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Endocrinology > Introduction to Diabetes Mellitus: Insulin action (5) > Flashcards

Introduction to Diabetes Mellitus: Insulin action (5) Flashcards

1
Q

What effect does insulin have on glucose

A

it decreases hepatic glucose output and increases uptake of glucose by muscles

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2
Q

What effect does insulin have on protein

A

it decreases proteolysis (breakdown of protein)

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3
Q

What effect does insulin have on lipids

A

it decreases lipolysis and decreases ketogenesis

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4
Q

What other effects does insulin have

A

growth, vascular effects, ovarian function, clotting and energy expenditure

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5
Q

what transporter is glucose uptake through

A

Glucose Transporter 4 (GLUT 4)

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6
Q

Where is GLUT 4 particularly abundant

A

in muscle and adipose tissue

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7
Q

What stimulates GLUT 4

A

insulin

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8
Q

Describe the structure and location of GLUT 4 in cells

A

It has hydrophobic elements on the outside embedded in the membrane and a hydrophilic core which allows glucose into the cell. GLUT-4 sits in vesicles within the cytoplasm

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9
Q

How does insulin cause a 7 fold increase in glucose uptake

A

insulin recruits GLUT 4 to the membrane. they are insulin responsive

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10
Q

What does cortisol do in muscle cells when we are stressed

A

increase proteolysis

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11
Q

what effect does insulin have on amino acids in muscle cells

A

prevents the oxidation of them and increases the re-synthesis of proteins from amino acid

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12
Q

what are gluconeogenic amino acids

A

amino acids that have entered the circulation and moved to the liver where they are used to produce glucose

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13
Q

how do gluconeogenic amino acids enter the liver

A

via specific transporter channels.

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14
Q

what increases the uptake of amino acids into the liver

A

glucagon

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15
Q

what does insulin stimulate in the liver

A

protein synthesis

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16
Q

What increases gluconeogenesis in the liver

A

Somatotrophin, Cortisol, Catecholamines and Glucagon

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17
Q

What inhibits gluconeogenesis in the liver

A

insulin

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18
Q

what is hepatic glucose output (HGO)

A

glucose produced by gluconeogenesis in the liver that enters the circulation

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19
Q

What are triglycerides broken down by before they can enter the adipocyte

A

lipoprotein lipase stimualated by insulin

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20
Q

what is the triglyceride broken down into

A

glycerol and non esterified fatty acids

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21
Q

why does glucose enter the adipocyte

A

to be used to make NEFA with glycerol and non esterified fatty acids

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22
Q

how can glucose be used to make triglycerides

A

it can be chopped up to make 2 glycerols and the fatty acids can be stuck to the glycerol to make triglycerides

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23
Q

what effect does insulin have on fat in the blood

A

breaks down fats so it can enter the adipocyte

24
Q

what effects does insulin have on fat in the adipocyte

A

promotes formation on triglyceride and storage of fat and inhibits lipolysis

25
Q

why is waist circumference a simple indicator of an individuals risk of ischaemic heart disease

A

blood reaches the gut and there is a portal system connecting the intestines to the liver. the blood passes through the liver for the absorbed food to be processed. adipocutes in the gut are different in activity and endocrine regulation compared to the rest of the body

26
Q

what is glycerol from adipocytes and food entering the liver used for

A

to make triglycerides which then enter lipoprotein particles

27
Q

what can glycerol also be used to make

A

glucose and this supports hepatic glucose ouput

28
Q

why cant fat do even though glycerol can be used to make glucose

A

reenter the glucose pathway

29
Q

what happens after a 10 hour fast

A

25% of our hepatic glucose output is supported by new glucose production

30
Q

what fuel can the brain use and not use

A

can use glucose and ketone bodies but cannot use fatty acids

31
Q

what can fatty acids made from lipolysis be used to make in the liver

A

ketone bodies

32
Q

what is the effect of insulin on ketone body synthesis in the liver

A

it inhibits the conversion of Fatty Acyl CoA to ketone bodies

33
Q

high blood glucose + high ketone bodies =

A

insulin deficient

34
Q

definition of ketones

A

three water soluble molecules that are produced by the liver from fatty acids during periods of low food intake or carbohydrate restriction.

35
Q

what are the three ketone molecules

A

acetone, acetoacetic acid, beta-hydroxybutyric acid

36
Q

what promotes hepatic glycogenesis

A

insulin, glucagon and catecholamines

37
Q

what is glucose converted to in the liver

A

glucose-6-phosphate

38
Q

what are the 2 processes that support hepatic glucose output

A

gluconeogenesis and glycogenolysis

39
Q

what promotes uptake of glucose by GLUT-4

A

insulin

40
Q

what inhibits uptake of glucose by GLUT-4

A

stress hormones - GH, CATS, CORT

41
Q

what is glucose stored as in muscle cells

A

glycogen

42
Q

characteristics of the fasted state

A

low insulin : glycogen ratio. normal blood glucose concentration due to the change in ratio. muscle uses lipid. brain uses glucose and then at a later stage ketone bodies

43
Q

what is there an increase of in the fasted state

A

concentration of NEFA, proteolysis, lipolysis, hepatic glucose output

44
Q

what is there a decrease of in the fasted state

A

amino acid concentration when prolonged

45
Q

characteristics of the fed state

A

high insulin:glucagon ratio. stored insulin released then you get 2nd phase insulin release. stop hepatic glucose output

46
Q

what is there an increase of in fed state

A

glycogen, protein synthesis and lipogenesis

47
Q

what is there a decrease of in fed state

A

gluconeogenesis, proteolysis

48
Q

presentation of type 1 diabetes mellitus

A

Absolute insulin deficiency. Proteolysis with weight loss. Hyperglycaemia. Glycosuria with osmotic symptoms. Ketonuria

49
Q

Insulin induced hypoglycaemia causes an increase in:

A

insulin, glucagon, catecholamines, cortisol and somatotrophin, HGO and lipolysis

50
Q

What is insulin induced hypoglycaemia and how is it treated

A

Treatment induced complication. Increased insulin from SUBCUTANEOUS stores –> glucose uptake into muscle –> low plasma glucose concentration. TREATMENT: Increased INTRAMUSCULAR glucagon –> increased HGO, Glycogenolysis and gluconeogenisis and increased lipolysis –> increased plasma glucose

51
Q

Insulin resistance and its effects

A

It resides in the liver, muscle and adipose tissue. Increase in LDL (dyslipidaemia), circulating NEFA, triglyceride. decrease in lipoprotein lipase activity, VLDL clearance and HDL cholesterol.

52
Q

in T2DM what is there enough insulin to suppress

A

ketone production and proteolysis

53
Q

what 2 pathways does insulin have an effect on

A

mitogenic pathway (MAPK) and metabolic pathway (PI3K-Akt)

54
Q

compensatory hyperinsulinaemia

A

someone with insulin resistance makes enough insulin to maintain normal blood glucose

55
Q

features of insulin resistance

A

hypertension (BP>135/80), high triglyceride, high ldl, fasting blood glucose > 6.0mmol/L, adipocytokines, inflammatory state, energy expenditure, large waist circumference

56
Q

presentation of T2DM

A

Insulin resistance. 60-80% obese. Dyslipidaemia. Later insulin deficiency. Hyperglycaemia. Less osmotic symptoms. With complications

57
Q

management of T2DM by controlling diet

A

Control total calorie intake. reduce fat, refined carbohydrate and sodium. increase complex carbohydrate and soluble fibre

Endocrinology (12 decks)

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