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Hormones 2 Flashcards

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1
Q

What is the function of the small intestine?

A
  • digest and absorb nutrients
  • glucose, amino acids, and triacylglycerols are absorbed from the intestine into the blood stream to reach each cell
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2
Q

What is different about RBC from other cells?

A
  • no organelles, nucleus
  • concave shape
  • only uses glucose, needs consistent supply
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3
Q

What does the brain use for energy?

A
  • ketone bodies (preference)
  • glucose (uses most of the time)
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4
Q

What nutrients does the heart/skeletal muscle use for energy?

A
  • less specific
  • fatty acids
  • ketone bodies
  • lactate, alanine
  • glucose
  • muscle can store glycogen
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5
Q

What does adipose tissue store? usage?

A
  • triacylglycerol, stores for energy
  • when glycogen storage has filled up, extra energy is stored as fat
  • two way path for fatty acids and glycerol into and out of adipose tissue by beta oxidation
  • one way for glucose
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6
Q

Role of liver in metabolism?

A
  • stores glucose as glycogen
  • breaks down glycogen into glucose
  • stores fatty acids as triacylglycerols, releases them by beta oxidation
  • glycolysis (lactate)
  • gluconeogenesis (lactate)
  • releases ketone bodies
  • brings in glycerol, fatty acid synthesis
  • VLDL
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7
Q

Pancreas Anatomy? Functions? (4)

A
  • under liver, behind stomach, above small intestine
  • Head
  • Neck
  • Body
  • Tail
  • Uncinate
  • Exocrine (95%)- release enzymes for digestion
  • Endocrine-islet of langerhans have beta cells for secretion of insulin, alpha cells secrete glucagon
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8
Q

Exocrine functions of pancreas? enzymes?

A
  • synthesize and secrete digestive enzymes/zymogens
  • trypsinogen
  • chymotrypsinogen
  • pancreatic lipase- digest lipids
  • amylase
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9
Q

Endocrine functions of pancreas? hormones?

A
  • synthesize and secrete hormones, formed by the islets of langerhans
  • insulin (beta cells- found in core)
  • glucagon (alpha cells-located in periphery)
  • gastrin and somatostatin (delta cells)
  • pancreatic polypeptide (F cells)- inhibits somatostatin
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10
Q

What composes the core of the islets of langerhans in the pancreas? mantle? (6)

A
  • core- beta cells that produce insulin
  • mantle- outer shell, contains alpha, delta, and F cells
  • alpha cells produce glucagon
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11
Q

Precursors of insulin? C peptide? (7)

A

preproinsulin gene -> proinsulin -> insulin

  1. connecting peptide (C peptide) is cut off by two digestive enzymes
  2. C peptide is secreted together with insulin
    - usually 1:1 ratio with insulin
    - use it to measure amount of insulin b/c insulin get used
    - insulin is conserved peptide
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12
Q

Steps of insulin synthesis and secretion in beta cells? (8)

A
  1. DNA transcription in nucleus produces mRNA for preproinsulin production
  2. transported to cytosol where translation begins from N terminal (leader sequence) to C terminal
  3. transported to rough ER where translation finishes of preproinsulin, leader sequence is cleaved by signal peptidase to form proinsulin
  4. packaged in Golgi, removes C peptide, convert proinsulin to insulin, insulin and c peptide packaged together and released into blood
  5. Calcium and glucose are the signal
    - degradation of C peptide is slower
  6. Secretory granules (condensation and storage)
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13
Q

Steps of the signal that regulates insulin secretion and synthesis? (9)

A
  1. increased glucose levels in blood
  2. glucose is transported by GLUT 2 into beta cells
  3. glucose catabolism by glycolysis to generate ATP and pyruvate
  4. ATP/ADP ratio increases to shut off potassium (K+) channel, depolarizing membrane
  5. force open calcium channel, 2nd signal, calcium moves into cell (influx)
  6. calcium signal squeezes sacks containing insulin and C peptide into bloodstream, and also for regulation of the calcium activated insulin gene expression via CREB leading to transcription activation of insulin gene to produce more insulin
    - insulin is water soluble so it doesn’t need a carrier protein to travel in blood stream
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14
Q

What is the role of glucose transporter 2 (GLUT 2)?

