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Physio Exam 3 - Endocrine > 18 | Endocrine Pancreas, Metabolism > Flashcards

18 | Endocrine Pancreas, Metabolism Flashcards

1
Q

fat storage

A
  • largest energy reservoir
  • stored in adipose tissue as form of triglyceride
  • broken down to FFAs (used for B-oxidation) and glycerol (liver converts to glucose)
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2
Q

glucose storage

A
  • glycogen in the liver

- after a meal can be used by liver or adipose for triglyceride synthesis

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3
Q

protein “storage”

A
  • protein synthesis from AA’s in all tissues, most active after a meal
  • no real storage form, all protein have a purpose
  • during fast, protein breakdown in tissues. AA’s used by liver for gluconeogenesis
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4
Q

anabolism

A

storage of fuels

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5
Q

catabolism

A

mobilization of fuels

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6
Q

insulin (general role)

A

regulates anabolism + catabolism

-integrates body fuel metabolism between fed and fasting states

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7
Q

fed state

A

anabolic - high insulin

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8
Q

carbohydrate digestion

A

increase levels of glucose in blood

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9
Q

glucose (stim vs. inh actions)

A

stimulates insulin release

inhibits glucagon release

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10
Q

fed state - carbohydrate meal
[brain]
(1)

A

energy needs

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11
Q

fed state - carbohydrate meal
[liver]
(5 uses, 3 effects)

A
  • energy needs
  • converted to glycogen, storage
  • converted to triglyceride, exported as lipoproteins
  • amino acid synthesis
  • nucleic acid synthesis
  • inh protein breakdown
  • inh glycogen breakdown
  • inh glucose synthesis
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12
Q

fed state - carbohydrate meal
[muscle]
(1, 2)

A

-increased glucose uptake, energy needs

  • stim protein synthesis
  • inh protein breakdown
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13
Q

fed state - carbohydrate meal
[adipose]
(3, 1)

A
  • increased glucose uptake, energy needs
  • conversion to triglycerides
  • increased TG uptake from circulating lipoproteins, produced by liver

-inh lipolysis

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14
Q

protein digestion

A

increased amino acids

  • stim insulin production AND
  • stim glucagon production (counteracts some insulin effects, prevents hypoglycemia)
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15
Q

fed state - protein meal
[brain]
(1)

A
  • no use for AA’s alone

- uses glucose made from AA’s in liver

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16
Q

fed state - protein meal
[liver]
(3)

A
  • AA’s for protein synthesis
  • gluconeogenesis (local energy, and glycogen)
  • metabolized to TGs, exported as lipoproteins
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17
Q

fed state - protein meal
[muscle]
(2)

A
  • increased AA uptake, used for protein synthesis

- used for local fuel

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18
Q

fed state - protein meal

[adipose]

A

-inc TG uptake from circ lipoproteins produced by liver

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19
Q

fat digestion

A

dietary TGs absorbed as FFAs and monoglycerides

  • reesterified into TGs, exported from enterocyte in chylomicron, enters lymph
  • TGs can be broken down by lipoprotein lipase in adipose capillaries
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20
Q

fed state - fat meal

[adipose]

A

FFA’s from TG lipolysis taken up

-used for TG resynthesis (storage)

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21
Q

fed state - fat meal

[muscle]

A

takes up FFAs for fuel use

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22
Q

post-absorptive state

interprandial) (3

A

decreased insulin
increased glucagon
use of fuel stores

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23
Q

post-absorptive state: brain (2)

A

depends on glucose from glycogenolysis and gluconeogenesis in liver

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24
Q

post-absorptive state: liver (3)

A

inc glucagon, dec insulin promote
-glycogenolysis
-gluconeogenesis
FFAs from adipose used as fuel

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25
Q

post-absorptive state: muscle (3)

A
  • glycogen breakdown
  • dec glucose use
  • inc FFA uptake for fuel
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26
Q

post-absorptive state: adipose (2)

A
  • dec glucose uptake + use

- inc lipolysis, liberates glycerol and FFAs

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27
Q

brief starvation: brain (1)

A

con’t use of glucose from liver gluconeogenesis

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28
Q

brief starvation: liver (3)

A
  • glycogen stores depleted
  • inc gluconeogenesis, use AA’s and lactate
  • inc ketone body formation from FFAs, into circ
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29
Q

brief starvation: muscle (3)

A
  • glycogen stores depleted
  • inc protein breakdown + AA export (for gluconeogenesis)
  • dec use of FFAs for fuel, inc use of ketone bodies from liver
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30
Q

brief starvation: adipose (1)

A

-lipolysis + FFA release

31
Q

prolonged starvation: liver (1)

A

-inc ketogenic enzyme activity, for ketone body formation

32
Q

prolonged starvation: muscle (2)

