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Pathohysiology > Insulin Resistance > Flashcards

Insulin Resistance Flashcards

1
Q

why do we get fat?

A

endocrinology
genetics
chemicals
bacteria

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2
Q

why is obesity a problem?

A

Because it leads to insulin resistance which leada to diabetes.
High insulin is a cause and consequence of fat gain.

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3
Q

Diabetes

A

to pass through

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4
Q

mellitus

A

sweet or honeyed

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5
Q

Where is insulin synthesized?

A

in the pancreatic beta cells

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6
Q

what are some ways we can check for insulin production?

A

you can check insulin levels but some people have anti insulin antibodies so in cases like that we can check the c-peptide levels bc we release that along with insulin into our blood stream. That way we can see if we are even producing insulin.

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7
Q

guconeogenesis

A

generation of glucose

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8
Q

how does blood glucose increase?

A

increase in uptake from digestive tract
increase glucose recovery from the kidneys
increase glucose release form the liver.
Glucose clearance.

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9
Q

how is glucose recovered from the kidneys or up taken from the digestive tract?

A

glucose is transported against a concentration gradient by a sodium glucose symport.

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10
Q

SGLT

A

Sodium-Glucose symport.
Present in epithelial cells in the gut and kidney. They utilize the Na gradient as the energy source for glucose transport

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11
Q

what would happen if we has a sodium free diet?

A

our blood glucose levels would be really low because we wouldnt have the Na necessary for the SGLT. Glucose would be stuck in our kidneys or intestines

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12
Q

Which organ is the only one who can dephosphorilate glucose?

A

the liver

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13
Q

why doesn’t glucose leave cells?

A

because once it is in a cell that wants it, it is phosphorilated and can’t pass.

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14
Q

glucose transporters

A

get glucose in and out of all cells of the body.

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15
Q

how many types of glucose transporters are there?

A

13

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16
Q

which glucose transporters are not regulated by insulin?

A

GLUT 1-3 and 5-13. they are found in the RBCs, brain, kidney, liver, intestine, etc.

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17
Q

which glucose transporters are regulated by insulin?

A

GLUT 4
glucose can only go into the cell is insulin is present.
Found in skeletal muscle, cardiac muscle, and adipocytes.

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18
Q

When is insulin acutely high?

A

After meals.

Insulin is highest after breakfast, then dinner and then lunch.

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19
Q

When is insulin chronically high?

A

when you are insulin resistant (pre-diabetes) or when you have type II diabetes

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20
Q

how does your sympathetic nervous system regulate insulin?

A

it increases glucagon and decreases insulin

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21
Q

how does your parasympathetic nervous system regulate insulin?

A

increases insulin and decreases glucagon release.

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22
Q

What does thinking about food, relaxation, etc do to insulin?

A

it increases insulin and reduces glucagon

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23
Q

what does stress do to insulin?

A

decreases insulin and increases glucagon

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24
Q

which cells have insulin receptors

A

all cells have insulin receptors but muscle, cardiac, and adipose cells need it the most.

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25
Q

what does insulin do to your liver?

A

inhibits ketgenesis
activated lipogenesis
activates glycogenesis
tells liver to make fat and glycogen

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26
Q

what does insulin do to your muscle cells?

A

causes glucose uptake and anabolism. muscle growth.

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27
Q

what does glucose do to your adipose cells?

A

activates glucose uptake, lipogenesis and adipogenesis

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28
Q

role of glucagon

A

glucagon has the opposite affects as insulin

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29
Q

what is the primary regulator of insulin and glucagon release?

A

plasma glucose concentration

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30
Q

what does insulin do to glucagon?

A

insulin inhibits glucagon secretion directly

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31
Q

what does glucagon do to insulin?

A

glucagon stimulates insulin secretion directly and indirectly

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32
Q

what affect does glucagon have on the liver?

A

glycogenolysis
gluconeogenesis
ketogenesis

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33
Q

what affect does glucagon have on muscle cells?

A

no effect because they dont have glucagon receptors.

34
Q

what affect does glucagon have on adipose cells?

A

causes lipolysis (break down of fat)

35
Q

overall affects of glucagon:

A

increases glucose, fat and ketones

36
Q

effects of carbs on fat hormones:

A

increases insulin, decreases glucagon. overall, fat increase and muscle growth.

37
Q

affects of protein on fat hormones:

A

increases insulin, increases glucagon. little to no fat gain. insulin is more potent than glucagon so while insulin is creating fat and glucagon is breaking it down then eventually insulin will win.

38
Q

effects of fat on fat hormones:

A

no effect on insulin, increase glucagon. overall it will tell fat cells to lyse. so fat lose.

