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psc2002 > lecture 24 > Flashcards

lecture 24 Flashcards

1
Q

what does blood glucose homeostasis require?

A

effective regulation

(usually driven by insulin and glucagon)

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2
Q

what occurs to blood glucose after a meal?

A

-increase
-comes down with time

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3
Q

what occurs to insulin with low blood glucose levels?

A

insulin levels low

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4
Q

what occurs to insulin with high blood glucose levels?

A

insulin levels also high

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5
Q

what is hyperglycaemia?

A

blood glucose levels are too high

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6
Q

what does hyperglycaemia cause?

A

high blood glucose to stimulates insulin secretion

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7
Q

what occurs with hyperglycaemia and glucagon?

A

inhibits glucagon secretion

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8
Q

when is glucagon at highest?

A

when glucose levels are low

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9
Q

what is the role of insulin?

A

-secreted in conditions of high blood glucose
-insulin decreases blood glucose levels to normal range

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10
Q

what is the role of glucagon?

A

-secreted in conditions of low blood glucose
-increases the blood glucose levels

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11
Q

what occurs after a meal?

A

-increase blood glucose levels
-signals pancreas to release insulin
-insulin is signal to decrease blood glucose levels

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12
Q

where is the signal sent to?

A

liver, adipose tissue and muscle

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13
Q

what does the insulin signal mean?

A

increase glucose uptake, don’t produce any more glucose, form glycogen with the insulin

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14
Q

what occurs after exercise/prolonged periods of not eating?

A

-blood glucose decreases
-pancreas detects the change and releases glucagon
-glucose levels increased to normal range

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15
Q

where does the glucagon act upon?

A

liver

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16
Q

what are the main functions of the liver?

A
  1. exocrine - releases digestive enzymes into gut
  2. endocrine - blood glucose homeostasis
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17
Q

what are the pancreatic islets (islets of langerhans)?

A

-scattered throughout pancreas
-comprise of alpha, beta and delta that secrete hormones
-small and different
-regulate blood glucose

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18
Q

what do the pancreatic alpha cells release?

A

glucagon

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19
Q

what do the pancreatic beta cells release?

A

insulin

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20
Q

what do the pancreatic delta cells release?

A

somatostatin

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21
Q

what are the regulators of insulin release?

A

glucose
amino acids
gut hormones
neural input (cholinergic)
adrenaline (inhibitory action)
somatostatin (inhibitory action)

22
Q

what are the regulators of glucagon release?

A

glucose (inhibitory action)
insulin (inhibitory action)
amino acids
neural input (stress)
adrenaline
cortisol
gut hormones (inhibitory action)

23
Q

how is insulin produced by pancreatic beta cells? complex

A

-gene transcription produces unfolded structure
-needs to be folded so transported to ER
-forms preproinsulin (has n terminal signal peptide, beta chain of insulin connected to a chain)-not active
-cleaved to proinsulin
-transported to Golgi (packages proteins)- production off disulphide bonds between b and a chains
-cleavage of c peptide forming mature insulin

24
Q

how is insulin formed? simple

A

-produced in islet beta cells as pre-proinsulin
-intramolecular disulphide bonds formed between b and a chains, cleaving a C-peptide (inactive) and insulin

25
Q

how is insulin stored?

A

-hexatrimeric form (to add stability)
-complexed with zinc

26
Q

what is C peptide used for?

A

-diagnosis (type 1 diabetes) to see whether people are producing their own insulin
-used as insulin has short half life

27
Q

what occurs in basal/resting state?

A

-glucose moves via concentration gradient from blood into cell
-glucose needs to be metabolised in cell by glucokinase (low activity so not much glycolysis, low energy levels)
-potassium atp channels remain open
-voltage calcium channels closed at resting
-membrane hyperpolarisation
-no insulin secretion

28
Q

what occurs with higher blood glucose levels?

A

-more glucose entering cell
-glucokinase activity higher so more metabolism
-raised ATP
-K+ channels closed
-membrane becomes depolarised
-Ca2+ channels open - influx into the cell
-high insulin secretion

29
Q

what occurs in glucose metabolism?

