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PSL300 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What is metabolism?

A

Sum of all chemical reactions in a body

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2
Q

Anabolic

A

large molecules synthesised from smaller ones

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3
Q

Catabolic

A

Breakdown of larger molecules into smaller ones

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4
Q

What are the two states?

A

Fed (absorptive) and Fasted (postabsorptive)

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5
Q

Fed state

A

anabolic state
Uses glucose for energy

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6
Q

Fasted state

A

catabolic, uses glucose, fat for energy

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7
Q

Basal Metabolic rate (BMR)

A

An individual’s energy expenditure when resting, comfortable temperature, fasted

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8
Q

Energy balance

A

we control caloric intake and exercise

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9
Q

Glycogenolysis

A

Breakdown of glycogen from liver and muscle to glucose

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10
Q

Glycogenesis

A

creation of glycogen from glucose

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11
Q

Glycolysis

A

the breakdown of glucose releasing ATP (energy and pyruvic acid)

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12
Q

what does glycolysis occur along with ?

A

tricarboxylic acid cyle and oxidative phosphorylation

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13
Q

Lipogenesis

A

fatty acid and glycerol to triglycerides (adipose tissue)

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14
Q

Lipolysis

A

break down of trigylcerides to fatty acids and glycerol

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15
Q

what happens when fatty acid and glycerol breakdown ?

A

beta oxidation of FFA, releases ATP

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16
Q

Protein synthesis

A

amino acids to protein (muscle)

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17
Q

Protein degradation

A

protein to amino acids

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18
Q

Gluconeogenesis

A

synthesis of glucose from non-carbohydrate substrates such as glycerol and amino acids

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19
Q

How does glucose get inside cells?

A

Glucose transporters (there are 14 different types)

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20
Q

2 main types of glucose transporters that were are focusing on?

A

GLUT 2 and GLUT 4

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21
Q

GLUT 2

A

Liver, Pancreas (intestines, kidneys)
Glucose transport and insulin secretion

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22
Q

GLUT 4

A

Adipose tissue, skeletal muscle
Glucose transport (insulin dependent)

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23
Q

what does beta cells in the pancreas contain and release?

A

it contains proinsulin, it releases insulin+c peptide

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24
Q

what do alpha cells in pancreas release?

A

glucagon

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25
Q

what do delta cells in pancreas release ?

A

somatostatin

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26
Q

exocrine (acinar cells) of the pancreas

A

contain zymogens
The produce bicarbonates and proenzymes that are used for digestion

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27
Q

islet of Langerhans

A

cluster of cells in the pancreas (alpha, beta, delta epsilon) that release different hormones

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28
Q

glucagon and glucose

A

opposing actions
Glucagon increases when glucose is lowered

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29
Q

insulin and glucose

A

same action
insulin gets lowered when glucose is lowered

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30
Q

insulin

A

the dominant hormone of the fed state, it is synthesized as a typical peptide

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31
Q

what receptor does insulin bind to?

A

tyrosine kinase

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32
Q

what does insulin do?

A

it helps reduce blood glucose and promotes the formation of glycogen, fat, and protein

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33
Q

Mechanisms of insulin action

A
  1. Insulin binds to tyrosine kinase receptor
  2. Receptor phosphorylates insulin-receptor substrates (IRS)
  3. Second messenger pathways alter protein synthesis and existing proteins
  4. membrane transport is modified
  5. Cell catabolism is changed
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33
Q

Low insulin/glucagon ratio

A

fasted

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34
Q

High insulin/glucagon ratio

A

fed

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35
Q

Insulin and Glucose transport in liver through GLUT2

A

Liver expresses GLUT2 transporter on the plasma membrane (independent of insulin)

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35
Q

what happens when there is a high insulin/glucagon ratio?

A
  1. Insulin binds to the receptor.
  2. Signal transduction cascade.
  3. exocytosis of GLUT 4 onto the plasma membrane
  4. glucose enters cell from bloodstream
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36
Q

GLUT2 mechanism

A

In the fed state, Insulin activates hexokinase maintaining a high glucose concentration gradient which indirectly increases glucose uptake by the liver.

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37
Q

Intravenous v/s intrajejunal glucose infusion

A

intrajejunal causes a much HIGHER increase in insulin after the addition of glucose

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38
Q

Incretin effect

A

the difference in plasma insulin after intravenous and intrajejunal glucose addition.
higher plasma insulin for intrajejunal

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38
Q

What does hexokinase help with?

A

Hexokinase-mediated conversion of glucose to glucose 6-phosphate keep intracellular (glucose) low

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39
Q

Insulin release mechanism

A
  1. Increase of glucose in the blood
  2. glucose will enter beta cell through GLUT
  3. Increase in glycolysis and citric acid cycle
  4. Increase in ATP
  5. the potassium channels close
  6. Less K+ leaves the cell
  7. cell depolarizes
  8. Ca2+ channel opens
  9. Ca2+ entry triggers exocytosis and insulin is released
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40
Q

what was GIP-1 previously known as?

