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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Alternative effects of insulin

A 
Lipoproteins
Smooth muscle hypertrophy
Ovarian function
Clotting
Energy expenditure
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2
Q 
GLUT-4
Structure
Which cells have it?
Where are they in cells?
Increased number from?
A

Hydrophobic, outer part sits in membrane
Hydrophilic core= glucose enters into cells

Muscle+ adipose tissue
Membrane, but also lie in vesicles, recruited+ enhanced by insulin

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3
Q

Muscle cell
Proteolysis inhibited by?
Stimulated by?
Protein synthesis stimulated by?

A

Insulin, amino acids could be used as energy source (gluconeogenic amino acids could go to liver+ used to make glucose)
Cortisol
Insulin, Growth Hormone, IGF1

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4
Q

Liver cell
Glucagon effect?
Insulin effect?

A
  1. Gluconeogenic amino acids enter liver, stimulated by glucagon
  2. Protein synthesis (from aas), stimulated by insulin OR
  3. Protein lysis (protein to aas), stimulated by protein deficiency or glucagon
  4. Amino acids could also be converted to glucose, inhibited by insulin, stimulated by glucagon, catecholamines, cortisol= GLUCONEOGENSIS
  5. Glucose leaves cells into blood
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5
Q

Carbohydrates, Proteins, Fat
Most energy from?
Used for the longest amount of time?

A

Fat

Fat

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6
Q

Adipocyte

Insulin effect?

A
  1. Triglyceride broken down in vessels by lipoprotein lipase, stimulated by insulin= increase glycerol in blood
  2. NEFA (Non-esterified fatty acids) cross vessel membrane into adipocytes
  3. Glucose also cross into adipocytes through GLUT-4, stimulated by insulin, can be broken down into NEFAs
  4. Glucose can also be converted into glycerol-3-phosphate
  5. Glycerol+ NEFAs combine to form triglyceride in adipocytes, stimulated by insulin
  6. Triglycerides broken down to glycerol leaves adipocytes, inhibited by insulin, NEFAs also leave adipocytes, stimulated by glucagon, catecholamines, cortisol
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7
Q

Hepatic gluconeogenesis pathway

Know flashcard 4 for all pathways+ more detail

A
  1. Glycerol enters hepatocytes, converted to glycerol-3-phosphate
  2. Glycerol-3-phosphate converted into glucose+ leaves to blood
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8
Q

Energy that brain can/not use

A

Can use
Glucose
Ketone Bodies

Can’t use
Fatty acids

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9
Q

NEFA conversion to ketone bodies
Glucagon effect?
Insulin effect?

A
  1. NEFA enters hepatocyte
  2. Shuttle on mitchondrial membrane= converted to fatty acyl CoA
  3. Fatty acyl CoA→ Acetyl CoA→ Aceoacetate→ Acetone+ 3-hydroxybutarate (ketone bodies), inhibited by insulin, stimulated by glucagon
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10
Q

Hepatic glycogenolysis

A
  1. Glucose enters hepatocytes, converted to glucose6- phosphate
  2. Glucose 6 phosphate→ glycogen, stimulated by insulin (reverse reaction stimulated by glucagon, catecholamines)
  3. Glucose-6-phosphate→ glucose, released into liver
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11
Q

Fatty acids+ Glycogen+ muscle cells

Insulin effect?

A
  1. Glucose enters muscle cells by GLUT-4, stimulated by insulin, inhibited by glucagon, catecholamines, cortisol
  2. Glucose either converted to glycogen or acetyl-CoA
  3. Fatty acids also enter muscle cells+ can be converted to acetyl CoA
  4. Acetyl CoA enters TCA cycle for respiration
    Muscle can use+ store glycogen but can’t release it again (unlike liver)
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12
Q

Fasted state

A

Low insulin: glucagon ratio
Increase NEFAs
Low amino acids when prolonged fasting
Increased proteolysis from muscles
Increased lipolysis to glycerol+ fatty acids
Increase HGO from glycogen+ gluconeogenesis
Muscle uses lipids
Brain uses glucose+ later ketones
Increased ketogenesis when prolonged fasting

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13
Q

Fed state

A 
Stored insulin released
High insulin: glucagon ratio
Stop HGO
Increase glycogen
Decreased gluconeogenesis
Increased protein synthesis in muscles
Decreased proteolysis
Increase lipogenesis in adipose
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14
Q

Type 1 diabetes presentation

A 
Absolute insulin deficiency
Increased proteolysis (increased amino acids)= weight loss
Increased lipolysis (increased glycerol+ amino acids)
Increased HGO (increased glucose+ ketones)= hyperglycaemia+ glycosuria (glucose in urine) with osmotic symptoms, ketonuria (ketones in urine)
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15
Q

Insulin induced hypoglycaemia

Treatment?

A

Increased insulin
Increased glucagon, catecholamines, cortisol
Increased growth hormone
Glucose enters muscle
Increased HGO later with glycogenolysis+ gluconeogenesis (gets better)
Increased lipolysis

Intramuscular glucagon

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16
Q

Insulin pathway in normal cells

Insulin resistance?

A

Binds to receptor, then 2 pathways:

  1. MAP Kinase pathway= growth + proliferation (especially in children)
  2. Insulin Receptor Substrate activated and activates PI3K- Akt pathway → Metabolic actions on fat, glucose, amino acids

Insulin resistance= only in PI3K- Akt pathway (IRS function)= more insulin secreted in Type II Diabetes (compensatory hyperinsulinaemia)
Consequence= excessive MAPK pathway stimulation= high blood pressure even if there aren’t any diabetic symptoms

17
Q

Clinical features of Insulin resistance

A 
Hypertension (140/80)
Waist circumference
Fasting glucose> 6mmol/L
High TG
Low HDL
Insulin resistance, Adipocytokines, Inflammatory state, Energy expenditure
18
Q

Presentation of Type 2 diabetes

A 
Insulin resistance
Dislipidaemia (abnormal carriage of lipids in circulation)
Later insulin deficiency
Hyperglycaemia
Less osmotic symptoms than Type 1
19
Q

Healthy diet

A 
Total calories control
Reduce fat calories
Reduce refined carbohydrate
Increase complex carbohydrate
Increase soluble fibre
Decrease sodium

Endocrinology (11 decks)

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