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Unit 10 > Week 5:Endocrinology 3 Glucose levels > Flashcards

Week 5:Endocrinology 3 Glucose levels Flashcards

1
Q

What are the main cell types that depend on glucose for their energy?

A

Red blood cells
Brain
Renal Medulla

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2
Q

What are the main regulators or blood glucose?
Why?

A

INsulin
Glucagon
Respond directly to levels of blood glucose

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3
Q

What are the consequences on the brain of long term starvation?

A

Reduced blood glucose
No blood glucose available
Relatiant on ketone bodies for alternative source of energy
Can result in permanent and grave brain damage

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4
Q

What is the average level of bloodstream glucose?

A

4.5 to 7 mM

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5
Q

What is the basic role on insulin?

A

Promote glucose uptake in muscle and adipose tissue
Glucose usage in glycolysis
Glycogen synthesis
Protein synthesis
Uptake of ions (k+ and phosphate)
Prevents hyperglycemia

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6
Q

What is the basic role of glucagon?

A

Promote glycogenolysis
Gluconeogenesis
Lipolysis
Glycogenolysis
Ketogenesis
Proteolysis
Prevents hypoglycemia

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7
Q

What is the role of the endocrine pancreas?

A

Structure = islets of Langerhans
Alpha cells - secrete glucagon
beta cells - secrete insuline
D cellls - secrete somatostatin - inhibits insulin and glucagon release
F cell/PP cell - release Pancreatic polypetide

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8
Q

What cell types are most abundant in the islet of langerhan?

A

Beta cells
Alpha cells
D cells
Level of PP cells varies.

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9
Q

What is the structure of insulin?

A

Made of two polypetide chains - a shorter alpha chain and a longer beta chain
These chains are crosslinked by two disulfide bonds
The alpha chain also has an intrachain disulfide bond

Produces alongside a C-peptide but this is cleaved in active insulin.
In total consists of 51 amino acids.

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10
Q

What is the half life on insulin and C-peptide?
Why is this important for clinical investigations?

A

Insulin - 4-6 minutes
C-peptide - 30 minutes
C-peptide preferred in clinical measurements to estimate levels of insulin when trying to differentiate between type 1 and type 2 diabetes - less random and more accurate of an average
High in type 2, low in type 1

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11
Q

Describe how insulin is formed

A
  1. Preproinsulin - consists of a signal sequence, beta chain, C-peptide and an alpha chain
  2. Signal sequence is cleaved by an enzyme in the endoplasmic reticulum - forms proinsulin
  3. C-peptide is cleaved and disulfide bonds form in the golgiapparatus - forms insulin.
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12
Q

How does high blood glucose lead to insulin release?

A
  1. Beta cells in the islet of langerhans take up glucose, convert to glucose 6 phosphate by action of glucokinase, which is then used in oxidative phosphorylation to produce ATP
  2. ATP : AMP ratio increases to high level at blood glucose greater than 5mM. THis causes ATP-sensitive K+ channels to close
  3. K+ build up inside the cytoplasm causing membrane depolarisations
  4. THis opens voltage gated calcium ion channels - influx of calcium
  5. High levels intracellular calcium results in release of stored granules containing insulin and C-peptide. (1;1 ratio)
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13
Q

Where are GLUT4 receptors found and what is their role?

A

Are insulin dependent
In skeletal muscle - cause inc glucose uptake, glycogen synthesis and protein synthesis
In adipose tissue - cause inc glucose uptake, inc lipogenesis and decreased lipolysis

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14
Q

Where are GLUT 2 receptors found and what is their role?

A

Are insulin independent
Found in liver - increase lipogenesis + glycogen synthesis and decrease gluconeogenesis
Found in basolateral enterocytes - absorption of monosaccharides from GIT

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15
Q

What factors cause insulin secretion from beta cells?

A

Blood glucose conc above 5mM - main factor
Can also be enhanced by
1. amino acids - arginine, leucine and glutamine
2. Gut hormones - incretin (GLP and GIP)
3. Neural output - parasympathetic ACh after a meal

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16
Q

What factors inhibit insulin release?

A

Sympathetic - adrenaline and noradrenaline

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17
Q

What is the detailed version of insulin production and secretion?

A

Stimulated by high blood glucose
Genes encoding for insulin are transcribed to mRNA in the nucleus
Translation occurs when bound to ribosome, forms an N-terminal hydrophobic signal sequence that aids in the transport of mRNA and ribosomes to RER
N-terminal sequence - penetrates the RER resulting in preproinsulin production and continues to elongate into RER
Signal sequences is cleaved in RER forming proinsulin
Transport to golgi -cleaved to insulin and C-peptide that are stored in secretory granules
Released by excytosis

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18
Q

What type of receptor is the insulin receptor?
How does it bring about its effects?

A

Is a tyrosine kinase - binding of insulin triggers a conformational change that results in autophosphorylation
Activates MAP kinase signalling pathway
Activates PI-3K pathway

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19
Q

What are the consequences of the activation of the MAP kinase signalling pathway by insulin?

A

Cell growth
Cell proliferation
Gene expression

20
Q

What are the consequences of the activation of the Pi-3K signalling pathway by insulin?

A

Synthesis of lipids, protein and glycogen
Cell survival and proliferation
Fusion of vesicles containing GLUT 4 within cell membrane - increases amount of functional GLUT 4 on membrane

21
Q

What is meant by the fasted and the fed state?

A

Fed - 2 hours after a meal
Fasted - 5-6 hours after a meal

22
Q

What are the conditions of glucose metabolism in the fasted state?