A

Gastric inhibitory peptide

40
Q

Incretin hormones

A

GIP-1 (Glucose-dependent Insulinotropic polypeptide) and GLP-1 (Glucagon-Like peptide)

41
Q

What does glucagon do?

A

Increases glycogenolysis, gluconeogenesis, and ketogenesis.
it prevents hypoglycemia.

41
Q

what releases GLP-1?

A

It is released by L cells in the small and large intestine in response to nutrients in the intestinal lumen.
GLP-1 Receptor (GPCR, Gas) on beta cells to stimulate insulin release.

41
Q

what releases GIP-1?

A

it is released by K cells in the small intestine in response to nutrients in the intestinal lumen.
GIP-1 Receptor (GPCR, Gas) on beta cells to stimulate insulin release.

41
Q

Mechanism of GLP-1

A
  1. GLP-1 binds to the GLP-1 receptor
  2. the G alpha S subunit is activated
  3. adenylate cyclate is released, that releases cAMP
  4. cAMP will activate EPAC (exchange protein activated by cAMP)
  5. insulin is released from beta cell

this work in conjunction with Ca2+ mechanism

42
Q

Stimulation of insulin secretion

A
  1. increase in plasma glucose
  2. Intestinal (incretin) hormones such as GLP-1 and GIP-1, both releases in response to nutrient ingestion=feedforward regulation
  3. increased plasma amino acids
  4. parasympathetic nervous system - rest and digest
43
Q

inhibition of insulin secretion

A
  1. sympathetic nervoud system- fight/flight
43
Q

what does glucagon target?

A

liver

44
Q

in what state does glucagon dominate?

A

fasted

45
Q

mechanism of glucagon

A

in reponse to fasting, glucagon triggers the activation of a cascade of signalling molecules inside the hepatocytes, each transmitting and amplifying the fastest signal.

it promotes the transport of glucose out of hepatocytes through GLUT2

46
Q

what is there inside hepatocytes

A

glycogen stores and glconeogenesis

47
Q

What is needed for the full activity of glucagon and epinephrine?

A

cortisol

48
Q

Stimulation of glucagon secretion

A
  1. decreased plasma glucose
  2. increased plasma amino acids
  3. sympathetic nervous system
49
Q

what three hormones does proglucagon contain

A

glucagon, GLP-1, GLP-2

49
Q

inhibition of glucagon secretion

A
  1. glucagon-like peptide-1 (GLP-1)
50
Q

where is proglucagon expressed

A

alpha cells, L cells on intestine and brain

51
Q

The main product in alpha cells

A

glucagon

52
Q

The main product in L cells of the intestine and brain

A

GLP-1 and GLP-2

53
Q

Key points- insulin

A

Insulin (prevents hyperglycemia): Beta cells (islet of Langerhans) – secreted in response to glucose, GLP1, PNS, amino acids – decreases blood glucose, promotes anabolic pathways, involved with growth

54
Q

Key points - GLP-1

A

released from intestine in response to glucose/amino acids – stimulates insulin secretion, increases beta cell mass, anorexigen, decreases glucagon

55
Q

Key points- Glucagon

A

Glucagon (prevents hypoglycemia):Alpha cells secrete
Glucagon in response from low glucose, SNS, amino acids
– increases blood glucose, gluconeogensis, glycogenolysis
– catabolic pathways to increase energy.

56
Q

Type-1 Diabetes

A

Insulin dependent diabetes- juvenile
-10%
-Insulin secretion reduced or absent
- treated by insulin injections or pumps

57
Q

Type 2 diabetes

A

Non-insulin dependent diabetes, mature onset
- 90%
- Defect in insulin secretion and target cells responsiveness to insulin is reduced.
- treated by diet, exercise, (translocation of GLUT4 to membrane), oral hypoglycemic (Sulfonylurea, GLP1)

58
Q

Actions of GLP-1 as medication

A

reduces inflammation, myocardial infarction, atheroscleoris, diabetic kidney disease, metabolic liver disease

59
Q

What is the posterior pituitary?

A

Neural tissue; extension of the brain that secretes neurohormones made in the hypothalamus.

60
Q

what is the anterior pituitary?

A

true endocrine gland

61
Q

2 hormones released by posterior pituitary

A

vasopressin and oxytocin

62
Q

6 hormones secreted by the anterior pituitary

A

prolactin, thyrotropin. adrenocorticotropin, growth hormone, follicle-stimulating hormone, luteinizing hormone

63
Q

Stalk connecting posterior pituitary and hypothalamus

A

infundibulum

64
Q

How to hypothalamic hormones reach the anterior pituitary?

