Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GIT physiology > Effects of insulin > Flashcards

Effects of insulin Flashcards

You may prefer our related Brainscape-certified flashcards:
Git Commands flashcards
1
Q

Effects of insulin within cell

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 effects of insulin on the liver

A
  1. Increased glycogen synthesis 2. Increased glycolysis 3. Decreased gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 effects of insulin on fat

A
  1. Increased glucose transport 2. Increased lipogenesis 3. Decreased lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 effects of insulin on skeletal muscle

A
  1. Increased glucose transport (= fat) 2. Increased glycogen synthesis (= liver) 3. Decreased gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effect of insulin on glycogen metabolism (in hepatocytes)

A

see folder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Insulin regulated metabolism in an adipocyte

A

see folder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Relationship between EC & IC glucose and insulin

A

Linear relationship (graph)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What does insulin stimulate (5) 2. What does insulin inhibit (5)
A

Image

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the structure of glucagon

A

Peptide hormone 29 AAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is glucagon produced by

A

Alpha cells -20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the half life of glucagon

A

5-10 mins degraded by liver tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

2 factors that decrease glucagon secretion

A
  1. Increase blood glucose 2. Insulin (feed-forward mechanism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Target tissues of glucagon

A

Liver muscle adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Glucagon action on cells

A

see folder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Response to decreasing glucose levels

A

photo

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
Q

Tissue-specific isoform of SS-28

A

Major isoform in intestine

26
Q

Which SS isoform is more potent in inhibition of GH secretion

A

SS-28

27
Q

Which SS isoform is more potent in inhibition of glucagon release

A

SS-14

28
Q

What are the microvascular complications of diabetes (4)

A
  1. Diabetes eye disease (retinopathy & cataracts) 2. Renal disease 3. Erectile dysfunction 4. Peripheral neuropathy
29
Q

What are the macrovascular complications of diabetes (4)

A
  1. Stroke
  2. Heart disease & hypertension - 2-4x increased risk
  3. Peripheral vascular disease
  4. Foot problems
30
Q

Type I diabetes mellitus/Insulin dependent/Juvenile onset

A

5-10% of all DM Absolute insulin deficiency Pancreatic cell destruction photo

31
Q

Type II diabetes mellitus/non-insulin dependent/Adult onset

A

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
Q

Where are Glucagon-Like Peptide 1 receptors located

A

L-cells located primarily in distal ileum & colon but also jejunum & duodenum

33
Q

What accounts for 90% of the incretin effect

A

Glucose Dependent Insulinotrophic polypeptide (K cells intestinal epithelia - mainly duodenum epithelia)

34
Q

Glucose stimulated secretion of insulin

A

photo

35
Q

Pathophysiology of type 2 diabetes

A
  1. Insulin resistance 2. Incretin effect 3. Relative insulin deficiency
36
Q

Contents of posionous venom of gila monster

A
  • serotonin - hyaluronidase - phospholipases/diesterases - proteases
37
Q

What is the biologically active peptide associated with gila monster

A

Exendin-4

38
Q

What does exendin-4 do

A

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
Q

Pre-receptor resistance

A

ANTIBODIES TO INSULIN

No insulin receptor binding

MUTANT INSULIN STRUCTURE

Beta chain mutations - inactive

FAMILIAL HYPERPROINSULINEMIA

Increase in proinsulin - inactive

40
Q

Receptor resistance

A
  • Decrease in insulin receptor number/receptor affinity for insulin
  • Mutation or auto-antibody to insulin receptor
41
Q

Post receptor resistance

A

Down regulation of beta-cell glucose transporters

42
Q

MODY - Mature Onset Diabetes of the Young

A

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
Q

MODY 1

A

HNF4A

Transcription factor; decreased insulin secretion

44
Q

MODY 2

A

GCK

Decreased glucose sensitivity due to phosphorylation defect; decreased glycogen storage

45
Q

MODY 3

A

HNF1A

Transcription factor; decreased insulin secretion, progressive beta cell damage

46
Q

MODY 4 (not as common)

A

PDX1/IPF1

Impaired pancreas development; homozygotes experience pancreas agenesis

47
Q

MODY 5

A

HNF1B

Transcription factor; decreased insulin secretion

48
Q

DIABETES - disease of the 3 Polys

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions