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GI > Regulation of glucose > Flashcards

Regulation of glucose Flashcards

1
Q

what are the 2 types of glucose transport?

A

passive and active

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2
Q

which passive glucose transporter is found on the basolateral membrane of ileum?

A

GLUT2

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3
Q

which passive glucose transporter is responsive to insulin?

A

GLUT4

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4
Q

which passive insulin transporter has a high affinity for glucose?

A

GLUT4

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5
Q

which sodium glucose symporter is found on the apical surface of the ileum?

A

SGLT1

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6
Q

which sodium symporter has a high affinity for glucose?

A

SGLT1

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7
Q

which organ produces insulin and glucagon?

A

pancreas

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8
Q

where are the b cells located in islets of langerhans and which hormone do they produce?

A

core (more central)

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9
Q

what do delta cells in the islets of langerhan produce?

A

SST

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10
Q

which hormone do a cells produce?

A

glucagon

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11
Q

how does glucose enter pancreatic b cells?

A

passively via GLUT2 transporters

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12
Q

why does Ca enter the B cells in response to the entry of glucose?

A

glucose –> glycolysis 00> ATP –> inhibits exit of K –> depolarisation –> Ca entry via voltage gated ion channels

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13
Q

what are the other modulators of insulin secretion?

A

CCK and Ach

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14
Q

how is insulin secreted?

A

exocytosis via vesicles

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15
Q

what happens to insulin in golgi bodies?

A

disulphide bridges formed between chains that fold the hormone

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16
Q

what happens to insulin in golgi and secretory granules?

A

cleaved into A+B chain and C peptide

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17
Q

what clinical role does c peptide have?

A

helps to monitor endogenous insulin levels (clinical marker)

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18
Q

in what form is insulin produced?

A

preprohormone –> cleaved –> prohormone –> golgi bodies

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19
Q

what are the inhibitors of insulin release and how do they work?

A

SST, sympathetic nervous system via Gi

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20
Q

Which part of the ANS drives insulin secretion?

A

parasympathetic nervous system

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21
Q

what type of receptor is the insulin receptor?

A

tyrosine kinase receptor

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22
Q

which AA is the insulin binding domain rich in?

A

cysteine

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23
Q

what happens in the tyrosine kinase domain of insulin receptors?

A

neighbouring domains phosphorylate each other and neraby proteins by adding phosphate to tyrosine AA of proteins

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24
Q

what are the 2 main pathways of insulin receptor signalling?

A

P13K and PKB

MAPK

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25
Q

what does the MAPK pathway do?

A

phosphorylates transcription factors –> modifies gene expression –> growth/ mitogenic pathways

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26
Q

what do P13K and PKD do?

A

GLUT4 insertion into membranes by phosphorylating proteins

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27
Q

does oral or IV glucose cause a greater response in insulin?

A

oral

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28
Q

is the release of insulin biphasic or monophasic?

A

biphasic

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29
Q

what form is glucagon released in?

A

proglucagon

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30
Q

what effect does glucose have on glucagon release?

A

inhibits

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31
Q

what stimulates glucagon release?

A

AAs

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32
Q

what is GLP1 and where is it secreted?

A

L cells in small intestine

incretin like glucagon –> stimulates insulin release

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33
Q

which metabolic processes does insulin stimulate in the liver?

A

glycolysis, lipogenesis, protein and lipid synthesis

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34
Q

which metabolic processes does insulin inhibit in the liver?

A

gluconeogenesis, ketone body formation

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35
Q

do liver hepatocytes express GLUT4?

A

no

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36
Q

what happens when there is low insulin?

A

gluconeogenesis, glycogenolysis

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37
Q

which metabolic pathways are stimulated in muscle cells by insulin?

A

glycogen synthesis, triglyceride synthesis, protein synthesis

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38
Q

how does glucose enter muscle and fat cells in response to insulin?

A

GLUT4

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39
Q

which metabolic pathways does insulin stimulate in adipocytes?

A

triglyceride synthesis
free fatty acids exported
lipogenesis into lipid droplets
LPL extracts free fatty acids from VLDLs

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40
Q

what is induced in exercise via adrenaline?

A

GLUT4 insertion

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41
Q

what does somatostatin inhibit?