A

portal system

65
Q

Inhibitor of prolactin

A

dopamine (PIH)

66
Q

Hypothalamic releasing hormone and inhibiting hormone of growth hormone/somatotropin

A

Hypothalamic releasing hormone- GHRH
Hypothalamic releasing hormone-Somatostatin (Growth hormone inhibiting hormone)

67
Q

The trend seen for bone mass

A

Decreasing bone mass with age

68
Q

Bones: Adult

A

Growth plates closed
Bone loss >40 years

68
Q

Bones: adolescent

A

Bones fully ossified
Growth plates closing towards end of puberty

69
Q

Bones: in-utero

A

Cartilage not fully ossified
Active growth plates

69
Q

Mechanism of growing bones

A
  1. Osteoblasts lay down on top of bone cartilage
  2. Old chondrocytes disintegrate
  3. Chrondocytes produce cartilage, causing the epiphyseal plate to widen
  4. Diving chronodocytes add length to bone
70
Q

Chrondocytes

A

They produce cartialge

71
Q

What does IGF-1 do?

A

Increase recruitment, proliferation, and matrix of chondrocytes.

72
Q

Where does growth hormone act and what does it stimulate?

A

It acts in the liver to stimulate IGF (Insulin-like growth factors) release

73
Q

Receptor for growth hormone

A

tyrosine kinase

74
Q

Glucose sparing effect: Catabolic action of GH

A

ulates adipose cells to breakdown stored fat, fueling growth effects

75
Q

Growth effect: catabolic action of GH

A
  1. Increases uptake of amino acids from blood.
  2. Enhances cellular proliferation and reduces apoptosis
76
Q

Diabetogenic effect_ Catabolic effects of GH

A

GH stimulates the liver to break glycogen into glucose, fueling growth effects. It also stimulates IGF1 release which stimulates growth effects.

77
Q

Age (Thyroid hormones)

A

Early years and puberty

78
Q

Age (growth hormone)

A

More or less consistent, decreases after 16

79
Q

Androgens and estrogens

A

Peak during puberty

80
Q

Gigantism

A

Too much growth hormone is childhood

81
Q

Acromegaly

A

Too much GH in adulthood - long bones fuse together, thickening at the end of bones

82
Q

Parts of thyroid gland

A

C cell, Follicular cells, capillary, colloid

83
Q

What are thyroid hormones made from?

A

Iodine and tyrosine

84
Q

How are thyroid hormones made

A
  1. A Na+-I- symporter brings I- into the cell. the pendrin transported moves I- into the colloid.
  2. Follicular cells synthesizes enzymes and thyroglobulin for colloid.
  3. Thyroid peroxidase adds iodine to tyrosine to make T3 and T4.
  4. Throglobulin is taken back into the cell by vesicles.
  5. Intracellular enzymes separate T3 and T4 from the protein.
  6. free T3 and T4 enter circulation.
85
Q

T3

A

MIT+DIT

86
Q

T4

A

DIT +DIT

87
Q

What does TSH do?

A

Activates G protein-linked membrane receptors acting via adenylate cyclase. Stimulates the synthesis and activity of enzymes T3 and T4. Activates transcription factors c-fos and c-myc
Stimulates thyroid growth.

88
Q

Mechanism of action of thyroid hormones

A

T3 and T4 circulate in blood bound to plasma proteins.
Both bind to nuclear thyroid receptors ( form homodimers or heterodimers with retinoic acid receptors)

89
Q

What is more potent: T3 or T4?

A

T3 (3-5X)
T4 is converted to T3 in target tissues

90
Q

Functions of thyroid hormones

A
  1. metabolic (metabolic rate, oxygen consumption, heat production, protein degradation, lipolysis)
  2. nervous system (enhances speech, thinking, reflexes)
  3. Growth and development (essential in children, works with GH)
  4. Cardiovascular (enhances heart rate and contractility; peripheral blood flow, works in part by increasing the number of beta-adrenergic receptors + other proteins.)
  5. Muscular (too much causes muscle weakness)
91
Q

causes of hyperthyroidism

A

tumors
thyroid-stimulating immunoglobulins (Grave’s disease)

92
Q

Symptoms of hyperthyroidism

A

goiter, nervousness, insomnia, anxiety, weight loss, high heart rate, exophthalmos

93
Q

Grave’s disease

A

autoimmune disease: abnormal antibodies against the TSH receptor are produced. =

94
Q

Causes of hypothyroidism

A
  1. under active throid gland
  2. iodine deifiency
95
Q

Symptoms of hypothroidism

A

goiter, slowed heart rate, slowed speech, fatigue, cold-intolerance, cretinism (infants), stunted growth (infants), weight gain

96
Q

iodine deficiency

A
  1. leaves thyorid gland uanble to produce T3 and T4
  2. Lack of negative regulation leads to excess TSH secretion
  3. TSH stimulates growth of thyroid gland, goiter may be present

PSL300 (9 decks)

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