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Y1 LCRS Endo > Metabolism and insulin > Flashcards

Metabolism and insulin Flashcards

Glucose homeostasis; Pancreas anatomy; Insulin; Glucagon; Intermediary metabolism; Diabetes mellitus; Isulin resistance

1
Q

What is the cellular structure of an Islet of Langerhans?

A

70% Insulin secreting β cells
Glucagon secreting α cells
Somatostatin secreting δ cells
Tight junctions between cells to produce extracellular regions of high hormone concentration for paracrine signalling

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2
Q

What is the purpose of somatostatin in the release of pancreatic hormones?

A

Paracrine effect to inhibit release of pancreatic hormones

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3
Q

What is the purpose of glucagon?

A

Increases transport of amino acids to the liver
Lipolysis
Hepatic glycogenolysis and gluconeogenesis

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4
Q

What stimulates glucagon secretion?

A

Sympathetic and parasympathetic activity
GI hormones
Certain amino acids

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5
Q

What inhibits glucagon secretion?

A

Insulin

Somatostatin

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6
Q

What is the purpose of insulin?

A

Increase glycogenesis and decrease glycogenolysis in muscle and liver
Decrease gluconeogenesis in liver
Incrase glycolysis in liver and adipose tissue
Decrease breakdown of amino acids in liver
Increased amino acid uptake and protein synthesis in muscle, liver and adipose tissue
Decreased lipolysis
Increased lipogenesis and esterification of fatty acids in liver and adipose tissue
Inhibits production of ketone bodies from NEFA
Increased GLUT4 transport to increase glucose uptake into cells

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7
Q

What stimulates insulin secretion?

A

Parasympathetic activity via β receptor
GI hormones
Certain amino acids

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8
Q

Which cell produces insulin?

A

β cells in the Islet of Langerhans

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9
Q

Which cell produces glucagon?

A

α cells in the Islet of Langerhans

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10
Q

What inhibits insulin secretion?

A

Sympathetic activity via the α receptor

Somatostatins

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11
Q

How is insulin synthesised?

A

Insulin translated to preproinsulin which has a signal sequence
Converted to proinsulin in the ER/Golgi with signal sequence removed
Disulfide bonds are formed to hold A and B chains together
When stimulated to be secreted, C Chain cleaved upon cell exit to release the C peptide

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12
Q

What can be studied to monitor insulin production?

A

C peptide concentration - it has no glucose-lowering effect but is released with every insulin synthesised

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13
Q

Where is insulin stored?

A

In vesicles as proinsulin in β cells

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14
Q

How is insulin secreted?

A

1) Glucose binds to GLUT2 receptor on β cell
2) Glucose→glucose6phosphate by glucokinase (RATE LIMITING STEP)
3) Glycolysis occurs - ATP produced
4) ATP binds to ATP sensitive K+ channels, closing them
5) This allows Ca2+ influx
6) Influx of C2+ causes release of insulin vesicles

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15
Q

How is exocrine and endocrine function divided in the pancreas?

A

98% exocrine function

2% endocrine function - Islets of Langerhans

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16
Q

Where are insulin receptors found and how are they activated?

A

Found on cell membranes of liver, adipose and skeletal muscle tissues
Insulin binds to α subunit causing auto-phosphorylation of receptors to activate β subunit tyrosine kinases
These phosphorylate cell protein substrates

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17
Q

What is the structure and purpose of GLUT4?

A

Muscular insulin transporter
hydrophilic pore and hydrophobic outside
Causes 7 fold increase in glucose uptake when fused with cell membrane
Normally stored in vesicles

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18
Q

What is the effect of insulin on GLUT4?

A

Causes increased GLUT4 synthesis

Causes exisiting GLUT4 vesicles to fuse w the membrane to increase glucose uptake

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19
Q

What is glycogenolysis?

A

Breakdown of glycogen to produce Glucose-6-phosphate

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20
Q

What is the role of insulin in the liver?

A

Stimulates storage of glucose as glycogen
Inhibits gluconeogenesis and increases protein synthesis, reducing concentration of free AAs
Decreases ketone production by decreasing the production of acetoacetate from fatty acyl CoAs

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21
Q

What is the role of insulin in muscle?

A

Stimulates GLUT4 vesicle fusion with membrane to increase glucose uptake for aerobic respiration and storage as glycogen
Inhibits proteolysis and increases protein synthesis, reducing the concentration of free AAs

22
Q

What is the role of catecholamines in the liver and muscle?

A

Stinmulates glycogenolysis in liver

Inhibits GLUT4 glucose uptake in muscle

23
Q

What is the role of growth hormone in muscle?

A

Inhibits GLUT4 glucose uptake to promote glycogenolysis

Increases protein synthesis to build proteins for growth

24
Q

What is the role of glucagon in the liver?

