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GIT physiology > Effects of insulin > Flashcards

Effects of insulin Flashcards

1
Q

Effects of insulin within cell

A
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2
Q

3 effects of insulin on the liver

A
  1. Increased glycogen synthesis 2. Increased glycolysis 3. Decreased gluconeogenesis
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3
Q

3 effects of insulin on fat

A
  1. Increased glucose transport 2. Increased lipogenesis 3. Decreased lipolysis
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4
Q

3 effects of insulin on skeletal muscle

A
  1. Increased glucose transport (= fat) 2. Increased glycogen synthesis (= liver) 3. Decreased gluconeogenesis
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5
Q

What receptors does the heart have

A

GLUT 1 & some GLUT 2

=> heart gets a low level of glucose all of time even in the absence of insulin

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6
Q

Effect of insulin on glycogen metabolism (in hepatocytes)

A

see folder

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7
Q

Insulin regulated metabolism in an adipocyte

A

see folder

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8
Q

Relationship between EC & IC glucose and insulin

A

Linear relationship (graph)

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9
Q
  1. What does insulin stimulate (5) 2. What does insulin inhibit (5)
A

Image

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10
Q

What is the structure of glucagon

A

Peptide hormone 29 AAs

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11
Q

What is glucagon produced by

A

Alpha cells -20%

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12
Q

What is the half life of glucagon

A

5-10 mins degraded by liver tissue

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13
Q

3 factors that increase glucagon secretion

A
  1. Blood glucose < 70 mg/dL 2. AAs (high protein, low CHO meal) 3. Stress - adrenaline via beta-adrenergic receptors on alpha cells
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14
Q

2 factors that decrease glucagon secretion

A
  1. Increase blood glucose 2. Insulin (feed-forward mechanism)
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15
Q

Target tissues of glucagon

A

Liver muscle adipose tissue

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16
Q

What is the mechanism of action of glucagon

A

Binds to Gs-coupled receptor, resulting in increased cAMP and increased PKA activity - also activated IP3 pathway => increase in Ca2+

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17
Q

Action of glucagon on the liver (3)

A

PRIMARY TARGET - increase blood glucose

  1. Increased glycolysis - Activates a phosphorylase - cleaves a 1-P off glycogen
  2. Inhibits glycogenesis - Inactivates glycogen synthase by phosphorylation
  3. Increased gluconeogenesis - Increases phosphoenolpyruvate carboxykinase
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18
Q

Action of glucagon on lipids

A

Increases lipolysis - activates lipases - breaking down of triglycerides

  • inhibits acetyl CoA carboxylase - stops FFA from becoming acetyl CoA
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19
Q

Glucagon action on cells

A

see folder

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20
Q

Response to decreasing glucose levels

21
Q

Where was somatostatin first discovered and where is it found now

A

Hpothalamus - GHIH

Pancreas, intestinal tract, CNS

22
Q

What does somatostatin do

A

Inhibits secretion of many other hormones: 1. GH 2. Insulin 3. Glucagon 4. Exocrine pancreatic secretions

23
Q

What are the 2 forms of somatostatin

A

SS-14 & SS-28

24
Q

Tissue-specific isoform of SS-14

A

Sole isoform from pancreas Major isoform in CNS

25
Tissue-specific isoform of SS-28
Major isoform in intestine
26
Which SS isoform is more potent in inhibition of GH secretion
SS-28
27
Which SS isoform is more potent in inhibition of glucagon release
SS-14
28
What are the microvascular complications of diabetes (4)
1. Diabetes eye disease (retinopathy & cataracts) 2. Renal disease 3. Erectile dysfunction 4. Peripheral neuropathy
29
What are the macrovascular complications of diabetes (4)
1. Stroke 2. Heart disease & hypertension - 2-4x increased risk 3. Peripheral vascular disease 4. Foot problems
30
Type I diabetes mellitus/Insulin dependent/Juvenile onset
5-10% of all DM Absolute insulin deficiency Pancreatic cell destruction photo
31
Type II diabetes mellitus/non-insulin dependent/Adult onset
Insulin resistance Can lead to beta cell exhaustion resistance to insulin begins 10 yrs before diagnosis most common in those \> 40 (children being diagnosed more regularly) photo
32
Where are Glucagon-Like Peptide 1 receptors located
L-cells located primarily in distal ileum & colon but also jejunum & duodenum
33
What accounts for 90% of the incretin effect
Glucose Dependent Insulinotrophic polypeptide (K cells intestinal epithelia - mainly duodenum epithelia)
34
Glucose stimulated secretion of insulin
photo
35
Pathophysiology of type 2 diabetes
1. Insulin resistance 2. Incretin effect 3. Relative insulin deficiency
36
Contents of posionous venom of gila monster
- serotonin - hyaluronidase - phospholipases/diesterases - proteases
37
What is the biologically active peptide associated with gila monster
Exendin-4
38
What does exendin-4 do
Interacts with the GLP-1 receptor stimulates insulin release - over stimulation of pancreas in vivo - Development of synthetic exendin-4 BYETTA as a treatment of diabetes
39
Pre-receptor resistance
ANTIBODIES TO INSULIN No insulin receptor binding MUTANT INSULIN STRUCTURE Beta chain mutations - inactive FAMILIAL HYPERPROINSULINEMIA Increase in proinsulin - inactive
40
Receptor resistance
* Decrease in insulin receptor number/receptor affinity for insulin * Mutation or auto-antibody to insulin receptor
41
Post receptor resistance
Down regulation of beta-cell glucose transporters
42
MODY - Mature Onset Diabetes of the Young
Group of monogenic disorders characterised by autosomal dominantly inherited non-insulin dependent form of diabetes classically presenting in young adults before the age of 25 years - 2-5% of diabetics
43
MODY 1
HNF4A Transcription factor; decreased insulin secretion
44
MODY 2
GCK Decreased glucose sensitivity due to phosphorylation defect; decreased glycogen storage
45
MODY 3
HNF1A Transcription factor; decreased insulin secretion, progressive beta cell damage
46
MODY 4 (not as common)
PDX1/IPF1 Impaired pancreas development; homozygotes experience pancreas agenesis
47
MODY 5
HNF1B Transcription factor; decreased insulin secretion
48
DIABETES - disease of the 3 Polys
POLYPHAGIA No glucose entering cells =\> hunger Hyperglycemia - increased blood glucose Glucosuria - Glucose Tmax exceeded in kidney =\> glucose lost in urine POLYURIA Glucose drags water into urine POLYDIPSIA Increased thirst to replace water loss

GIT physiology (11 decks)

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