A

glucose absorption in liver and pancreas

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15
Q

Insulin signaling path in the muscle and adipose tissue? (10)

A
  1. increased insulin binds to insulin receptors on outside of cell, insulin receptor is heavily glycosylated tetramer consisting of two subunits (alpha2beta2), beta subunit has tyrosine kinase activity in cytoplasm
  2. inner side of receptor is autophosphorylated, activated
  3. other molecules (IRS) become phosphorylated, leading to translocation of GLUT 4
    - GLUT 4 normally located in cell, when insulin is present it moves to cell membrane
  4. glucose comes into cell by GLUT 4
  5. in muscle, glycolysis happens in order to create energy to do work
    - extra glucose is stored as glycogen
    - still extra, glucose turns into pyruvate to synthesize fatty acids and stored in adipose tissue
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16
Q

Effects of insulin on liver? (11)

A
  • increased glycolysis
  • decreased gluconeogenesis
  • increased glycogen synthesis
  • decreased glycogenolysis
  • increased fatty acid synthesis
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17
Q

Why doesn’t glucose uptake occur in liver but does in adipose and skeletal muscle?

A

liver uses GLUT 2 (not regulated by insulin) but adipose and skeletal uses GLUT 4 which is regulated by insulin

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18
Q

effects of insulin on adipose tissue?

A
  • increased glucose uptake
  • increased glycolysis
  • decreased lipolysis
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19
Q

effects of insulin on skeletal muscle?

A
  • increased glucose uptake
  • increased glycolysis
  • increased glycogen synthesis
  • decreased glycogenolysis
  • increased protein synthesis
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20
Q

Biochemical and physiological effects of insulin?

A
  • enhance anabolism, inhibit catabolism
  • insulin is a growth hormone
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21
Q

Where is glucagon synthesized and secreted? precursors?

A

-alpha cells in pancreas when blood glucose levels are low

preproglucagon gene -> proglucagon -> glucagon

-mature glucagon is a single chain polypeptide of 29 amino acids

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22
Q

What inhibits glucagon?

A

insulin and glucose

  • inverse relationship between glucagon and insulin
  • low glucose = high glucagon
  • low insulin = high glucagon
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23
Q

What increases glucagon secretion?

A
  • amino acids (Arginine, Alanine, GABA)
  • catecholamines (epinephrine)
  • glucocorticoids (GI hormones)
  • nervous system
  • high levels of circulating FFA
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24
Q

Target of glucagon?

