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Signalling and Men > The Homosexual community > Flashcards

The Homosexual community Flashcards

1
Q

(1) The 6 types of cell to cell communication

A

1) Autocrine (Regulates itself)
2) Paracrine (Hormone to target cell)
3) Endocrine (Hormone to target cell via bloodctream)
4) Neurocrine (Neurone –> bloodstream –> Target
5) Exocrine (Ducts to target)
6) Juxtacrine (Cell-cell close contact)

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2
Q

(1) 3 hormones derived from amino acids

A
  • AVP
  • Insulin
  • Gonadotrophins
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3
Q

(1) 3 hormones derived from cholesterol derivatives

A
  • Cortisol
  • Testosterone
  • Vitamin D
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4
Q

(1) Characteristics of peptide hormones

A
  • Rapid changes in [plasma]
  • Short half life
  • Receptors: Membrane
  • Mech: Activate pre-formed enzymes
  • Rapid effect
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5
Q

(1) Characteristics of steroid hormones

A
  • Slow fluctuations in [plasma]
  • