metabolism and insulin Flashcards

insulin resistance: define insulin resistance and explain the relation to diabetes, dyslipidaemia, hypertension and ischaemic heart disease, and explain the consequences on metabolism

1
Q

define insulin resistance

A

where insulin is produced but target cells are not sensitive to it, resulting in elevated levels of blood glucose

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2
Q

insulin action in insulin resistance: effect on glucose

A

decrease hepatic glucose output (HGO), increase glucose muscle uptake

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3
Q

insulin action in insulin resistance: effect on protein

A

decrease proteolysis (breakdown of proteins into amino acids; oxidised for energy source in gluconeogenesis)

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4
Q

insulin action in insulin resistance: effect on lipid

A

decrease lipolysis (breakdown of lipids into glycerol and fatty acids using lipoprotein lipase)

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5
Q

why does lipolysis decrease when insulin acts in insulin resistance

A

after meal, lipids should be stored in adipocytes but can only enter as glycerol; once entered, stored as triglyceride by reaction of glycerol-3-P (from glucose) and non-esterified fatty acids (from triglycerides)

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6
Q

insulin action in insulin resistance: effect on ketone bodies

A

decrease ketogenesis (production of ketone bodies by the breakdown of fatty acids and ketogenic amino acids)

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7
Q

how is hepatic glucose output (HGO) increased

A

absence of insulin increases glycogenolysis and gluconeogenesis (triglycerides and glucogenic amino acids converted to glucose)

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8
Q

what part of triglycerides can the liver use in gluconeogenesis

A

glycerol, not non-esterified fatty acids

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9
Q

where does insulin resistance reside

A

liver, muscle and adipose tissue

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10
Q

what does insulin resistance effect

A

intermediary metabolism, glucose and fatty acids

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11
Q

with insulin resistance, what is there sufficient insulin to suppress

A

enough insulin to suppress lipolysis, ketogenesis and proteolysis, so break down of fat or protein doesn’t occur, so no weight loss

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12
Q

how are adipocytes in central circulation different to those in the limbs

A

central circulation anatomical sites have possibility of changing metabolism

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13
Q

how is insulin resistance and waist:hip circumference associated with ischaemic heart disease

A

if insulin resistant, gluconoegensis increases including breakdown of triglycerides in adipose tissue to glycerol and free fatty acids; increased production of free fatty acids is associated with the expansion of adipose mass, and due to atherosclerosis, ischaemic heart disease can be predicted by waist:hip circumference; obesity also increases amount of central adipocytes and are more likely to be insulin resistant as not enough insulin in circulation compared to mass; greater insulin production so greater mitogenic pathway stimulus

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14
Q

insulin resistance contributors to ischameic heart disease

A

dyslipidaemia and hypertension

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15
Q

how can an individual be insulin resistant with ischaemic heart disease, dyslipidaemia and hypertension without having type II diabetes mellitus

A

high insulin (hyperinsulinaemia) causes glucose to be normal but overstimulates mitogenic pathway so major growth and proliferation (high lipoproteins but low HDL, smooth muscle hypertrophy, ovarian function, clotting, energy expenditure)

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16
Q

what is insulin resistance associated with

A

high triglyceride, low HDL, high fasting glucose (not diabetic), high waist circumference, hypertension, adipoctyokines, inflammatory state, energy expenditure

17
Q

how is someone diagnosed as insulin deficient

A

high ketone presence in urine (insulin prevents ketogenesis) and high glucose level

18
Q

insulin induced hypoglycaemia: effect on hormones secreted

A

insulin remains high; increased insulin, glucagon, catecholamines, cortisol, growth hormone secretion to counter effect

19
Q

insulin induced hypoglycaemia: effect on HGO

A

glucose still continues to enter muscle; glucagon will manage to increase HGO with glycogenolysis and gluconeogenesis (lipolysis increased); without medical intervention it will get better long-term but should be prevented short-term

20
Q

insulin induced hypoglycaemia: treatment

A

subcutaneous insulin injection decreasing HGO; corrected by intramuscular glucagon increases HGO