HUBS 191 Lecture 29 Flashcards

(45 cards)

1
Q

why are brain cells so dependent on glucose

A

because unlike other cells they aren’t able to use alternative substrates to produce ATP

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2
Q

what can prolonged high BGLs cause

A

blood vessel and nerve damage

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3
Q

where is the pancreas located and what does it consist of

A

it is located in the curve of the duodenum (the first part of the small intestine) and it consists of a head, tail and body

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4
Q

99% of pancreatic cells are clustered into ___ that secrete _______ into ducts which empty into the duodenum

A

acini - digestive enzymes

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5
Q

what are the clusters of endocrine cells in the pancreas called and how many are typically in the human pancreas

A

islets of langerhans or pancreatic islets - there are normally 1-2 million islets in the pancreas

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6
Q

what are the two types of pancreatic endocrine cells that you need to know for HUBS 191

A

alpha and beta cells

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7
Q

what do alpha cells secrete and what do they secrete it in response to

A

they secrete glucagon in response to low blood glucose which increase BGL back to normal

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8
Q

what do beta cells secrete and what do they secrete it in response to

A

they secrete insulin in response to high blood glucose which reduces BGL back to normal

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9
Q

how is insulin synthesised

A

insulin is a protein hormone that is initially synthesised on the rough ER of beta cells as preprohormone with A, B and C chains. the C chain is removed in the Golgi and packaged into secretory vesicles to be exocytosed into the blood

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10
Q

is insulin bound in circulation and how long does it remain in circulation for

A

insulin circulates unbound in plasma and is mostly cleared from circulation within 10-15 minutes

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11
Q

how can the C chain of insulin be useful

A

if someone is administering their own insulin we can look for the C chain to see if they are producing any of their own insulin because artificial insulin doesn’t contain any of the C peptide chain

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12
Q

does insulin correct hypo or hyperglycaemia

A

hyperglycaemia - increased BGL

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13
Q

how does insulin correct hyperglycaemia

A

by facilitating glucose uptake into cells of most body tissues. without insulin glucose can’t be utilised by most cells for energy and blood glucose level will be too high

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14
Q

what happens when BGLs go up

A

released insulin binds to insulin receptors which triggers a cascade of reactions that results in transporters that are stored inside cells like muscle and fat cells being incorporated into the plasma membrane

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15
Q

what tissues have different glucose transporters and therefore don’t rely as heavily on insulin

A

the liver and brain

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16
Q

what are insulin receptors made up of

A

alpha and beta subunits

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17
Q

how do insulin receptors function

A

insulin binds to the alpha subunit which causes beta subunits to then get the phosphate groups from ATP for themselves. beta subunits are then able to phosphorylate proteins inside the cell that mediate insulins effects (insulin response substrates) - this leads to the insertion of GLUT4 transporters into the cell membrane of muscle and fat cells

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18
Q

what are the effect of insulin on skeletal muscle

A

increased glucose energy into muscle cells via GLUT4
increased glycogen synthesis (glycogenesis)
increased transport of amino acids into the muscle and other cells
increased protein synthesis
inhibition of protein breakdown

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19
Q

why do muscle store glucose in the form of glycogen

A

glycogen doesn’t exert an osmotic effect unlike glucose which would cause water to be drawn into the cell

20
Q

what are the effects of insulin in adipose tissue

A

increased glucose transport via GLUT4
increased synthesis and storage of triacylglycerides
insulin inhibits lipolysis - stops the breakdown of fatty acids and triglycerides

21
Q

what are the effects of insulin on the liver

A

uptake of glucose and conversion to glycogen
fatty acid synthesis
inhibits glyconeogenesis
suppresses the formation of ketone bodies

22
Q

what is the entry of glucose into hepatocytes (liver cells) dependent on

A

GLUT2 which is insulin independent

23
Q

why does insulin increase fatty acid synthesis in the liver

A

when the quantity of glucose entering the liver cells is more than can be stored as glycogen (or used for hepatocyte metabolism) then insulin promotes the conversion of excess glucose into fatty acids

24
Q

can fatty acids in the liver be used by other parts of the body

A

yes - fatty acids are packaged into VLDL as a triglyceride. VLDL enters the bloodstream and transports triglycerides to other tissues

25
what is glycogenolysis
the breakdown of glycogen to glucose
26
what is gluconeogenesis
the break down of proteins into their constituent amino acids which can be used for energy or to make new glucose in the liver
27
what are ketone bodies
the liver can produce ketones when you are breaking down a lot of fat - they can be used by other cells for energy (even the brain). however, these are acidic and if you build up too many of them in your blood stream it will make your ECF too acidic
28
what is glucagon
a polypeptide hormone secreted by alpha cells of the pancreatic islets primarily in response to hypoglycaemia
29
glucagon exerts it's effects (primarily on the _____) via activation of receptors that utilise _____ as a second messenger
liver - cAMP
30
glucagon activated enzymes which...
cause the breakdown of glycogen to glucose (glycogenolysis) promote the production of new glucose by hepatocytes (gluconeogenesis) promote the release of glucose from liver cells into the blood promote the breakdown of triglycerides and release of fatty acids from adipose
31
what are the three historical characteristics of diabetes mellitus
polyuria, polyphagia, poldipsia
32
what is polyuria
the passing of large volumes of water caused by glucose acting osmotically and attracting water with it when it leaves the blood stream meaning that as you lose glucose you are also losing water
33
what is polydipsia
excessive drinking/thirst - because your losing water and becoming dehydrated the osmolarity of your bodily fluids is going to go up meaning that everything that eft begins is more concentrated and that will stimulate osmoreceptors in the hypothalamus and you will feel thirsty
34
what is polyphagia
excessive hunger - you can't make ATP which signals feelings of intense hunger
35
what is type 1 diabetes
essentially no insulin is produced by the beta cells
36
how is type 1 diabetes thought to be caused
autoimmune destruction of pancreatic beta cells, thought to be due to some environmental trigger combined with a genetic predisposition
37
what are the chronic symptoms of type 1 diabetes
poor healing increased infection risk because glucose is a good medium for bacteria to grow cardiovascular disease due to blood vessel damage renal disease diabetic retinopathy diabetic neuropathy
38
what is ketoacidosis
when your producing so many ketone that your level of consouness will reduce as well as problems with blood pressure and blood volume
39
what causes ketoacidosis
when diabetes goes untreated for long periods of time
40
what is the treatment for type 1 diabetes
insulin - other dietary and exercise management strategies many be involved but insulin is needed
41
what is type 2 diabetes
reduced sensitivity to the effects of insulin (hyposensitivity)
42
what are common causes of type 2 diabetes
inactivity, poor diet and obesity
43
later in type 2 diabetes beta cells may get work out leading to...
progressively lower insulin secretion and worsening blood glucose control (hypo secretion)
44
what are the treatments of type 2 diabetes
aim to reduce weight by 10-15% in early disease to achieve remission metformin - improves insulin sensitivity of cells and reduced hepatic gluconeogenesis drugs that cause glucose to be lost to urine drugs that increase insulin secretion drugs that slow down absorption of glucose from the intestines
45
what is gestational diabetes
diabetes in women during pregnancy