A

insulin and glucagon release

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42
Q

where does glucagon mainly act?

A

liver

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43
Q

what sort of receptor is the glucagon receptor?

A

GPCR attached to Gs –> PKA –> phosphorylates key enzymes

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44
Q

what does glucagon stimulate in liver cells?

A

gluconeogenesis, glycogenolysis, fatty acid uptake

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45
Q

why does the shift in metabolism occur in muscle cells and adipocytes?

A

drop in insulin

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46
Q

why would glycogen be at very high levels?

A

pathological reason eg ketoacidosis, sepsis

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47
Q

what do very high levels of glycogen stimulate in adipocytes and muscle cells?

A

lipolysis in adipocytes

proteolysis in muscle cells

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48
Q

where is most glucagon metabolised?

A

liver

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49
Q

what is he cori cycle?

A

lactate produced in anaerobic respiration in the muscle used in gluconeogenesis in the liver to produce glucose

50
Q

what effect does adrenaline have during exercise?

A

liver –> enhance glucose production
muscle –> glucogen breakdown and fatty acid breakdown
adipocytes –> fatty acids released into blood

51
Q

which 3 hormones work together to control growth?

A

thyroid hormone, growth hormone, insulin

52
Q

what are the acute effects of glucocorticoids?

A

diabetogenic effects (antagonise the effects of insulin)

53
Q

how do glucocorticoids affect growth in the long term?

A

antagonise growth

54
Q

what happens with an excess of GH in children?

A

gigantism

55
Q

what happens with an XS GH in adults?

A

acromegaly

56
Q

what happens with a deficiency of GH in children?

A

dwarfism

57
Q

what happens with a deficiency of GH in adults?

A

no obvious disease but more adipose tissue, less muscle bulk, replacement increase vigour

58
Q

What part of the body integrates signals for growth?

A

hypothalamus

59
Q

where is GH released from?

A

anterior pituitary

60
Q

what increases GH release from the anterior pituitary?

A

GHRH

61
Q

what increases GRH release from the hypothalamus?

A

amino acids, low glucose, stress, exercise, sleep, TRH, ghrelin

62
Q

what inhibits GH release?

A

Somatostatin

63
Q

by what mechanism does GHRH increase GH secretion?

A

coupled to Gs which increases cAMP

64
Q

describe the secretion of GH

A

pulsatile, more during the night

65
Q

what are the acute effects of GH release?

A

diabetogenic, enhancing gluconeogenesis

66
Q

how does GH bring about acute reponses?

A

tyrosine kinase associated receptor causes protein phosphorylation

67
Q

what is the benefit of the diabetogenic effects of GH?

A

more glucose available for the brain

68
Q

what mediates the long term effects of GH?

A

Insulin-like growth factor 1 (somatomedin) released from many tissues in response to GH

69
Q

How do IGFs (somatomedin) increase protein synthesis?

A

cross reactivity with insulin increases growth

70
Q

how does insulin effect growth in utero?

A

enhances growth (growth stimulus as suggests plenty of food)

71
Q

how do sex steroids effect growth?

A

increase growth but premature puberty

72
Q

is glucocorticoid a type of steroid?

A

yes

73
Q

what is the thyroid gland anchored to?

A

thyroid cartilage

74
Q

What do C cells of the thyroid hormone release?

A

calcitonin

75
Q

what stimulates the release of thyroid hormones?

A

TSH (thyroid stimulating hormone) released from the anterior pituitary)

76
Q

what does the parathyroid gland secrete?

A

parathyroid hormones

77
Q

what are thyroid hormones essential for?

A

essential for normal growth and development

78
Q

what does TH signal there is enough of?

A

energy

79
Q

what are the effects of TH?

A

increases metabolic rate, heat production

80
Q

How are TH carried in the blood?

A

bound to proteins predominantly thyroid binding globulin and transthyretin

81
Q

Which form of TH is more active?

A

T3

82
Q

what does TSH stimulate?

A

nearly all processes in thyroid hormone production

83
Q

what is thyroglobulin and where is it found in the thyroid gland?

A

is is a long AA chain with tyr sticking off the end found in the lumen

84
Q

which enzyme is involved in adding iodine to thyroglobulin?

A

iodinase

85
Q

what is iodine added on to?

A

2 tyr AAs on thyroglobulin

86
Q

what happens after iodine has been added to thyroglobulin?

A

endocytosis and cleaved

87
Q

Which 3 types of TH are produced?

A

T3 T4 rT3

88
Q

what happens to T4?

A

deiodinated into T3

89
Q

which 2 enzymes are involved in deiodinating T4?

A

type 1 and type 2

90
Q

where is type 1 enzyme found?

A

liver kidneys thyroid

91
Q

what is the type 1 enzyme inhibited by?

A

stress and caloric restriction

92
Q

where is type II found?

A

pituitary CNS placenta

93
Q

what initiates gene transcription?

A

nuclear receptors

94
Q

what are the acute effects of TH?

A

wasting energy, heat production, increasing basal metabolic rate, mitochondrial decoupling

95
Q

What does TH stimulate in the liver?

A

gluconeogeneis and glycogenolysis

96
Q

How do THs affect lipid metabolism?

A

lipogenesis and lipolysis (free glycerol available for gluconeogenesis)

97
Q

how do THs affect protein metabolism?

A

proteolysis and synthesis, net muscle wasting (increase AAs for gluconeogenesis)

98
Q

how do THs affect B receptor?

A

increase B receptor expression which increases sensitivity to SNS

99
Q

what is the chronic effect of TH and what is it crucial for?

A

brain development and growth crucial in infancy

100
Q

what does infant TH deficiency lead to?

A

cretinism and dwarfism

101
Q

what does TH deficiency in later childhood lead to?

A

stunted growth

102
Q

What happens to the thyroid gland if TH levels are very low?

A

goitre because high levels of TSH

103
Q

what are the symptoms of hypothyroidism?

A

weight gain, cold, bradycardia, tiredness, constipation, hair loss, decreased sweating

104
Q

why might primary thyroid failure occur?

A

autoimmune or drug induced

105
Q

how is hypothyroidism diagnosed and what is the treatment?

A

static tests –> low TH and high TSH (if primary)

T4 replacement

106
Q

What are the symptoms of hyperthyroidism?

A

sweating, overeating but weight loss, taccycardia, tremor

107
Q

what are the main causes of hyperthyroidism?

A

Graves disease = 80% (autoimmune) toxic nodule = 15% thyroiditis = 1%

108
Q

what are the clinical signs of grave’s disease?

A

eye swelling and eye ball protrusion, muscle paralysis

109
Q

what would be found on examination of someone with hyperthyroidism?

A

sweating, lid lag, tender thyroid, big goitre, sweaty palms, hand tremor

110
Q

what are the treatment options for hyperthyroidism?

A

anti-thyroid drug and supplement 6-18 months 50% –> remission block and replace T4 levels
radioactive iodine to destroy gland –> NOT FOR EYE PROBLEMS
surgery –> risky not 1st option

111
Q

what is the main glucocorticoid?

A

cortisol

112
Q

what is the role of the hypothalamus in glucocorticoid release?

A

integrates stress factors and diurnal rhythm

113
Q

what does corticotrophin releasing hormone stimulate?

A

anterior pituitary to release ACRH adrenocorticotrophin releasing hormone

114
Q

where is cortisol produced?

A

adrenal glands

115
Q

which disease results from adrenocorticoid deficiency?

A

Addison’s disease

116
Q

what do iatrogenic steroids do?

A

strong negative feedback inhibiting production of ACTH so adrenal atrophy

117
Q

what are the acute effects of glucocorticoids?

A

diabetogenic, inhibit insulin responses, increase lipolysis, glucose targetted to brain, gluconeogenesis and glycogenolysis

118
Q

what are the chronic effects of glucocorticoids?

A

immunosuppression, decrease in inflammation and decrease in cytokine production, fat redistribution –> central obesity, skin thinning, muscle wasting, osteoporosis

119
Q

what happens with excess glucocorticoids?

A

cushings disease

120
Q

what are the symptoms of cushings disease?

A

truncal obesity, growth arrest in children, moonlike face in adults, acne, poor wound healing, thin skin, easy bruising, striae on abdomen

GI (10 decks)

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