32
Q

Cholecystokinin/PYY

A

Intestine

-: Suppresses appetite

33
Q

Incretin

A

Intestine

Promotes insulin release, inhibits glucagon release

34
Q

What do AMP-dependent protein kinases do?

A

Act as fuel sensor

35
Q

AMP-dependent protein kinase

A

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
Q

AMP PK effects

A

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
Q

Why does insulin secretion cease with the drop in circulating glucose?

A

Glucose will be available for brain

38
Q

How do liver and kidneys respond to continued demand for glucose?

A

increasing the rate of gluconeogenesis, using noncarbohydrate precursors such as amino acids (derived from protein degradation) and glycerol (from fatty acid breakdown)

39
Q

Fasting burns more…

A

Fatty acids

40
Q

body weight that remains constant and independent of energy intake/expenditure even over many decades.

A

Set point

Regulated by leptin

41
Q

named for its high mitochondrial content, is specialized for generating heat to maintain body temperature.

A

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
Q

Type 1 (juvenile or insulin-dependent):

Type 2 (adult or non-insulin-dependent):

A

Immune system destroys pancreatic beta cells

Insulin resistance- failure of body to respond to normal or even elevated concentrations of the hormone

43
Q

high levels of glucose in blood. Loss of responsiveness of tissues to insulin = cells fail to take up glucose

A

Hyperglycemia

Insulin insensitivity

44
Q

Glucose + NADPH + H⁺ —ALDOSE REDUCTASE→ Sorbitol + NADP⁺

A

Sorbitol accumulation and disruption of osmotic balance; renal stress; protein precipitation leads to cataracts

45
Q

Diabetic Ketoacidosis:

A

Uncontrolled diabetics also metabolics fatty acids instead of carbs, resulting in over production of ketone bodies.

46
Q

Metabolic syndrome

A

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
Q

Warburg effect

A

aerobic glycolysis

Cancer cells have oxidative phosphorylation, but consume glucose and waste is lactate. Why? Make precuors for cell growth

48
Q

How does glutamine support cancer growth?

A

Provides the nitrogen
Converts to other stuff
CAC flux increases

49
Q

What is a control point for cancer metabolism?

A

Glutamate dehydrogenase

Activated by ADP/Leucine
Inhibited by GTP/Palmitoyl-CoA

50
Q

Extreme loss of weight/muscle in cancer patients, only cure is food. White fat to brown

A

Cachexia

Cellular Biochemistry (15 decks)

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