A
  • after 3-4 days, ketone bodies used as major fuel

- day 24 switches to FFA for fuel, conserve ketones for brain

33
Q

prolonged starvation: adipose (1)

A

-lipolysis for FFA release

34
Q

prolonged starvation: brain (1)

A

-con’t to use glucose until day 24, ketone bodies become major fuel

35
Q

exercise (4, 2)

A

-dec circ glucose
-dec insulin
-dec glucagon
-inc catecholamines
glycogenolysis
gluconeogenesis

36
Q

exercise - muscle (2)

A
  • initial use of local glycogen and TG stores for fuel

- then use circulation FFAs as fuel (preserve glucose for brain)

37
Q

severe exercise - muscle

A

-increased dependence of glucose as more fibers are recruit, can preserve as much for brain

38
Q

exercise recovery - muscle (3)

A
  • accelerated replenishing of glycogen stores
  • plenty of FFAs for fuel (liberated from exercise), so glucose can be stored not used
  • enhanced insulin sensitivity, further promotes glucose uptake + glycogen formation
39
Q

pancreas hormones (4) + their cells

A

insulin (B cell - 60%)
glucagon (A cell - 20%)
somatostatin (D cell)
pancreatic polypeptide (PP cells)

40
Q

endocrine cells of the pancreas

A

islets of Langerhans

41
Q

islet structure + blood flow

A

b-cells located at center
surrounded by other cells
blood flow center out
paracrine regulation of glucagon A-cells by insulin B-cells

42
Q

insulin structure

A

(in B-cells)

  • pre-proinsulin
  • ER cleaves to proinsulin (A, B, C chain)
  • packaged into secretory vesicles in golgi, in vesicle C peptide (pro) is proteolytically cleaved
  • 1:1 ratio, insulin (A+B) : C-peptide
  • A+B chains linked by disulfide bridges, required for biological potency
  • most C-peptide excreted in urine, can use to measure endogenous insulin levels + B-cell function
43
Q

incretins

A

intestinal peptide hormones

  • greater insulin production following oral glucose vs. IV
  • oral glucose stimulates GLIP + GIP (incretins) from endocrine cells of SI
  • circulating incretins promote more insulin sec from B-cells for a given level of plasma glucose
44
Q

effects of insulin (4)

A

fat, carb, protein metabolism
ion flux
growth factor prod
hormone action

45
Q

insulin release stimulators (6)

A

[reciprocally inhibit glucagon]
glucose (also enhances stimulatory effect of others)
amino acids
fatty acids
catecholamines (B-adrenergic)
neural ACh
intestinal peptide hormones (incretins GLIP + GIP)

46
Q

insulin release inhibitors (4)

A

catecholamines (a-adrenergic, net inc of catecholamines inhibits insulin sec)
somatostatin
serotonin
prostaglandin E

47
Q

glucose tolerance test

T1D v. T2D

A

-capacity to clear glucose from blood w/ 75g oral dose
-measure rise and recovery
-detect insulin resistance or glucose tolerance
T1D: high glucose, little to no insulin
T2D: high glucose, may have high insulin

48
Q

glucose-induced insulin release

A
  1. inc EC gluc, inc IC gluc in B-cell. enters through insulin-insensitive GLUT 2 transporter
  2. inc glucose metabolism increases ATP/ADP ratio, closes ATP sensitive membrane K+ channel
  3. membrane depolarization (no longer hyperpol)
  4. opening of VGCaC, Ca2+ enters cell
  5. exocytosis of containing secretory granules
49
Q

insulin receptor functions(on target cells) (2)

A
  1. rec recognizes and binds insulin with high affinity + specificity
  2. generate signals that modulate insulin’s effector- function
50
Q

insulin receptor structure

A
  • glycoprotein
  • 2 EC a subunits, insulin binding site
  • 2 TM b subunits, signal transmission
  • disulfide bonds a-a, a-b, a-b
  • insulin binding activates tyrosine kinase in b subunits
  • autophosphorylation of receptor, signaling cascade
51
Q

insulin signaling cascade

A
  • autophosphorylation
  • phosphorylation of insulin receptor substrates (IRS-1, -2)
  • IRS’s bind and activate PI3-K, Grb-SOS and protein tyrosine phosphate (SHPTP2)
  • activate downstream enzymes, more specific roles
  • many of insulin’s effects mediated by phosphorylation and dephosphorylation reactions*
52
Q

insulin receptor activation

A
  • ligand/rec complex rapidly internalized
  • insulin lysosomally degraded
  • receptor recycled
53
Q

insulin clearance

A

receptor mediated insulin/rec endocytosis

impaired ability causes hyperinsulinemia

54
Q

insulin regulation of glucose homoeostasis

A

controls hepatic glucose production and use of glucose by muscle + adipose
-use determine by rate of glucose transport into cells r

