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A Physiology > 7.4. Insulin secretion and the regulation of the secretion. The effects of insulin on the intermediary metabolism. Diabetes mellitus. > Flashcards

7.4. Insulin secretion and the regulation of the secretion. The effects of insulin on the intermediary metabolism. Diabetes mellitus. Flashcards

1
Q

I. Basics
1. What is Intermediary metabolism?

A
  • Metabolic steps within the cells in which the nutrient molecules or foodstuffs are metabolized and converted into cellular components and/or provide energy => it provides the appropriate energy supply for the cells and tissues.
  • Energy donors: carbohydrates, fats/lipids, AAs
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2
Q

I. Basics
2. What are the energy donors of intermediary metabolism

A

carbohydrates, fats/lipids, AAs

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3
Q

I. Basics
3. Is the site of storage extracellular or intracellular?

A

INTRACELLUAR!!!

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4
Q

I. Basics
4. Describe the intracellular storage of amino acids

A
  • Can be glycogenetic
  • But too “valuable” because of other functions of proteins
  • During breakdown, NH3 or urea is produced
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5
Q

I. Basics
5. Describe the intracellular storage of lipids

A
  • Ideal storage property
  • Only oxidative breakdown
  • Not suitable for every tissue
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6
Q

I. Basics
6. Describe the intracellular storage of carbohydrate

A
  • Appropriate for every tissue
  • Bad storage properties
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7
Q

I. Basics
7A. What are the 3 Major players ‘’effectors’’ of the intermediary metabolism

A

The regulation depends on hormones produced by different endocrine organs
1. Liver: ‘’the center’’
2. Adipose tissue:
3. Skeletal muscle

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8
Q

I. Basics
7B. One of Major players ‘’effectors’’ of the intermediary metabolism is
“LIVER”
=> Explain

A

Liver: ‘’the center’’
- Gluconeogenesis can direct sources to provide glucose

(The regulation depends on hormones produced by different endocrine organs)

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9
Q

I. Basics
7C. One of Major players ‘’effectors’’ of the intermediary metabolism is
“ADIPOSE TISSUE”
=> Explain

A
  • White adipose tissue: storage site of fat/lipids
  • Actually the largest endocrine tissue => produces regulatory molecules
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10
Q

I. Basics
7D. One of Major players ‘’effectors’’ of the intermediary metabolism is
“SKELETAL MUSCLE”
=> Explain

A
  • Largest energy consumer if we exercise
  • Other energy consumers: Brain, CT, bone tissue, skin, kidney etc.
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11
Q

I. Basics
8. Depending of the demand
=> What are the processes that lead to elimination of transport nutrients?

A
  • Protein synthesis
  • Lipogenesis
  • Glycogenesis
  • Glycolysis
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12
Q

I. Basics
9. Depending of the demand
=> What are the processes that lead to production of transport nutrients?

A
  • Proteolysis
  • Lipolysis
  • Glycogenolysis
  • Gluconeogensis
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13
Q

I. Basics
10A. What are the 3 basic rules of the regulation of intermediary metabolism?

A
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14
Q

I. Basics - basic rules of the regulation
10B. How do we keep the plasma [glucose] at the normal level?

A
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15
Q

I. Basics - basic rules of the regulation
10C. What is the major regulator?

A

Insulin

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16
Q

I. Basics
11. Make a schematic diagram of regulation in intermediary metabolism?

A
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17
Q

II. Insulin synthesis and secretion
1. How is insulin secreted?

A

Insulin is secreted by β-cells in the endocrine regions of the pancreas: the islets of Langerhans.

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18
Q

II. Insulin synthesis and secretion
2A. How does synthesis of insulin occur?

A
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19
Q

II. Insulin synthesis and secretion
2B. How is pro-insulin processed?

A
  • Pro-insulin is sent to the ER and folded properly, the connecting peptide (C-peptide) is cleaved, and the mature insulin + C-peptide are packaged in equal amounts in secretory granules (Golgi)
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20
Q

II. Insulin synthesis and secretion
3. What are the values of secretion of insulin during fasting, mixed feeding? Also the insulin content of pancreas

A
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21
Q

II. Insulin synthesis and secretion
4A. Insulin is secreted by β-cells due to a variety of factors
=> What are these factors?

A
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22
Q

II. Insulin synthesis and secretion
4B. What are the features of incretins?

A
  • Incretins (GLP + GIP): hormones that stimulate a decrease in blood glucose levels
    +) Released due to orally ingested glucose, regulates insulin release by feed- forward mechanism
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23
Q

II. Insulin synthesis and secretion
5. How does glucose affect the cell?

A
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24
Q

II. Insulin synthesis and secretion
6. What is the mechanism of ↑[glucose] that leads to ↑insulin secretion

A
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25
Q

II. Insulin synthesis and secretion - Pharmacological regulation of the inwardly rectifying KATP-channel
7. What should we do if the production of insulin on the β-cells is insufficient?

