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Cell and molecular extras > Lecture 11 Cell communication > Flashcards

Lecture 11 Cell communication Flashcards

1
Q

Adrenaline secreted form, binds to, for the

A

Adrenal glands, adrenergic receptors, fight or flight

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2
Q

How is adrenaline transported

A

Blood

every cell exposed yet only some have correct receptors

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3
Q

Describe endocrine signalling

A
  • Long distance: a cell signals to cells distributed widely in body
  • A Hormone is a chemical mediator that is released in one part of the body but regulates the activity of cells in other parts of the body
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4
Q

What drug is specific for beta 1 adrenergic receptors

A

Bisoprolol

This is only expressed in the heart so the it is less responsive to adrenaline, yet the rest of the body is unaffected.

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5
Q

Result of hormones being present in low concentrations

A

Receptor specific and sensitive to change

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6
Q

Synaptic signalling

A

Physical linkage

Target determined by neurones that synapse onto them

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7
Q

Gateway between neuronal and endocrinological systems

A

Hypothalamus/pituitary gland

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8
Q

What makes up cholesterol

A

Lipid - hydrophobic

Alcohol - hydrophilic

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9
Q

Structure of cholesterol allows it to

A

travel through PM and dissolve in aq solution

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10
Q

% of PM made up by cholesterol

A

30

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11
Q

How much cholesterol is synthesised per day

A

10g in 37 step biosynthetic pathway

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12
Q

Cholesterol is the precursor for

A

Steroid hormone

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13
Q

4 examples of steroid hormones

A

Vit D3
Testosterone
Cortisol
Estradiol

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14
Q

Steroid hormone structure allows it to

A

pass through BBB and CM as alcohol/lipid

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15
Q

Structure of nuclear receptors

A 
A/B C terminus
C  DNA BD
D Hinge
E Ligand BD
F C terminus
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16
Q

DNA binding domain encodes

A

ZInc fingers that contain 4 cysteine residues that coordinate with a zinc atom to formed a looped structure allowing it to access a major groove of DNA double helix

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17
Q

All nuclear receptors share

A

The same primary structure

C term - DNA BD - N term

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18
Q

2 forms of nuclear receptors

A

Inactive - inhibitory proteins present
Active - ligand binds, coactivator proteins, C terminus locks ligand in, high affinity –> conf change –> DNA BD –> transcription

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19
Q

Name 2 transcriptional responses of nuclear receptors

A
  1. primary response

2. secondary response

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20
Q

Primary response of steroid hormones

A

Proteins made by R itself

R-steroid hormone activates primary response genes to form primary response hormones

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21
Q

Secondary response of steroid hormones

A

DELAYED response

Primary response proteins shut off primary response genes + turn on 2nd response genes to form 2nd response proteins

