The Endocrine Pancreas - Part 2 Flashcards

1
Q

What happens if there is more glucagon than insulin?

A

Glucose released into plasma from stores and BG conc. increases
Increased glycogenesis, gluconeogenesis and ketogenesis

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2
Q

Describe glucagon

A

Peptide hormone produced by alpha cells of pancreatic islet cells
Glucose mobilizing hormone, acting mainly on the liver

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3
Q

What is the plasma half life of glucagon?

A

5-10 mins
Degraded mainly by the liver

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4
Q

When is glucagon most active?

A

In post absorptive state

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5
Q

What are glucagon receptors?

A

G protein coupled receptors
Linked to adenylate cyclase/cAMP system which when activated phosphorylate specific liver enzymes

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6
Q

What is the action of glucagon?

A

Opposes the action of insulin, part of the glucose counter regulatory control system which included epinephrine, cortisol and GH

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7
Q

What does phosphorylation of specific liver enzymes result in?

A

Increased glycogenolysis
Increased gluconeogenesis
Formation of ketones from FAs

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8
Q

What is glycogenolysis?

A

Breakdown of glycogen to return to glucose

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9
Q

How does fasted state metabolism maintain plasma glucose for brain?

A

Liver glycogen becomes glucose
Adipose lipids become free FAs and glycerol that enter blood
Muscle glycogen is used for energy -use FAs and break down proteins into aa
Brain can only use glucose and ketones

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10
Q

How are ketone bodies formed?

A

Beta oxidation from free fatty acids

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11
Q

What do amino acids stimulate and why is it important?

A

Stimulate glucagon and insulin
If no glucagon stimulation then glucose uptake into cells and lowered BG conc.
Potentially catastrophic for brain - hypoglycaemia
Adaption was for high protein meals

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12
Q

What happens if someone consumes a very high protein meal?

A

Amino acids stimulate insulin causing decreased BG conc.
Also stimulates glucagon causing increased BG conc.
This maintains BG conc.

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13
Q

Explain glucose sparing for obligatory glucose users

A

In post absorptive state then there is low insulin levels so a large mass of tissue like muscle and fat can not readily access glucose

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14
Q

What are some stimuli which promote glucagon release?

A

Low BG conc. (under 5 mM)
High conc. of amino acids
Sympathetic innervation and epinephrine, Beta 2 effects
Cortisol
Stress

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15
Q

What stimuli inhibit glucagon release?

A

Glucose
Free fatty acids and ketones
Insulin
Somatostatin

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16
Q

What happens if increased parasympathetic innervation on islets cells?

A

Increased insulin and lesser increase of glucagon
Association with anticipatory phase of digestion

17
Q

What happens if increased sympathetic innervation on islets cells?

A

Promotes glucose mobilization
So increased glucagon, epinephrine and inhibition of insulin so brain had enough energy

18
Q

How does epinephrine help control BG conc.?

A

Muscle and liver glycogenolysis
Gluconeogenesis
Lipolysis

19
Q

How does cortisol and GH help control BG conc.?

A

Gluconeogenesis
Inhibition of glucose uptake
Lipolysis
Cortisol only - protein catabolism

20
Q

What is somatostatin?

A

SS is a peptide hormone secreted by D cell of the pancreas
Main pancreatic function is to inhibit activity of GI tract

21
Q

What is another action of somatostatin?

A

Supresses the release of both insulin and glucagon
If SS tumour then can have symptoms of diabetes

22
Q

Describe the effect of exercise on conc. of BG?

A

Entry of glucose into skeletal muscle increases even in absence of insulin
There is insulin independent increase in GLUT4 in muscle membrane
Also increases insulin sensitivity of muscle

23
Q

Explain GLUT4 transporters in active muscle

A

Can migrate to membrane without insulin being present
Exercise causes glucose uptake independent of insulin

24
Q

Describe what happens during starvation

A

Adipose tissue is broken down - fatty acids are released
Most tissues can used FFAs to make energy and liver converts excess to ketones - additional source of energy

25
Q

What happens to the brain after a period of starvation?

A

Brain adapts to be able to use ketones

26
Q

Why does the brain adapt to use ketones as energy source?

A

Serves to save protein breakdown as can become weak and vulnerable to infection
Ketone body uptake is insulin dependant

27
Q

Describe Type I diabetes (IDDM)

A

Inulin dependant diabetes mellitus
Autoimmune destruction of the pancreatic beta cells destroys ability to produce insulin and compromises ability to absorb glucose

28
Q

What are the results of type I diabetes?

A

Absolute need for insulin - insulin injections
Without then develop ketoacidosis, coma and die

29
Q

Describe the breakdown of homeostatic regulation in diabetes

A

Meal increases BG conc. but lack of insulin effect so liver produces more glucose by gluconeogenesis because body thinks its starving - further increase in BG conc.

30
Q

Describe ketoacidosis in type I diabetes

A

Lack of insulin depresses ketone body uptake so build up rapidly in plasma - acidic so create life threatening acidosis with plasma less than 7.1

31
Q

How are ketones detectable?

A

Detectable in urine and produce distinctive acetone smell to breath

32
Q

Describe type II diabetes

A

Non-insulin dependant diabetes mellitus
Peripheral tissues become insensitive to insulin - insulin resistance
Either abnormal insulin response of receptors or reduction in number of receptors

33
Q

What are the beta cells like in type II diabetes?

A

Intact and appear normal
Can sometimes even be hyperinsulinemia

34
Q

What are major contributions to type II diabetes?

A

High sugar and animal fat diet with little exercise

35
Q

Describe the glucose tolerance test in diabetes

A

Type I and type II give raised BG conc.
Type I - inadequate release of insulin
Type II - inadequate tissue response
Patient ingests glucose after fasting BG measures then if elevation after 2 hrs - indictive of diabetes

36
Q

How is mg/dl converted to mM?

A

Ex. 90mg/dl x 100 to make L
900mg/l
MW of glucose is 180
900/180 - 5mM

37
Q

What are some diabetic complications of long term hyperglycaemia?

A

Retinopathy
Neuropathy
Nephropathy
CVD

38
Q

What can hypoglycaemia in type I diabetes cause?

A

Type I on exogeneous insulin
Can lead to permanent brain damage and death in end
Only needs to be over short period to see complications