A

When the production of insulin on the β-cells is insufficient
-> diabetes (↑[glucose]).

=> Since the KATP-channels has sulphanylurea (SU)-receptors, we can use sulphanylurea to bind and close the channel
-> depolarization
-> insulin secretion

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26
Q

II. Insulin synthesis and secretion - Pharmacological regulation of the inwardly rectifying KATP-channel
8. What should we do if there is an overactivation of β-cells?

A

If there is an overactivation of β-cells, we can use diazoxide.
- It allows KATP to remain opened even when ATP is present, thereby hyperpolarizing the cell => inhibits insulin secretion

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27
Q

II. Insulin synthesis and secretion - β-cell mechanism
9A. Describe β-cell mechanism

A
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28
Q

II. Insulin synthesis and secretion - β-cell mechanism
9B. Describe β-cell mechanism When the cell is well supplied with energy donors?

A

When the cell is well supplied with energy donors:
- AMP
-> ADP -> ATP
=> insulin secretion

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29
Q

II. Insulin synthesis and secretion - β-cell mechanism
9C. Describe β-cell mechanism When energy donors are sufficient?

A
  • When energy donors are sufficient ↑[AMP] (no ATP produced) AMP will also regulate AMP-kinase, which inhibits the insulin synthesis = NO INSULIN SECRETION
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30
Q

II. Insulin synthesis and secretion - β-cell mechanism
9D. Describe β-cell mechanism When glucose enters the cell?

A
  • When glucose enters the cell, AMP -> ATP and ↓[AMP] = no AMP-kinase produced
    => insulin synthesis starts (with help of Ca2+-calmodulin)
    => insulin secretion
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31
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
10A. What are the activators in β-cell regulation?

A
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32
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
10B. What are the AAs that act as activators of β-cell regulation?

A

lysine, arginine, leucine

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33
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
10C. What is the role of incretins as activators of β-cell regulation?

A

Incretins: GIP (glucose-dependent insulinotropic peptide) and GLP (glucagon-like peptide) are released due to orally ingested glucose and have stimulatory effect on
insulin

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34
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
10D. What is the role of Glucagon as activators of β-cell regulation?

A

Glucagon: induces insulin by activating a Gq-protein that causes ↑[Ca2+] and thus insulin release

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35
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
10E. What is the role of Vagus as activators of β-cell regulation?

A

ACh -> (Gq)M1-receptor -> PLC -> IP3 -> ↑[Ca2+]
=>↑[cAMP] is the 2nd messenger for most of them

36
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
11A. What are the inhibitors of β-cell regulation?

37
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
11B. What happen if there is an Acute exposure of the pancreatic β-cell to FFA?

A

Acute exposure of the pancreatic β-cell to FFA results in an increase of insulin release.
=> BUT a chronic exposure results in desensitization and suppression of insulin secretion

38
Q

II. Insulin synthesis and secretion - Components of the β-cell regulation
12. Make the schematic diagram for the β-cell regulation?

39
Q

II. Insulin synthesis and secretion
13. What is the structure of Insulin receptor?

40
Q

II. Insulin synthesis and secretion
14. What is the mechanism of Insulin receptor?

41
Q

II. Insulin synthesis and secretion
15. What are the steps of GLUT4 transposition?

42
Q

II. Insulin synthesis and secretion
16. How does Exercise-responsive GLUT4-containing vesicle work?

43
Q

II. Insulin synthesis and secretion
17. Glucose transport into the cells increases, wherever GLUT4 transporters are present:
=> T/F??

44
Q

II. Insulin synthesis and secretion
18. What are the features of Insulin-dependent glucose uptake?

A

Insulin-dependent glucose uptake: (GLUT4)
- Pancreas α-cell, CT, lymphoid tissue
- Adipose tissue and skeletal muscle (they also have GLUT1 present – allows only smaller glucose transport)

45
Q

II. Insulin synthesis and secretion
19. What are the features of Insulin-independent glucose uptake?

A
  • GLUT2: liver, kidney, intestine
  • GLUT3: brain, RBC, cornea
46
Q

III. ACTION OF INSULIN
1. What are the features of insulin?

A
  • Insulin a strongly anabolic hormone, and it is often taken by bodybuilders to help them gain more muscles.
  • Insulin promotes the uptake of AAs (proteins) into the cells  contributing to its anabolic effect (muscles bruv!!)
47
Q

III. ACTION OF INSULIN
2. What are the 4 general insulin effects?

A

General insulin effects: (exerted in all the tissues)
1. Amino acid transport into the cells↑
=> protein synthesis↑
2. K+-transport into the cells↑ (activation of Na+/K+-ATPase)
3. Activation of phosphodiesterase
=> ↓[cAMP]
4. Growth promoting effect

