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Endocrinology > Introduction to DM > Flashcards

Introduction to DM Flashcards

1
Q

General effects of insulin?

A

decrease hepatic glucose output
increase glucose uptake by muscles
decrease lipolysis/ketogenesis
decrease proteolysis

MITOGENIC PATHWAY 
lipoproteins
smooth muscle hypertrophy
ovarian function
clotting 
energy expenditure
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2
Q

Where is GLUT 4 abundant?

A

muscle and adipose tissue

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3
Q

How is glucose up-taken?

A

via GLUT4 transporters
insulin stimulates GLUT4
has hydrophobic elements on outside and hydrophilic core that allows glucose into cell (insulin responsive)

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4
Q

When is GLUT4 recruited?

A

sits in vesicles in cytoplasm
insulin recruits them to membrane
causes 7x increase in glucose uptake

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5
Q

What is the effect of insulin on protein?

A

stops proteolysis
prevents AA oxidation in muscle cell
increase re-synthesis of proteins from AAs (also IGF1)

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6
Q

What increase proteolysis when stressed?

A

cortisol
these amino acids (gluconeogenic ones eg alanine) can enter circulation and move to liver to produce glucose

somatotrophin has opposite effect

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7
Q

What is the effect of insulin on the liver?

A

inhibits gluconeogenesis
cateacholamines, cortisol, somatotrophin and glucagon increase it
increase protein formation

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8
Q

What occurs in the liver?

A

gluconeogenic amino acids enter liver via specific transporter channels
glucagon increases uptake
protein synthesis stimulated by insulin
or amino acids used to generate glucose

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9
Q

What is the hepatic glucose output?

A

glucose produced from gluconeogenesis than enters circulation

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10
Q

What is our long term energy store?

A

fat

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11
Q

What are the effects of insulin on adipocytes?

A
  1. TGs from vasculature are too big to enter adipocyte directly
  2. broken down by lipoprotein lipase to glycerol and non esterified FAs
  3. stimulated by insulin
  4. Absorbed into adipocyte and used to make NEFA
  5. glucose may also generate 2 glycerols and FAs can be stuck to make TAGs

INSULIN STOPS LIPOLYSIS

  • in blood it breaks down fats so can enter adipocyte
  • adipocyte promotes formation of TG and storage of fat
  • inhibits lipolysis
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12
Q

Why is omental fat/waist circumference indicative of risk of heart disease?

A

adipocytes in gut are different in activity and endocrine regulation compared to rest of body

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13
Q

How is glycerol used by the liver?

A
  1. glycerol from adipocytes/food to liver
  2. used to make TGs
  3. these enter lipoproteins or used for gluconeogenesis or lipogenesis (but cannot re-enter glucose pathway)
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14
Q

What happens after 10hr fast?

A

25% of hepatic glucose output supported by new glucose production

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15
Q

What is the effect of insulin on ketone body synthesis?

A
  1. FAs from lipolysis used to make ketone bodies
  2. insulin inhibits conversion of fatty acyl CoA to ketone bodies
  3. glucagon promotes it
  4. ketone bodies enter circulation and mainly used by muscles
  5. if someone has high insulin they should stop making ketone bodies
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16
Q

What is caused by high glucose and high ketone bodies?

A

insulin deficiency

17
Q

What are ketone bodies?

A

3 water soluble molecules produced in liver from FAs during periods of low food intake/carb restriction

acetone
acetoacetic acid
beta-hydroxybutyric acid

18
Q

What is the effect of insulin on glycogenolysis?

A

insulin promotes storage of glucose at glycogen - inhibit

glucagon/catecholamine promote glycogenolysis

19
Q

What is the effect of insulin on glucose uptake by muscle?

A
  1. glucose enters via GLUT4
  2. insulin promotes uptake
  3. stress hormones inhibit uptake
  4. glucose stored as glycogen
20
Q

Describe the fasting state?

A

low insulin: glycogen ratio
normal blood glucose (change in insulin : glucagon ratio)
muscle uses lipid
brain uses glucose –> ketone bodies

21
Q

What is characteristic of fasting state?

A 
increase...
[] NEFA
proteolysis
lipolysis 
hepatic glucose output

decrease…
amino acid []
IF PROLONGED FASTING

22
Q

Describe the fed state?

A

high insulin:glycogen ratio
stored insulin release
then 2nd phase
stop hepatic glucose output

23
Q

What is characteristic of fed state?

A

increase…
glycogen
protein synthesis
lipogenesis

decrease…
gluconeogenesis
proteolysis

24
Q

How does T1DM present?

A

absolute insulin deficiency

  • proteolysis with weight loss
  • hyperglycaemia
  • glycosuria with polyuria/dipsia
  • ketonuria
25
Q

What occurs after insulin induced hypoglycaemia?

A

increase catecholamines, glucagon, cortisol, somatotrophin

decrease HGO, lipolysis
subcutaneous insulin switches off HGO

26
Q

What can increase HGO?

A

intramuscular glucagon

treat insulin induced hypoglycaemic attack

27
Q

Where is insulin resistance found?

A

liver, muscle, adipose tissue

28
Q

What is the effect of LDL/dyslipidaemia?

A

major cause of heart disease in diabetics due to vessel damage

increases...
circulating NEFA
TGs
LDLs
decreases...
lipoprotein lipase activity
VLDL clearance
HDL cholesterol
29
Q

What distinguishes T1DM from T2DM?

A

T1 is high glucose and ketones, losing weight, diabetic symptoms

T2 enough insulin to suppress ketone production and proteolysis

30
Q

What 2 pathways are affected by insulin?

A

mitogenic (MAPK)

metabolic (PI3K-Akt)

31
Q

What does the feedback loop for insulin production mainly work through?

A

blood glucose []

32
Q

What will someone with insulin resistance have?

A

compensatory hyperinsulinaemia

  • to make enough insulin to have normal blood glucose
  • this happens in T2DM person before glucose is elevated
  • high insulin still harming because increases mitogenic pathway
33
Q

Where does insulin resistance reside?

A

metabolic pathway

control of insulin depends on blood glucose [] and not downstream effects on mitogenic pathway

34
Q

What are features of insulin resistance?

A 
hypertension BP>135/80
high TG
low HDL
high LDL
fasting blood glucose >6
adipocytokines
inflammatory state
energy expenditure
high omental fat (waist circumference)
35
Q

How does T2DM present?

A 
60-80% obese
dyslipidaemia
later insulin deficiency (beta cells exhausted)
hyperglycaemia
fewer osmotic symptoms
36
Q

Complications and identifying diabetes?

A

T1DM hardly presents with complications

T2DM does

37
Q

How is T2DM controlled via diet?

A

control total calorie

increase. ..
- complex carbs
- soluble fibre
decrease. ..
- fat
- refined carbs
- Na (lower risk of hypertension)

Endocrinology (13 decks)

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