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22
Q

Example of nuclear receptor

A

Glucocorticoid receptor

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23
Q

Glucocorticoid receptor detects

A

Dexamethasone - cortisol

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24
Q

Glucocorticoid receptor location

A

IC receptor as dexamethasone diffuses through PM

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25
Dexamethasone complex translocates to..
Nucleus
26
Dexamethasone complex mostly expresses
TF | Consistent with primary/secondary responses
27
Dexamethasone pathway
GR + HSP70 + FKBP52 + Dex --> GR + Dex + DNA + tran machinery
28
Glucocorticoid receptor mainly target
Metabolism Catabolism Biosynthetic pathways
29
When is Dex/cortisol released
stress | decreased blood glucose
30
4 main points about glucorticoids
1. for medical therapy 2. immunosuppression/antiinflamm 3. broad effects, different organ systems 4. debilitating side effects = bone loss/glucose dysregulation
31
Describe hypothalamus- pituitary-adrenal axis
1. The hypothalamus produce a 41 aa peptide called corticotropin-releasing hormone (CRH). 2. This travels to the pituitary gland that releases ACTH which is a peptide hormone. 3. This stimulates the adrenal glands which then release cortisol/dexamethasone
32
What does cortisol effect
1. metabolism 2. immune system 3. Memory 4. electroyltes
33
Disease of too little cortisol + symptoms
Addison's disease | • Depression, flu-like symptoms, nausea, weight loss
34
Types of disease from too little cortisol
* Primary adrenal insufficiency – damage to the adrenal glands so cortisol is not made * Secondary adrenal insufficiency – lack of ACTH due to lack of activity or damage to pituitary gland so adrenal glands can’t be stimulated
35
Disease of too much cortisol + symptoms
Cushing's syndrome | Puffy face, weight gain, increase BP, facial growth
36
Causes of too much cortisol
Benign adenoma pituitary increases ATCH | LT steroid abuse and use
37
Insulin controls
Blood glucose levels
38
Insulin released from
Beta cells, Islets of Langerhans - stimulated after meal
39
Type 1 diabetes
Destruction of β cells – often as a result of auto-immune attack. This results in high levels of plasma glucose
40
Prevalence type 1 diabetes
1:300, age 18
41
Insulin receptor structure
Heterotetramer linked by disulfide bonds | Tyrosine kinase activity
42
Conformation changes when ligand binds to IR
2 kinases domains closer Kinase domains trans-phosphorylate Docking domain, insulin substrate 1 becomes tyrosine phosphorylated
43
3 major biochemical steps in insulin signalling
1. tyrosine phos of R and its substrate IRS 2. activation lipid kinase P13K 3. activation multiple serine/threonine kinases = AKT
44
6 step pathway of insulin signalling - more detail
1. Insulin binds to IR 2. IR tyrosine activated 3. Tyrosine phos of IR and IR substrate (IRS) 4. P-tyrosine sites on IRS allows binding of lipid kinase P13K which synthesises PIP3 at PM 5. PIP3 recrutis PDK and directly phos AKT and other serine/threonine kinases 6. AKT phos ser/thr residues substrates
45
What are the effectors of AKT
FOXO --> glucose production TSC2 --> mTORC1 --> S6K --> protein synth + --> SREBP1c --> lipid synth GSK3beta --> glycogen sytnh TBC1D4 --> glucose uptake
46
Types of insulin
long acting background insulin replacement | Fast acting bolus for meals
47
Excess insulin disease and symptoms
Hypoglycaemia - too little blood sugar, brain only metabolisrs glucose, live muscles take up glucose --> unconscious/death
48
Type 2 diabetes
dysreg lipid,carb,protein metab | impaired insulin sercretion/resistance
49
Prevalence type 2
1: 17 | 3. 8m UK
50
Correlation type 2 diabetes
There is a strong correlation between body mass index and risk of type 2 diabetes
51
Type 2 diabetes symptoms
``` Thirsty excess glucose in urine as kidneys cant reabsorb all increased urination weight/muscle loss slow heal cuts/ulcers thrush blurred vision ```
52
REmission trial
High intensity weight loss | 46% remission 12m, 36% 24m
53
Summary Remission results
Increase QOL, decrease systolic BP/triglycerides/SAEs 12-24m
54
Medication type 2
Metformin - antihyperglycameic agent of the biguanide class
55
Mechanism metformin
Insulin sensitiser - decrease insulin resistance - reduces plasma fasting insulin levels - weight loss
56
Where and why does metformin accumulate
Positively charged - in cells and mitochondria
57
Metformin inhibits
Mitochondria complex 1 preventing production of mito ATP --> increased cytoplasmic ADP:ATP and AMP:ATP ratio --> activated AMP-activated protein kinase which regulates glucose metabolism
58
2 classes of steroid hormones
corticosteroids - cortex adrenal gland | sex steroids - placenta/gonads
59
corticosteroids e.g. x2
gluco/mineralcorticoids
60
sex steroids
oestrogen, testosterone, progesterones

Cell and molecular extras (16 decks)

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