55
Q

glucose transport into cells + role of insulin

A

muscle + adipose: GLUT-4

  • low number of rec on membrane
  • glucose transport is rate-limiting for uptake and metabolism*
  • insulin increases transport by recruiting GLUT-4 from intracellular pool
56
Q

potassium uptake

A
  • insulin increase uptake of K+ into cells (esp liver + muscle), in absence of glucose movement or pH
  • due to insulin increasing activity of Na/K ATPase
  • but with low insulin (T1D), can lose K+ in the urine as it leaves cells
  • but treatment with insulin can lead to hypokalemia but promoting rapid uptake
57
Q

glucagon stimuli (3, 3)

A

-falling BG
-inc AA’s in plasma (alanine, arginine)
-S-ANS
(inc BG, SS, insulin inh)

58
Q

glucagon in circuation

A

blood flow from pancreas to liver

  • 90% glucagon removed passing liver
  • little peripheral effects
59
Q

insulin vs. glucagon (2)

A
  • glucagon has little effect on glucose uptake by muscle

- shift of anabolism/catabolism in liver are result of changes in insulin/glucagon ration, not absolute amounts

60
Q

glucagon receptor

A

GPCR linked with AC

-increase cAMP

61
Q

glucagon in liver

A

-promotes glycogenolysis
-promotes gluconeogenesis
(leads to increased glucose release)
-increases beta-oxidation of fatty acids

62
Q

type 1 diabetes (general)

A

“insulin-dependent”

-viral or immune-mediated destruction of B-cells

63
Q

type 2 diabetes (general)

A

“non-insulin dependent”

  • if insulin deficient, far less than T1. may have normal or high levels.
  • insulin resistant
  • more common in obese and elderly
64
Q

T1D: lack of insulin effects (2)

A

uncontrolled fuel catabolism

  1. hyperglycemia: high BG, no insulin to reduce it. increased gluconeogenesis.
  2. ketoacidosis: high levels of ketone bodies, FFAs from adipose converted to ketones in liver
65
Q

ketoacidosis: starvation

A

w/ starvation

  • gradual
  • not associated with hyperglycemia (have insulin)
  • only mild acidosis, increased renal NH3 enables H_ clearance
66
Q

diabetic ketoacidosis

A
  • rapid development
  • hyperglycemic
  • dehyrated due to osmotic diuresis
  • high levels of ketone bodies in blood, causing acidosis
  • kidney cant increase NH3 fast enough
  • w/out insulin muscle can’t take up ketone bodies quickly, ends up using FFAs for fuel
  • plasma glucose and ketone levels above renal threshold, appear in urine
  • Epi/Ne levels increase
67
Q

T2D: effects

A
  • disordered glucose metabolism

- varying degrees of inability to maintain normal BG, resulting hyperglycemia, and glucose in urine

68
Q

phsyiological risks of T1D + T2D

A

both at risk for atherosclerosis (T2D more)

both at risk for eye, kidney, nerve complications (T1D more)

69
Q

3 P’s of diabetes

A

(major clinical manifestations)
polyurea
polydipsia (inc thirst)
-low ECF vol, osmotic diuresis b/c of increase BG
polyphagia (inc appetite)
-“starved” for glucose due to poor uptake into cells

70
Q

sulfonylureas + insulin relase

A

-stimulate insulin release by blocking ATP-dep K+ channel, facilitate Ca2+ influx, promoting inuslin release
(used in T2D)

71
Q

insulin + T2D

A
  • use exogenous insulin when stimulate of endogenous secretion failed
  • could be due to down regulation of receptors, defective receptors, anti-insulin Abs, post-receptor defects
  • exogenous insulin important to facilitate glucose use
72
Q

hyperosmolar hyperglycemic nonketonic syndrome

A
  • individual w/ T2D doesn’t drink enough fluids
  • easer to become dehydrated with high BG
  • can lead to stupor as brain becomes dehydrated
73
Q

3 -pathy’s of diabetes

A

retinopathy
-inc risk for glaucoma and cataracts
neuropathy
-poor circulation + wound healing. decreased sensation - minor injuries unnoticed, can lead to infection and amputation. dec circ can also lead to arterial disease.
nephropathy
-kidney failure, degradation of microvasculature

74
Q

hypoglycemia symptoms

A
  • adrenergic: activation of S-ANS leads to sweating, weakness, palpitation, tremor, hunger, nervousness
  • neuroglycopenic: CNS symptoms such as headache, confusion, visual disturbances, motor weakness, personality changes

Physio Exam 3 - Endocrine (8 decks)

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