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Drew 922 > Block 3 Lecture 4 -- Hormonal Regulation of Fuel Metabolism > Flashcards

Block 3 Lecture 4 -- Hormonal Regulation of Fuel Metabolism Flashcards

1
Q

What tissue-specific hormone receptors are present in the liver?

A

1) GLUT-1
2) alpha-adrenergic
3) beta-adrenergic
4) glucagon

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2
Q

What tissue-specific hormone receptors are present in the muscle?

A

1) GLUT-4
2) beta-adrenergic
3) insulin

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3
Q

Typical FPG?

A

80-100 mg/dL

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4
Q

Typical post-prandial [glucose]?

A

120-140 mg/dL

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5
Q

MW of glucose?

A

180 g/mol

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6
Q

What happens if glucose < 80 mg/dL?

A

coma, death, hemolysis

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7
Q

What are the consequences of not storing fat?

A

1) atherosclerosis, LDL = stroke, MI

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8
Q

What happens if too much fat is stored?

A

fat-only catabolism

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9
Q

What are the functions of insulin?

A

1) promotes nutrient storage
2) anabolic for blood proteins
3) promotes utilization of glucose for fuel

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10
Q

What are insulin’s nutrient storage effects?

A

1) glycogen synthesis
2) protein synthesis
3) TG synthesis in liver
4) TG storage in adipose

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11
Q

How is insulin sotred?

A

as the Zn2+ complex

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12
Q

Describe the structure of insulin?

A

2 peptide chains connected by 2 disulfides

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13
Q

What is structure of proinsulin?

A

folded with formation of disulfide bonds

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14
Q

Structure of pre-proinsulin

A

translation product after processing removes signal sequence in the RER

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15
Q

Why is C-peptide a good diagnostic tool?

A

not cleared as rapidly as insulin

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16
Q

What factors stimulate insulin release?

A

1) parasympathetic stimulation
2) Ala/Arg
3) GIP

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17
Q

What factors inhibit insulin release?

A

insulin

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18
Q

How is insulin solubilized from its storage form?

A

Ca++ displaces Zn++

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19
Q

What stimulates glucagon release?

A

1) catecholamines
2) cortisol
3) GI hormones
4) AAs

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20
Q

What control glucagon release?

A

lack of insulin

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21
Q

What suppresses glucagon release?

A

insulin and glucose

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22
Q

half-life of glucagon?

A

4 minutes

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23
Q

functions of glucagon?

A

1) stimulates glycogenolysis and gluconeogenesis in liver

2) mobilizes FAs in adipose

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24
Q

What other factors affect glucagon release?

A

1) blood metabolite levels
2) neuronal signals
3) other insulin opponents

25
Q

What percentage of islet is beta cells?

A

75%

26
Q

What percentage of islet is alpha cells?

A

20%

27
Q

What percent of islet is delta cells?

A

5%

28
Q

What does the cholera toxin do?

A

inhibits GTP hydrolysis by Galpha

29
Q

What is the reaction catalyzed by adenylate cyclase?

A

4 ATP –> 4 AMP –> 4 cAMP

30
Q

What is the function of phosphodiesterase?

A

inactivates cAMP

31
Q

What substances inhibit PDE?

A

caffeine, theophylline, theobromine

32
Q

What does cAMP do?

A

binds regulatory dimer of PKA to allow catalytic dimer to phosphorylate shit

33
Q

What is a CRE?

A

cAMP Response Element, a DNA promoter that encodes gluconeogenesis enzymes

34
Q

How are CRE’s bound to stimulate transcription?

A

cAMP-PKA phosphorylates CREBs that then bind CREs

35
Q

What hormones function through membrane receptors?

A

1) glucagon
2) epinephrine
3) beta-receptors

36
Q

What hormones function through RTKs?

A

insulin

37
Q

Describe RTK action?

A

1) dimerizes

2) TK autophosphorylates Tyr residues

38
Q

What hormones function through PIP2 hydrolysis couplers?

A

epinephrine alpha receptors

39
Q

What hormones function through gated ion channels?

A

1) angII

2) neurotransmitters

40
Q

What do alpha1 receptors do?

A

vascular smooth muscle contraction via PIP2

41
Q

What do beta1 receptors do?

A

myocardial increase HR & contractility

42
Q

What do beta2 and 3 receptors do?

A

fuel metabolism

43
Q

How does the insulin RTK take effect?

A

IRS (insulin receptor substrate) has an SH2 domain that binds Tyr-PO4s of RTK

44
Q

What does IRS-1 do?

A

affects glucose metabolism

45
Q

What does IRS-2 do?

A

affects fat metabolism

46
Q

What are cortisol’s effects?

A

works synergistically with glucagon to…

1) mediate long-term changes in fuel metabolism

47
Q

What is the MoA of sulfonylureas?

A

blocks ATP-dependent K+ channels in beta cells to increase Ca++ mobilization

48
Q

What are the sulfonylureas?

A

1st gen: tolbutamide

2nd gen: glipizide, glimepiride, glibencalmide

49
Q

What is the MoA of repaglinide?

A

same as Sulfonylureas

50
Q

What is the MoA of metformin?

A

stimulates AMP-activated PK to decrease liver gluconeogenesis via expression of SHP which inhibits expression of PEPCK & G6Pase

51
Q

What class of hypoglycemic agents is Metformin from?

A

biguanide

52
Q

Where is metformin derived from?

A

french lilac

53
Q

What is salsalate’s mechanism of action?

A

NSAID with blood-sugar lowering activity, decreases inflammation, increases insulin sensitivity

54
Q

What drugs are DPP4 inhibitors?

A

sitagliptin, saxagliptin

55
Q

What is the MoA of DPP4-inhibitors?

A

inhibits dipeptidylpeptidase-4 (involved in glucagon release); also stimulate insulin release by inhibiting inactivation of insulin-stimulating incretins

56
Q

What is the MoA of exantide?

A

incretin mimetic

57
Q

What is the MoA of Liraglutide?

A

GLP-1 analog with palmitate side chain that acts like incretins

58
Q

How is synthetic glucagon administered?

A

IM or SQ

Drew 922 (12 decks)

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