39
Q

fasting glucose for a healthy person

A

75-100

40
Q

fasting glucose for type I diabetes

A

greater than 126

41
Q

fasting glucose for MODY

A

greater than 126

42
Q

Fasting glucose for type II diabetes

A

greater than 126

43
Q

Fasting glucose for IR

A

110-126

44
Q

fasting insulin for healthy person

A

1-10

45
Q

fasting insulin for type I

A

about 0

46
Q

fasting insulin for MODY

A

about 0

47
Q

fasting insulin for type II

A

greater than 12

48
Q

fasting insulin for IR

A

greater than 10

49
Q

Type I diabetes

A

destruction of pancreatic beta cells which is were the insulin is coming from. We lose all of them. Its a reaction from the auto immune system which produces anti beta cell antibodies which “eat up” the beta cells. occurs in childhood (1st decade) Insulin is the treatment

50
Q

MODY

A

no loss of pancreatic beta cells but a reduction in beta cell insulin production so you don’t have the enzymes to produce insulin. they still have beta cells though so that is how you can check for MODY vs Type I

51
Q

type 2 diabetes

A

normal or greater beta cell mass. excess insulin production. Usually occurs later in life. whats happening is that your insulin levels are constantly high due to constant high glucose that your cells receptors become desensitized to insulin. so you’re producing tons of insulin but not doing anything with it.

52
Q

AGE

A

formed when there is excess glucose. the glucose binds to an amino acid forming AGE.

53
Q

RAGE

A

AGE is bound to rage which increases swelling which then causes cellular damage in the long run. it also attracts pathogens when it is activated.

54
Q

Sorbitol

A

excess glucose in the cell turns into sorbitol. we cannot control sorbitol as well so it is just in the cells and we are slowing degrading it. Since its all in the cell it increases cell osmolarity and ultimately damages the cell.

55
Q

how are ketones formed? f

A

from amino acids and fatty acids.

they are formed in the liver

56
Q

examples of ketones

A

acetone
acetoacetate
B-hydroxybutyrate

57
Q

what does insulin do to ketogenesis?

A

INHIBITS!!! ALWAYS!!!

58
Q

what does glucagon do to ketogenesis?

A

it stimulates it.

59
Q

ketosis

A

regulated and controlled production of ketones.
happens often.
no change in blood pH
protects amino acid derived gluconeogenesis

60
Q

ketoacidosis

A 
extreme uncontrolled ketogenesis
exhausts buffering capacity (dangerous)
nausea
vomiting 
Kussmaul respirations (breathing quick in order to restore blood pH. releasing CO2)
61
Q

when are ketones used?

A

when we don’t have glucose in our blood (fasting) ketones are an important form of energy especially for our brains.

62
Q

what purpose do ketones serve during diabetes?

A

no purpose because our body as excess glucose so ketones are not needed.

63
Q

what fuel does the brain use?

A

glucose

64
Q

what fuel does muscle and adipose use?

A

fat

65
Q

which type of diabetes does ketoacidosis always accompany?

A

T1DM because you can’t metabolize glucose so your cells are essentially starving.
it almost never accompanies type 2.

66
Q

Insulin Resistance

A

normal to greater beta cell mass
excess insulin production
all T2DM started with IR

67
Q

symptoms of IR

A 
onset usually later in life
hyperinsulinemia
acanthosis nigricans (darkening of skin)
hypercholesterolemia
hypertension
68
Q

HOMA

A

insulinxglucose/405

69
Q

how does the liver change in IR?

A

it continues to inhibit ketogenesis and it continues to activate lipogenesis but it no long activated glycogenesis. It instead activates gluconeogenesis.

70
Q

metabolic syndrome

A 
insulin resistance
central obesity
hypertension
increased TAG
reduced HDL
71
Q

What advantage dies it provide the body to produce ketones during diabetes mellitus?

A

the ketones serve no useful role.

72
Q

what are the two adipose compartments?

A

Subcutaneous (giggly belly) and visceral (deeper hard belly. BAD)

73
Q

Is subcutaneous or visceral fat pro-inflammatory?

A

visceral

74
Q

what does ceramide do?

A

it accumulates in the muscle and liver due to an accumulation of cytokines.

75
Q

tell me about macrophages and cytokines in visceral fat

A

an increase of visceral fat causes an accumulation of macrophages. If visceral fat goes down so do macrophages. Af fast is released into the blood cytokines go with it which induce inflammation and then an accumulation of ceramide which then causes insulin resistance.

76
Q

why isn’t liposuction healthy?

A

because it only removes subcutaneous fat which is not the worse kind. it remoces adipose cells but then the other adipose cells in other places grow more.

77
Q

how can you treat insulin resistance?

A

inhibition of ceramide. doing so will impove insulin sensitivity and improve cardiovascular function as well as prevent weight gain.
lifestyle changes

78
Q

Metformin

A

most commonly used as an anti diabetic drug. it’s the most affective yet.

79
Q

true or false: reduced carb intake leads to increased weight loss and enhanced insulin sensitivity

A

true

80
Q

which disorder does gestational diabetes resemble?

A

insulin resistance. gestational diabetes increases your risk of T2DM. breast feeding for more than 3 months reduces the risk.

Pathohysiology (16 decks)

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