A

Stimulates glycogenolysis to increase hepatic glucose output
Causes transporter channels to open and allow gluconeogenic amino acids to enter liver
Stimulates proteolysis and gluconeogenesis
Increases production of ketone bodies by increasing production of acetoacetate as blood glucose is low

25
Q

What is the role of cortisol in muscle?

A

Inhibits GLUT4 glucose uptake to promote glycogenolysis
Increases proteolysis when stressed to release gluconeogenic amino acids into circulation to enter liver for gluconeogenesis

26
Q

Why must triglycerides be converted to ketones and glucose?

A

Brain cannot metabolise fatty acids but can metabolise ketones and glucose
fatty acids → ketones
glycerol → glucose

27
Q

What are adipocytes?

A

Specialised cells that store fat as triglycerides

28
Q

How are triglycerides modified in order for them to be able to enter adipocytes?

A

Those in blood are too large to enter directly

Lipoprotein lipase hydrolyses triglycerides that are too large so they can enter the cell

29
Q

What is the effect of insulin on adipocytes?

A

Insulin increases formation of triglycerides in adipocytes
Activates lipoprotein lipase to increase concentration of non-esterified fatty acids
Activates GLUT4 to increase glucose which is converted to NEFAs
NEFAs condensed with glycerol-3-phosphate to form triglycerides

30
Q

What is the effect of growth hormone and cortisol on adipocytes?

A

Increase hydrolysis of triglycerides to release NEFAs for growth

31
Q

What is gluconeogenesis and where does it happen?

A

Occurs in liver
uses glycerol-3-phosphate to produce glucose
25% of hepatic glucose output after 10 hour fast

32
Q

How are ketones produced and where?

A

Occurs in liver
Converts NEFAs to fatty acyl CoAs
These combine with acetyl CoA to form acetoacetate
Acetoacetate converted to ketone bodies that can be used by brain

33
Q

What would suggest an insulin deficiency?

A

High ketones and high glucose

No inhibition of ketone production, yet blood glucose high

34
Q

What are omental adipocytes?

A

More metabolically and endocrinolically active adipocytes

More omental fat leads to higher risk of coronary heart disease

35
Q

What is glycosuria?

A

Presence of glucose in the urine

36
Q

What is osmotic diuresis?

A

Osmotically active glucose pulls water into urine by osmosis

37
Q

What is the renal reabsorptive capacity?

A

Amount of glucose that can be reabsorbed by the kidneys - if exceeded leads to glycosuria

38
Q

How does T1D present?

A

Months after onset without complications

Polyuria and polydipsia secondary to absolute insulin deficiency

39
Q

What is the regular age of onset for T1D?

A

Young usually

40
Q

What is the mechanism of T1D?

A

Unabated proteolysis = muscle loss
Continual lipolysis of triglycerides
High hepatic glucose output leads to glycosuria and ketonuria

41
Q

What is the treatment available for T1D?

A

Insulin injections

42
Q

What is a potential complication of insulin injections?

A

May produce insulin induced hypoglycaemia because level of insulin not reduced as it is not endogenous
∴ keeps causing entry to muscle even at low blood glucose levels and in the face of high glucagon

43
Q

How does T2D typically present?

A

After years of onset without complications
Fewer osmotic symptoms
Results from end organ resitstance to insulin
60-80% obese
dyslipidaemia common

44
Q

What is the normal age of onset of T2D?

A

Older usually

45
Q

What is the mechanism of T2D?

A

Liver, muscle and adipose tissue resistant to insulin
Usually enough to suppress ketogenesis and proteolysis so no muscle loss
Not enough insulin to stop other effects

46
Q

What is the treatment available for T2D?

A

Diet and exercise
Control of total calories
reduction in number of fats and refined carbs and sodium
Increase in number of complex carbohydrates and soluble fibre

47
Q

What two pathways does insulin binding activate and what do they do?

A

MAP Kinase pathway - growth in utero and children

PI3K-Akt pathway - leads to metabolic actions such as GLIT4 production

48
Q

How does insulin resistance arise and what does it affect?

A

Arises in all organs at the same time
affects PI3K-Akt pathway
Prevents glucose from being taken up from blood
fasting glucose >6mmol

49
Q

What are the features of insulin resistance?

A 
hypertension
high blood concentration of triglycerides and LDLs
Low HDL concentration
Fasting glucose >6mmol 
High omental fat
50
Q

What is compensatory hyperinsulaemia and what does it cause?

A

Because blood glucose doesn’t fall when insulin is secreted, mitogenic MAPK pathway is over activated
Produces hypertension and dyslipidaemia see in in diabetes
Abnormal lipid carriage leading to isachemic heart disease

51
Q

What does dyslipidaemia cause?

A

Higher LDL and NEFA/triglyceride concentration in blood due to MAPK pathway
Causes damage to blood vessels and hypertension
Lower lipoprotein lipase activity
Causes isachemic heart disease

Y1 LCRS Endo (7 decks)

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