A

liver for glucose metabolism

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25
Glucagon signal transduction? (16)
- water soluble so it cannot penetrate membrane 1. glucagon binds to receptor on cell surface, form complex 2. G protein subunits bind the receptor 3. adenylate cyclase interacts with G proteins to form an active complex with the alpha subunit 4. ATP is used to turn adenylate cyclase-alpha into cAMP 5. cAMP interacts with protein kinase A (repressor group releases from catalyzing groups) 6. protein kinase A is active leading to phosphorylation of many substrates (some active, some inactive) hormone amplifies: - 1 hormone leads to 20 G proteins activated **-\> 100 cAMP -\> 100-1000 phosphorylation -\> net effect is 10^5 or 10^6** -hormonal function is very sensitive
26
How many binding sites for cAMP does protein kinase A have? (17)
4
27
What can stop the glucagon signal? (17)
1. receptor for glucagon can turn GDP into GTP 2. Adenylate Cyclase converts ATP to cAMP 3. **phosphodiesterase** can break down cAMP into AMP to stop the signal
28
glucagon effects on blood glucose levels? (18)
1. low glucose 2. increased glucagon 3. increased cAMP 4. increased PKA - different enzymes then lead to different pathways to increase glucose levels
29
Glycogen synthase pathway? (19)
low glucose levels 1. increased glucagon 2. binds glucagon receptor 3. increased cAMP 4. increased PKA 5. increased phosphorylation 6. glycogen synthase decreases which decreases glycogen synthesis 7. glycogen phosphorylase increases to increase glycogen degradation 8. increased glucose
30
Glucagon effects on target cells? (20)
- decreased glycolysis - increased gluconeogenesis - decreased glycogen synthesis - increased glycogenolysis - decreased fatty acid synthesis - increased fatty acid oxidation
31
What is the insulin/glucagon ratio after a meal? during fasting? how does this relate to glycolysis/gluconeogenesis? (21)
meal: - increased insulin/glucagon ratio - PFK 2 activity - high dephosphorylation fasting: - decreased insulin/glucagon ratio - F2,6P bisphosphatase activity - phosphorylation high F2,6P activates PFK1 which increases glycolysis low F2,6P activates activates F1,6P Base which increases gluconeogenesis
32
Blood glucose levels in a diabetic vs normal person? (3 things) (22)
1. basal level of diabetic is higher, over 100 mg/dL 2. given glucose tolerance test, there is a bigger spike in the diabetic 3. healthy person reaches basal levels quickly, diabetic takes a long time to reach basal levels - diabetic doesn't deal with glucose very efficiently
33
What is glucagon like peptide (GLP-1)? Functions? (23)
- comes from gut genes (small intestines) - intestines L cells proglucagon -\> GLP-1 -C terminus of GLP-1 is modified to amide Functions: - targets stomach- slows down release of food (gastric emptying) for better digestion - activates pancreas beta cells to generate insulin - inhibits glucose release from liver - enhance muscle glucose uptake, heart - brain helps to stop eating - lowers blood glucose - increases glucose consumption - decreases glucose generation - decreases appetite
34
GLUT 1? GLUT 2? GLUT 3? GLUT 4? affinity? capacity? (24)
1- transport glucose to RBC, high affinity, low capacity, function all the time no matter blood glucose levels (low Km) 2- transport glucose to liver, low affinity, high capacity, efficient when blood glucose levels are high (high Km) 3- transport glucose to brain, high affinity, low capacity, functions all the time, when glucose is low (low Km) 4-transport glucose to adipose and muscle tissues, insulin affects glucose uptake, functions at normal range of glucose
35
Relationship between glucose levels and insulin during starvation? glucagon?fatty acids? ketone bodies? (25)
- high glucose= high insulin - high glucose= low glucagon - high glucose= low fatty acids - high glucose= low ketone bodies During prolonged starvation: - insulin decreases - glucagon increases then levels off - fatty acids increase linearly - ketone bodies increases exponentially
36
Hormonal regulation in type 1 diabetes? type 2? remedy?
Type 1: - childhood, thin, 10% of people - low insulin - high glucagon (normally inhibited by insulin) - high gluconeogenesis - high blood glucose, sweet urine - insulin injection remedy Type 2: - adolescence, obese, 90% of people - low insulin receptor pathway - glucagon normal - low nutrient usage - high blood glucose, cholesterol, fatty acid - remedy: exercise, diet
37
What is insulin induced lipohypertrophy?
injecting insulin into somewhere other than the bloodstream, such as stomach
38
Examples of catecholamines? where are they derived from?
Neurotransmitter (brain): - DOPA - Dopamine Hormone (adrenal medulla): - norepinephrine (transmitter) - epinephrine - derived from tyrosine
39
What is the steps from tyrosine to epinephrine? (28)
1. tyrosine is oxidized by using the enzyme tyrosine hydroxylase and BH4 (rate limiting) to turn into DOPA 2. DOPA decarboxylation by DOPA Decarboxylase to generate Dopamine 3. Dopamine is oxidized by Dopamine Hydroxylase using ascorbate (vitamin C) to form norepinephrine 4. Amino group is methylated to form epinephrine- vit B6, vit B12, and folate are important - BH4 is important for each step
40
Where is epinephrine and norepinephrine synthesized and secreted? what increases it?
- synthesized in adrenal medulla (inner portion) - increased by stress (physical exertion, psychological stress, cold) - hypothalamus -\> anterior pituitary -\> adrenal medulla -water soluble
41
catecholamine receptors and signal transduction?
- signal transduction of beta 2 receptor is identical to glucagon receptor - 7 transmembrane receptors on cell membrane - activate adenylate cyclase - increase cAMP - activate PKA
42
Effects of catecholamines?
- fight or flight - adrenaline - slow down digestion - speed up heart rate - increase sweating - mobilize stores of energy (glycogen and fat) - same as glucagon, but different tissues - uses hypothalamic-pituitary-adrenal axis (HPA)