A

Low glucose levels
Glycogen stores are depleted to supply more glucose
Muscles and adipose tissue switch to an alternative supply - mainly Fatty acids and ketons

23
Q

What are the conditions of glucose metabolism in the fed state?

A

High glucose levels
Hepatic gluose production is no longer required
Alternative fuels not required
Excess glucose is diverted to energy storage.

24
Q

What are some common pathologies of insulin?

A

Diabetes Mellitus
Maturity-onset diabetes of the young
Secondary diabetes
Gestational diabetes

25
Q

What are the different types and causes of diabetes mellitus?

A

TYpe 1 - normally autoimmune or viral in cause - atrophy or destruction of beta cells - no insulin production

Type 2 - insulin resistance - more insulin than normal needed to give response - leads to subsequent failure of beta cells.

26
Q

What is maturity onset diabetes in the young?

A

Syndrome of genetic mutations that leads to impaired insulin production or elevated blood glucose (unable to recognise high glucose levels)

27
Q

What are some common causes of secondary diabetes?

A

Acromegaly - increased GH
Cushing syndrome - increased cortisol
Haemochromatosis - excess iron damaged pancrease
Pancreatitis - low insulin production

28
Q

What is the common cause, treatment and presentation of type 1 diabetes?

A

10% of all diabetes cases
Autoimmune destruction of beta cells
Insulin levels are very low or absent
Starts in childhood or adolescence
Short history of osmlar symptoms - thirsy, polyuria, weight loss and lethargy
Common complication: diabetic ketoacidosis (more than type 2)
Treatment is lifelong insulin

29
Q

What are the common features, treatment and presentation of type 2 diabets?

A

Around 90% of diabets cases
Risks - obseity, sedentary lifestyle, strong familial tendency and ageing
Gradual onset - so often has incidental finding
Cause: target tissues resistant to insulin and insulin secretion may also decrease in later disease due to pancreas damage
Treatment: lifestyle, medications, insulin

30
Q

What are the classic triad of diabets symptoms?

A

Polyphagia
Polydipsia
Polyuria
* these are more common in type 1

31
Q

What symptoms may appear in diabetes mellitus?

A

Extreme fatigue
Blurry vision
Repeated infection
Slow wound healing
Weight loss
Numbness in hands and feet.

32
Q

What are the major microvascular complications in diabetes mellitus?

A

Eye - retinopathy, cataracts and glucoma due to high BG and BP damaging BV
Kidney - high BP and BG overwork kidnet - nephropathy
Neuropathy - High BG damages peripheral nerves - pain or numbness - feet wounds go undetected - can become infected or gangrenous

33
Q

What are the major macrovascular complications in diabetes mellitus?

A

Brain - increased risk of stroke, TIA and cognitive impairment
Heart - increase risk of coronary artery disease
Extermities - peripheral vascular disease resulting in narrowing of blood vessels - reduced blood flow to the lefs, slow healing feet wounds

34
Q

What vitamin supplement might be given in T2D?

A

VitB12 - prevent neurovascular complications

35
Q

What tests can be used to diagnose a patient with T2D?

A

Fasting plasma glucose - 8 hours after meal - above 7 mmol/L
Random plasma glucose - above 11.1 mmol/L and symptomatic
Elevated HbA1c 48mmol/mol
Oral glucose tolerance test

36
Q

What is the golden standard test for diagnosing diabetes mellitus?

A

Oral glucose tolerance test
positive result in 2 hours plasma glucose above 200mg/dL after 75 gms of glucose

Shows how well able to regulate glucose metabolism
Can identify prediabetes and diabetes.

37
Q

Why is HbA1c important in diabetes mellitus patients?

A

Is an indicator of long-term glucose control (over 3 to 4 months)
Is a Non-enzymatic glycation of hemoglobin (depends on blood glucose levels)
Hig HbA1c indicates poor blood glucose control and higher risk of complications
Greater than 6.5% is a positive result for T2D

38
Q

What is the structure of glucagon?

A

Peptide hormone with 29 amino acids in a single polypeptide chain
Proglucagon is first formed - this is a large protein precurso that is tissue specifically modified
Converted to glucagon in alpha cells of pancreas by selective proteolytic cleavage in the secretory granules

39
Q

What factors increase glucagon secretion?

A

Main - low blood glucose
Enhanced by:
amino acids - argininge and alanine
Stress hormones - nor(adrenaline) and long term cortisol
neural input - sympathetic stimulation during stress

40
Q

What factors inhibit glucagon secretion?

A

Insulin
Glucose

41
Q

Where are glucagon receptors mainly found?

A

Liver hepatocytes
Renal cortex cells

42
Q

What are the effects of glucagon at its receptor?

A

Glucagon binds to GPCR on plasma membrane
Activates adenylyl cyclase
Converts ATP to cAMP
cAMP binds to and activates regulatory subunits of cAMP dependent protein Kinase A
This frees the catalytic portion of protein Kinase A to phsopharylate target enzymes brining about effects.

43
Q

What are the effects of glucagon in the liver?

A

Activate - glycogenolysis, gluconeogenesis, lipolysis, beta oxidation adn ketone body synthesis
Inhibit - glycogenesis, lipogenesis and glycolysis

44
Q

What are the effects of glucagon in the renal cortex?

A

Activation of gluconeogenesis and inhibition of glycolysis

45
Q

What are the effects of glucagon in fat cells?

A

Indirect action via low serum insulin: glucagon ration
Activation of TAG/triglyceride degradation (together with epinephrine)

46
Q

Where does insulin have receptors that glucagon does not?

A

Skeletal muscle

Unit 10 (37 decks)

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