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endocrinology > insulin action > Flashcards

insulin action Flashcards

1
Q

describe insulin metabolic action

A 
decrease HGO
increase muscle uptake of glucose 
decrease proteolysis 
decrease lipolysis 
decrease ketogenesis
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2
Q

list the mitogenic actions of insulin in insulin resistance

A 
affects on: 
lipoproteins 
smooth muscle hypertrophy - important in high Bp 
ovarian function 
clotting 
energy expenditure
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3
Q

describe glucose transporter 4

A 
GLUT 4 
hydrophilic core 
hydrophobic outside 
in muscle and adipose tissue 
insulin responsive 
lies in vesicles 
recruited to membrane and enhanced by insulin 
7 fold increase in glucose uptake 
pre-made - allow glucose through membrane
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4
Q

describe action of insulin on muscle

A

stimulates protein synthesis

inhibits proteolysis and O2-CO2

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5
Q

what can AA in the circulation do

A

go to liver and used to make glucose - gluconeogenic eg alanine

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6
Q

describe glucose and glycogen

A

glucose in blood all time at low and regulated concentration
glycogen - short time store in liver

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7
Q

After fasting what happens in the liver

A 
glucagon enters 
proteolysis -- aa -- glucose 
maintain HGO
inhibited by glucose 
gluconeogenesis - gluconeogenic AA - pyruvate and lactate
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8
Q

what stimulates gluconeogenesis

A

Glyg
cats
Cort

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9
Q

how long are each of the fuel stores present

A

glycogen 16hours
protein 15days
fat 30-40days

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10
Q

describe the action of insulin after a meal

A

insulin stimulate break down of triglyceride by lipoprotein lipase in the blood vessel
nonesterified fatty acid and glycerol enter adipocyte
glucose enter through glut 4 -break into 2C segments - NEFA and glycerol enters normally and some is made from glucose
insulin then encourages the formation of triglycerides in the adipose cell

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11
Q

which hormones stimulate break down of triglycerides in fight/flight

A

catecholamines
cortisol
GH

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12
Q

describe the circulation in the blood

A

circles through omental circulation to gut and liver to pick up nutrients before entering systemic circulation.
adipocytes different in central circulation to in arms and legs - able to change met more, met and endo more active - predict ischemic heart disease - large stomach

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13
Q

describe hepatic gluconeogenesis

A

glycerol enter liver
phosphorylated – glycerol 3p – glucose
maintain HGO
glycerol 3 p can also make TG
NEFA enter TCA so can’t be used to make glucose `

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14
Q

what source of energy can the brain use

A

glucose and ketone bodies

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15
Q

what happens when NFEA enters body after fasting

A

shuttle on mt membrane – fatty acyl CoA make ketone bodies: acetoacetate and acetone + 3 OH-B
leave liver
sign of insulin deficiency because insulin stop ketone body production
if ketone bodies present with glucose - no insulin (T1DM)

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16
Q

describe hepatic glycogenolysis

A

glucose enter liver - phosphorylated glucose-6-p
insulin encourage to glycogen
Cats and glucagon encourage glycogenolysis forming glucose-6-p – glucose – increase HGO

17
Q

what happens when glucose enters the muscle

A

enter through glut 4
inhibited by GH, cats and cort
stored as glycogen
muscle can’t release glucose - stay in muscle and enter TCA for energy in muscle

18
Q

what happens in the fasted state

A

increased: proteolysis, lipolysis, HGO from glycogen and gluconeogenesis (from glycerol and AA - continually release glucose), muscle use lipids, brain use glucose then ketones, ketogenesis when prolonged, [NEFA]
low insulin to glucagon ratio, [glucose]=3-5.5mmol/l
decreased [AA] when prolonged

19
Q

what happens in the fed state

A

stop HGO (no need)
increase glycogen store, protein synth, lipogenesis
decrease the opposites
stored insulin release then 2nd phase high [insulin] to [glucagon] ratio

20
Q

link obesity to T2DM

A

insulin injections don’t work

obesity - 1 of many factors but not necessarily the cause of diabetes

21
Q

what is the presentation of T1DM

A 
absolute insulin deficiency 
high HGO 
glucose and ketones in  urine
loss of muscle - proteolysis and fat 
hyperglycaemia 
glycosuria with osmotic symptoms 
ketouria
22
Q

describe insulin induced hypoglycaemia

A

glucose enters muscle
eventually glucagon, cat, cort and GH increase HGO - imporove without intervention but may have accident in time
family can give intramuscular glucagon - better before paramedics turn up

23
Q

describe insulin resistance

A

affects intermediary metabolism
reside in muscle, liver and adipose - all 3
enough insulin to suppress ketogenesis and proteolysis - don’t lose weight and no inappropriate ketone production

24
Q

Insulin receptor and mitogenic

A

Insulin receptor MAPK pathway - growth and proliferation in utero and Children
high Bp and dyslipidaemia in adults

25
Q

Insulin receptor metabolic actions

A

IRS - insulin receptor substrates
PI3K-Akt pathway
Insulin resistance resides in this pathway
metabolic actions on glucose fat and AA
Functioning pancreas - insulin conc increases, glucose normal - don’t have diabetes - stimulate mitogenic pathway so people have High Bp and Abnormal lipid carriage lead to ischaemic heart disease
some therapeutic medications

26
Q

describe insulin action in insulin resistance

A

glucose protein and lipid normal
hyperinsulinaemic effect on mitogenic growth - excess stimulation of lipoproteins (less HDL - good cholesterol) abnormal lipoproteins - damage of arteries , smooth muscle hypertrophy - high Bp, ovarian function - polycystic ovarian syndrome, clotting, energy expenditure
2 major contributors to ischaemic heart disease - hypertension and lipoproteins

27
Q

what does insulin resistance cause - intermediary metabolism

A

high TG
low HDL
high fasting glucose >6mmol/l
high waist circumference
hypertension Bp >135/80
adipocytokines, inflammatory state, energy expenditure - used as a therapeutic target
might not have all of these in a person with diabetes

28
Q

presentation of T2DM

A

insulin resistance
60-80% people obese at presentation - central adiposity
dyslipidaemia - abnormal carriage of lipid in circulation, more subtle feature of IR at presentation
later insulin deficiency
hyperglycaemia
less osmotic symptoms
with complications

29
Q

management of DM

A

control: total calories, calories as fat, refined carb (more for T1 - match to insulin), increase calories as complex carbs - longer to absorb, increase soluble fibre, decrease sodium

endocrinology (12 decks)

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