48
Q

III. ACTION OF INSULIN
3A. The role of liver when it comes to insulin?

A
  • Liver is both a target organ for insulin action and a major site of insulin degradation.
  • Glucose enters the hepatocytes through GLUT2 transporters (insulin-independent).
  • Blood [insulin] in portal vein is 3-4 times greater than its concentration in the systemic circulation.
49
Q

III. ACTION OF INSULIN
3B. What are the 3 effects of insulin on the liver?

50
Q

III. ACTION OF INSULIN
4A. What are the effects of insulin in the adipose tissue?

A

Insulin-regulated GLUT4 translocation: insulin induces translocation of GLUT4 to PM via the PI3-kinase pathway
1) Insulin promotes lipogenesis (formation of triglycerides)
2) Also increased FFA synthesis from glucose

51
Q

III. ACTION OF INSULIN
5. What are the Effects of insulin on the skeletal muscle?

A

Glucose enters the muscle through GLUT4 (insulin- dependent). Insulin-regulated GLUT4 translocation induces translocation of GLUT4 to PM via PI3-kinase pathway

1) Insulin stimulates glycolysis and glycogenesis
2) Protein synthesis↑ & proteolysis↓

52
Q

III. ACTION OF INSULIN
6. Make a table to demonstrate the effects of insulin

53
Q

IV. DIABETES MELLTIUS
1. What are the features of Diabetes mellitus type 1 (1TDM)

54
Q

IV. DIABETES MELLTIUS
2. What are Abnormal metabolic processes in 1TDM?

A

Impaired β-cell function (insulin secretion↓)

55
Q

IV. DIABETES MELLTIUS
3. What are the effects of diabetes mellitus on Muscle?

A
  • Glycogen storage↓, because they do not absorb glucose due to the absence of GLUT4 on PM
  • Protein breakdown -> lactate -> gluconeogenesis in liver (↑blood sugar even
56
Q

IV. DIABETES MELLTIUS
4. What are the effects of diabetes mellitus on adipose tissue?

A
  • Never get the insulin signal to stop lipolysis: so they release glycerol
    (-> gluconeogenesis) + FFA ( -> ketogenesis) -> liver (↑glucose)
57
Q

IV. DIABETES MELLTIUS
4. What are the effects of diabetes mellitus on Pancreatic α-cells?

58
Q

IV. DIABETES MELLTIUS
5. Which hormone will we add during DM? Why?

A

Somatostatin added during DM, will reduce the liver-consequences of insulin deficiency:
- Insulin is still deficient, but
glucagon will be inhibited (only target α-cell)
- Only use somatostatin in tumors in this case

59
Q

IV. DIABETES MELLTIUS
6A. What are the 2 main Consequences of the metabolic disturbance?

A
  1. Hyperglycemia
  2. Ketonemia (acetoacetic acid, β-OH-butyric acid)
60
Q

IV. DIABETES MELLTIUS
6B1. One of Consequences of the metabolic disturbance is
“Hyperglycemia”
=> Explain

61
Q

IV. DIABETES MELLTIUS
6B2. One of Consequences of the metabolic disturbance is
“Hyperglycemia”
=> What is Osmotic diuresis?

A

water and electrolyte loss (Na+, Cl-)

62
Q

IV. DIABETES MELLTIUS
6C. One of Consequences of the metabolic disturbance is
“Ketonemia”

A

Ketonemia (acetoacetic acid, β-OH-butyric acid):
- Without insulin, the body is basically in starvation mode despite being extremely hyperglycemic.
- Ketone bodies are produced in the liver and released into the blood
=> diabetic ketoacidosis and all the problems associated with metabolic acidosis (hyperventilation + vomiting => H2O-loss + diabetic coma)

63
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
7. What are the 3 tests for Diagnosis of DM?

A
  1. Glucose tolerance test
  2. Glycated hemoglobin (HbA1c)
  3. C-peptide
64
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
8A. How do we take Glucose tolerance test?

A

Start out by fasting and then ingest a large amount of glucose, then test blood sugar every 30 minutes for 2 hours and see how it responds (old treatment method)

65
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
8B. What are the 2 main measurements of Glucose tolerance test?

A
  • IFG = impaired fasting glucose
  • IGT = impaired glucose tolerance
66
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
8C. What does IFG = impaired fasting glucose indicate in Glucose tolerance test?

A
  • Before the meal
  • Less than 6,1mM = normal, above 7,0mM = diabetic, in range of 6,1-7,0mM = IFG => glucose higher than it should be, but still not diabetic
  • If someone has IFG => glucose tolerance test
67
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
8D. What does IGT = impaired glucose tolerance indicate in Glucose tolerance test?

