Biochemistry: Chapter 43 Hormones That Regulate Fuel Metabolism

Front 1

What is the major anabolic hormone?

Back 1

insulin

Front 2

What are counter-insulin hormones?

Back 2

epi, norepi, cortisol, GH, somatostatin, TH

Front 3

proglucagon is synthesized at what sites in the body? What other hormones does this gene contain?

Back 3

1) pancreas and L-cells of intestine
2) GLP1 and GLP2

Front 4

What is the half life of glucagon?

Back 4

3-6 minutes it is removed by liver and kidney

Front 5

What is the main target of glucagon?

Back 5

liver

Front 6

What is glucagons action on insulin?

Back 6

it increases insulin release but insulin suppresses glucagon

Front 7

Where in the body is somatostatin produced?

Back 7

D cells of pancreas, gastric and duodenal mucosa, hypothalmus

Front 8

What is tolbutamide?

Back 8

a sulfonylurea that increases insulin release

Front 9

What molecules increase somatostatin release? what hormones increase its release?

Back 9

1) glucose, arginine, leucine
2) glucagon, VIP, CCK

Front 10

What pathway does somatostatin activate when it binds cells?

Back 10

G proteins and inhibits them decreasing cAMP and preventing PKA activation

Front 11

What hormones does somatostatin inhibit?

Back 11

GH, TSH, insulin, glucagon, TRH

Front 12

What effect does somatostatin have on gastric emptying?

Back 12

delays it, decreases acid secretion, and pancreatic enzyme release

Front 13

what is the half life of somatostatin?

Back 13

3 min

Front 14

What drug is an analog of somatostatin?

Back 14

octreotide with a long half life

Front 15

What is the half life of HGH?

Back 15

20-50 min

Front 16

What is a GH antagonist?

Back 16

pegvisomant

Front 17

To determine if someone has a GH tumor you would give them 100g of glucose. What should you see?

Back 17

a decrease in GH to less than 2ng/mL if it is not a tumor

Front 18

what is ornithine decarboxylase? What is GH effect on it?

Back 18

1) regulates cell proliferation
2) GH increases it

Front 19

GH acts on what type of receptor? what proteins are stimulated when GH binds adipose cells?

Back 19

1) a tyrosine kinase
2) increased lipolysis, inhibition of LPL, increased hormone sensitive lipase, decreased glucose transport, decreased lipogenesis

Front 20

Where is GHRH produced?

Back 20

arucuate nucleus

Front 21

What is IGF-1 effect on GH?

Back 21

negative feedback to somatotrope

Front 22

what molecules stimulate GH release?

Back 22

hypoglycemia, arginine,

Front 23

during prolonged fasting what hormone in particular increases lipolysis?

Back 23

GH spares glucose and protein

Front 24

increased amino acids have what effect on GH?

Back 24

increases its release

Front 25

what secondary condition develops with a GH tumor?

Back 25

diabetes

Front 26

What effect does estrogen have on GH? What about K+? Renal failure? progesterone?

Back 26

1) increases
2) increases
3) increases
4) decreases

Front 27

Someone taking an alpha antagonist will have high or low GH? What about a beta agonist

Back 27

low

Front 28

Obesity has what effect on GH production?

Back 28

decreases it

Front 29

dopamine agonists increase or decrease GH release?

Back 29

increase

Front 30

is ketogenesis increased or decreased by GH?

Back 30

increased

Front 31

What effect does GH have on glycogen synthesis? what about gluconeogenesis?

Back 31

increases both

Front 32

IGF-1 is also known as?

Back 32

somatocedin C

Front 33

IGF-II is also known as?

Back 33

somatocedin A

Front 34

What do IGF-1 and insulin have in common structurally?

Back 34

they both contain the C peptide domain

Front 35

What type of receptor does IGF1 activate?

Back 35

tyrosine kinase

Front 36

what is different about IGF1 and IGF2 release?

Back 36

IGF2 is independent of GH

Front 37

what is the precursor to all catacholamines?

Back 37

tyrosine

Front 38

What have high levels of IGF1 been linked to?

Back 38

breast prostate, colon and lung cancer

Front 39

what effect does hypoxia have of catacholamine release?

Back 39

increases their release

Front 40

What are the metabolites looked for in someone with a pheochromocytoma?

Back 40

metanephrines and vanilylmandelic acid (VMA)

Front 41

where in the CNS are the adrenergic nuclei?

Back 41

hypothalamus

Front 42

Do catecholamines have a high or low affinity for receptors?

Back 42

low so that their effects are short lived

Front 43

Where is CRH released from?

Back 43

paraventricular nuclei

Front 44

Where in the adrenal cortex does ACTH act?

Back 44

zona fasciculata and reticulosa

Front 45

cushings disease is what? cushings syndrome is what?

Back 45

1) pituitary tumor
2) adrenocortical tumor

Front 46

What is the effect of cortisol on fat, glucose and protein?