43
Epinephrine effect on liver? path? (31)
increased epinephrine 1. binds to adrenergic receptor 2. increases cAMP 3. increases protein kinase A 4. increases gluconeogenesis - decrease glycolysis - increases glycogenolysis - decreases glycogenesis 5. increases blood glucose - same as glucagon
44
Effects of epinephrine on heart and liver? (slide 32,33)
- it has opposite effects on heart vs liver - liver: reduces F2,6P bisP, slows glycolysis - heart: increase F2,6P bisP, increases glycolysis
45
What happens with cortisol and glucocorticoids under chronic stress? path? difference from epinephrine?
1. chronic stress 2. CRH from hypothalamus 3. stimulates ACTH from anterior pituitary gland 4. cortisol and glucocorticoids are released from adrenal cortex 5. bind to receptors causing change in gene expression 6. increased lipolysis (adipose) - high increased protein degradation (muscle) - increased gluconeogenesis (liver) - increased glycogen synthesis (liver) - difference- epinephrine works through induction of cAMP (fast, short lived), glucocorticoids act through regulation of target gene expression (slow, long lasting)
46
When low blood glucose, what hormones act? how fast?
- epinephrine/norepinephrine happens instantly, doesnt last long - glucagon happens over a few hours - cortisol happens slowly, days or weeks, effects are longer lasting
47
What is leptin? (37)
leptin: a hormone that inhibits appetite and weight (OB gene) - have leptin (OB) gene, normal weight - loss of leptin (OB) gene, cannot suppress appetite, leads to obesity - small peptide - synthesized in adipocyte - proportional to body fat
48
What does leptin function in?
- decreases food intake (satiety), inhibits appetite - increases energy expenditure (metabolism) - acts slowly like insulin to promote stability in body stores - from adipocytes - proportional to body fat
49
Weight gain vs weight loss and leptin? (38)
- weight gain = increased leptin to decrease food intake and increase energy expend - weight loss = decrease leptin to increase food intake and decrease energy expend - determined by setting point, can change set point, cells expand or shrink
50
What is the diabetes gene (DB)? (39)
- leptin receptor- membrane protein enriched in the hypothalamus - no DB gene= no receptor, more body fat, leptin cannot bind anywhere - with DB gene= normal, leptin can bind receptor
51
Parabiosis experiment? (40)
- circulatory systems of two mice are joined together - combine OB(no leptin gene) with wild, OB gets smaller because hormones are shared from the wild, wild stays same - combine DB(no diabetic gene- no receptor) with wild, DB didn't change and wild got smaller because DB has no receptor but higher leptin levels because of higher body fat, wild gets smaller because it has receptors for leptin and there is a lot of leptin circulating due to the DB mouse - combine OB (no leptin) with DB (no receptor), DB stays same size because it has no receptor, OB gets smaller because it is using the leptin from the DB - brain regulates appetite
52
Leptin therapy for patients who lack leptin?
- used in limited numbers of people with leptin deficiencies - effects not significant for individuals with no deficiency -patient loses weight
53
Exercise changes on adipocytes? (42)
- subcutaneous adipocytes from exercising mice can improve glucose homeostasis - darker color - increase mitochondria - Factor X enhances glucose uptake to muscle
54
Regulation of appetite in brain? (orexigenic/anorexigenic)?
2 sets of neurons: arcuate nucleus (ARC) orexigenic: - appetite stimulating - NPY- neuropeptide Y - AgRP- agouri related protein - ghrelin (stomach)- levels rise just before meals anorexigenic: - appetite suppressing - POMC- pro opiomelanocortin - alpa-MSH- alpha melanocyte stimulating hormone - PYY (intestine)- peptide YY - CCK (intestine)- promote sense of fullness, release bile and digestive enzymes from pancreas - Leptin (fat/adipose) - insulin (pancreas) - melanocortins - work together to balance
55
What does the arcuate nucleus do? (ARC)
- integrates all information together to make a decision - master center of weight regulatory systems
56
Insulin defects in Type 1 diabetes?
- result of failure in beta cells function in synthesis and secretion of insulin - due to autoimmune attack on beta cells
57
Insulin defects in Type 2 diabetes?
- more complicated - reduced insulin secretion and synthesis - target cells not responding to insulin signal (insulin resistance) - overweight, obese
58
Insulin defects in neonatal diabetes (ND)?
- between 0-6 months of age - mutations of GK and K+ channel protein - therapy- administer sulphonyluria, K+ channel inhibitor
59
Family of adrenergic receptors and their effects?
- alpha 1- increase IP3 - alpha 2- decrease cAMP - beta types- increase cAMP - epinephrine is potent on beta 2 receptors
60
Epinephrine effects on metabolism?
- inhibit insulin and enhance glucagon - cardio muscle only contains receptors for epinephrine, not glucagon - liver has receptors for both glucagon and epinephrine - quick and short lived - heart: - increases adenylate cyclase and cAMP in heart - increases glycogenolysis and reduces glycogen synthesis - liver: - glucagon and epinephrine decrease glucose uptake - increases glucose release -increases blood glucose levels
61
How does neuropeptide Y (NPY) stimulate appetite?
- NPY- accelerator neuron 1. decreases expression of POMC gene by brake neuron 2. decreases synthesis of TRH 3. increases synthesis of melanin concentrating hormone (orexigenic)
62
How does agouri related peptide (ARP) stimulate appetite?
- ARP- accelerator neuron 1. antagonizes alpha melanocyte stimulating hormone (alpha-MSH) 2. blocks neuronal melanocortin receptors
63
How does the brain suppress appetite?
- brake neuron, inhibitory - produces melanocortin peptides from POMC - alpha-MSH - ACTH
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