A

-glucose is phosphorylated to G3P and metabolised by glycolysis and mitochondrial oxidation to generate ATP

30
Q

what tissues does insulin affect in the postprandial state? (fed state)

A

-pancreas
-gut
-muscle
-adipose tissue
-brain
-liver

31
Q

how is insulin used in the muscle?

A

-stimulation of insulin allows glucose into muscle
-insulin tells it to store glucose as glycogen or use for energy production

32
Q

how is insulin used in the fat cells?

A

-insulin stimulates uptake of glucose
-stored as fat cells

33
Q

what happens to the glucose taken up by the liver?

A

-converts to glycogen
-converts to fat (transported out to be taken up by adipose tissue)

34
Q

what is glycogen?

A
35
Q

why is glycogen needed?

A

-glucose brings water into cell and is osmotically active so cant store much in cell
-glycogen is major glucose store in muscle and liver

36
Q

what is the aim of the glycogen store in the liver?

A

to maintain blood glucose levels when not eating

37
Q

what happens when the liver glycogen stores are full?

A

-glucose is converted to fat by glycolysis
-enters citrate cycle forming fatty acids -eventually packaged into lipoproteins that are taken up by adipose tissue to be stored for later

38
Q

what occurs in the liver in fasting state?

A

-glucose falling
-no insulin release from pancreas but glucagon release
-acts on liver as has receptors
-breaks down glycogen into glucose and release into bloodstream
-gluconeogenesis - converting other carbon precursors into glucose
-fatty acids made into ketone bodies which are taken into bloodstream - useful for brain as source of fuel

39
Q

what occurs in the adipose tissue in a fasting state?

A

-in adipose tissue, triglyceride starts to break down back to fatty acids and are related into bloodstream (another energy source)

40
Q

what occurs in the muscles in fasting state?

A

-muscle takes up fatty acids and uses for fuel
-muscle breaks down its protein to form amino acids

41
Q

how is glucose produced during fasting?

A
  1. glycogenolysis (breakdown of glycogen)
  2. gluconeogenesis (making glucose from other carbon compounds)
42
Q

what does insulin do in the muscle?

A

-increases glucose transport
-increase glycogen synthesis
-increase glucose oxidation
-increase protein synthesis

43
Q

what does insulin do in the adipose tissue?

A

-increase glucose transport
-increase triacylglycerol synthesis
-decrease triacylglycerol breakdown release of fatty acids

44
Q

what does insulin do in the liver?

A

-increase glycogen synthesis
-increase fatty acid and triglyceride synthesis
-increase protein synthesis
-decrease glycogen degradation
-decrease gluconeogenesis

45
Q

what molecular targets are present in the muscle for insulin to have this effect?

A

-glucose isn’t taken up in absence of insulin because GLUT4 (glucose transporter) is localised to intracellular vesicles- needs insulin signalling for the translocation to plasma membrane
-insulin promotes the conversion to glycogen by activating glycogen synthase enzyme
-insulin covalently modifies the sensor (removes a phosphate group)
-stimulates glucose oxidation by phosphorylating pyruvate dehydrogenase so it becomes activated

46
Q

what molecular targets are present in the adipose tissue for insulin to have this effect?

A

-increased translocation of GLUT4
-increased fatty acid synthesis by increasing acetyl-coA carboxylate and fatty acid synthase
-decreased hormone sensitive lipase by covalent modification

47
Q

how does insulin regulate the fat uptake in adipose tissue?

A

-stimulate glucose uptake
-triglyceride synthesis

48
Q

how is covalent modification activated in the liver?

A

glycogen synthase and acetyl coA carboxylase

49
Q

how is covalent modification deactivated in the liver?

A

phosphorylase

50
Q

how is gene transcription induced?

A

glucokinase, acetyl coA carboxylase, fatty acid synthase

51
Q

how is gene transcription repressed?

A

glucose 6 phosphatase

psc2002 (15 decks)

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