Back 46

increased lipolysis, decreased glucose uptake, proteolysis of skin, lymphoid cells and muscle

Front 47

What effect does cortisol have on phosphoenolpyruvate carboxykinase?

Back 47

increases it to increase gluconeogenesis

Front 48

cortisol has a catabolic effect on elastin. What results?

Back 48

sagging wrinkling skin and increased fragility of capillaries

Front 49

What causes plethora in people with cushings?

Back 49

thinning of facial skin

Front 50

What is the rate of iodide transport dependent on ?

Back 50

concentration of iodide in the thyroid cell

Front 51

Where is iodinium ion made?

Back 51

at the apical border of thyroid cell by thyroid peroxidase

Front 52

T4 is made up of what constituents?

Back 52

2 tyrosines, 4 iodine molecules

Front 53

In thyroglobulin what is the normal ratio of T4 to T3?

Back 53

13:1

Front 54

Is T3 or T4 the biologically active form?

Back 54

T3

Front 55

What is unique about the thyroid gland and its storage ability?

Back 55

it has a large storage capacity of amino acids linked to thyroglobulin in the colloid space

Front 56

what is the half of T4? T3?

Back 56

1) 7 days
2) 1 day

Front 57

How do T4 and T3 travel in blood?

Back 57

bound to thyroid-binding globulin and 0.03% T4 is unbound and 0.3% T3 is unbound

Front 58

T4 and T3 are stored in vesicles in cells. What happens when TSH stimulates cells?

Back 58

causes lysosome to fuse with vesicle and degrade thyroglobulin to release T4 and T3 in 10:1 ratio

Front 59

TSH follows a circadian pattern. What is it?

Back 59

surge in late afternoon and peaks before sleep. Does have a pulsatile pattern though where it is released every 2-6 hours

Front 60

what intracellular signaling molecules are increased when TSH binds?

Back 60

cAMP, DAG and Ca2+

Front 61

What inhibits TSH and TRH release?

Back 61

T3 and at high levels it inhibits TRH

Front 62

What is the effect of excess T3 on muscle and amino acids? What about normally?

Back 62

1) breaks down muscle and sends amino acids to liver
2) increases glucose uptake, stimulates protein synthesis, increases muscle growth, but also increases glycolysis by sensitizing cells to epinephrine

Front 63

What are the effects of T3 on the liver?

Back 63

1) increase glycolysis
2) increase cholesterol syn
3) increase production of bile salts
4) increase production of TAGs

Front 64

How does T3 effect adipocytes? What happens if insulin and glucose are high?

Back 64

1) sensitizes adipose cells to epinephrine action leading to increased lipolysis (indirectly effects)
2) increased glucose with insulin can be converted to glycerol 3-phosphate which will promote lipogenesis

Front 65

How does T3 effect glucose metabolism in liver?

Back 65

increases gluconeogenesis indirectly by sensitizing cells to epinephrine

Front 66

How would insulin be effected if T3 were absent?

Back 66

insulin release would be depressed because T3 increases sensitivity of beta cells to glucose

Front 67

How does T3 participate in "shivering" response to cold?

Back 67

sensitizes sympathetics which increases NE release and increases heat release by making cells more permeable to Na therefore increasing activity of Na/K atpase which breaks down ATP and releases heat

Front 68

What occurs in Refetoff disorder? What is the obvious physical exam finding?

Back 68

1) mutation in T3 receptor which causes symptoms of hypothyroidism
2) goiter occurs because T3 and TSH levels are very high

Front 69

What happens to insulin clearance when someone has hyperthyroidism?

Back 69

it increases

Front 70

What is metathyroid diabetes mellitus

Back 70

glucose intolerance that results with hyperthyroid because insulin is degraded quicker than normal

Front 71

Where is ghrelin made and what does it do?

Back 71

1) CNS, stomach, intestine
2) stimulates GH release during fasting

Front 72

Where is GLP-1 made and what does it do?

Back 72

1) L cells in ileum, colon and CNS
2) a. inhibits glucagon and increases insulin
b. acts as an incretin to increase sensitivity to glucose in beta cells

Front 73

Where is VIP made and what does it do? What causes its release?

Back 73

1) widely expressed in PNS and CNS
2) regulate insulin and glucagon release
3) mechanical stim of gut and activation of PNS and CNS

Front 74

Where is motlin produced? what does it do and when is it released?

Back 74

1) M cell in duodenum
2) induces phase III contractions in stomach, increases gastric acid and pancreatic secretion, gallbladder contraction
3) duodenal alkalinization, gastric distention, suppressed by nutrients in duodenum

Front 75

Where is GIP produced? What does it do? What causes its release?

Back 75

1) K cells of duodenum and jejunum
2) increases insulin (incretin), regulates glucose and lipid metabolism
3) increased by food, especially long chain fatty acids