A
  • Measured in the end
  • If concentration below 7,8mM = tolerance normal, if above 11,1mM = diabetic (exogenous hyperglycemia)
  • Between 7,8-11,1mM = IGT
68
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
9. How does Glycated hemoglobin (HbA1c) test work?

A
  • This is used to get a longer-term idea of the average blood sugar level.
  • In presence of continuously high blood glucose concentration, Hb tends to bond with some of the glucose and thus become ‘’glycated’’.
  • People with diabetes will have abnormally high levels of glycated hemoglobin.
69
Q

IV. DIABETES MELLTIUS - Diagnosis of DM
10. How does C-peptide test work?

A

C-peptide: a peptide fragment from insulin synthesis that can be detected in the urine and corresponds to the insulin secretion

70
Q

IV. DIABETES MELLTIUS
11. What are the features of Diabetes mellitus type II?

A

Diabetes mellitus type II: (non-insulin dependent, adult diabetes, insulin resistance)
- This is associated with lifestyle and the damaging effects of eating a diet that pushes the limits of the ability for the pancreatic β-cells to produce insulin.

71
Q

IV. DIABETES MELLTIUS
12. Diabetes mellitus type II is associated with lifestyle and the damaging effects of eating a diet that pushes the limits of the ability for the pancreatic β-cells to produce insulin.
=> Explain

A
  • Strong correlation with central obesity (abdominal fat) and lack of exercise.
  • DM type II often accompanies ‘’metabolic syndrome’’ – the 3 other major syndromes related to lifestyle: atherosclerosis, hypertension and coronary artery disease
72
Q

IV. DIABETES MELLTIUS
13. DM type II often accompanies ‘’metabolic syndrome’
=> What does it mean?

A

DM type II often accompanies ‘’metabolic syndrome’’ – the 3 other major syndromes related to lifestyle: atherosclerosis, hypertension and coronary artery disease

73
Q

IV. DIABETES MELLTIUS
14. What does a person with DM type II need?

A

A person with DM type II may need twice as much insulin necessary to maintain or keep glucose levels normal
=> so there is an impaired response to insulin and resistance from tissues that normally take it up

74
Q

IV. DIABETES MELLTIUS
15. What happen to Serine-phosphorylation of the insulin receptor substrate (IRS) if there is insulin resistance?

A
  • IRS-1 together with tyrosine kinase phosphorylates on several occasions (normal response)
  • But when substances (insulin, triglycerides, TNFalpha, resistin, IL6) are present, they cause serine-phosphorylation -> IRS = insulin resistance (signaling does not work)
75
Q

IV. DIABETES MELLTIUS
16. Make a schematic diagram for insulin resistance in DM type II

76
Q

IV. DIABETES MELLTIUS
17. What is The role of the adipose tissue in the energy metabolism?

A

1.Triglyceride storage
2. Production of regulating peptide mediators: adipocytokines => adipocytokine production reflects the triglyceride content of the adipocytes (the nutritional state)

77
Q

IV. DIABETES MELLITUS
18. What is the role of adiponectin?

78
Q

IV. DIABETES MELLITUS
19. Why does the central form (visceral) obesity have particular significance in the development of insulin resistance and NIDDM?

79
Q

IV. DIABETES MELLITUS
20. What is the role of 11Beta-hydroxysteroid dehydrogenase-1?

80
Q

IV. DIABETES MELLITUS
21. Make a schematic diagram for transcriptional regulation of adipocyte derived mediators

81
Q

IV. DIABETES MELLITUS
22A. What are the 3 treatments for T2DM?

A
  1. Diet
  2. Exercise
  3. Medications
82
Q

IV. DIABETES MELLITUS
22B. How should you treat T2DM with diet?

A
  • Reduces the lipid content of adipose tissue
  • Increases adiponectin secretion (in other insulin target tissues: triglyceride↓,
    (insulin resistance↓), resistin, TNFalpha and IL6 secretion↓)
83
Q

IV. DIABETES MELLITUS
22C. How should you treat T2DM with exercise?

A
  • GLUT4 translocation to the PM
  • Muscle glucose consumption↑
  • Blood plasma [glucose] ↓
84
Q

IV. DIABETES MELLITUS
22D1. How should you treat T2DM with MEDICATIONS?

A

Use
1. Sulfanylurea
2. GLP
3. TZD
4. Biguanidines

85
Q

IV. DIABETES MELLITUS - medications
22D2. What is the mechanism of Sulfanylurea in treatment for T2DM?

86
Q

IV. DIABETES MELLITUS - medications
22D3. What is the mechanism of GLP in treatment for T2DM?

87
Q

IV. DIABETES MELLITUS - medications
22D4. What is the mechanism of TZD in treatment for T2DM?

A Physiology (88 decks)

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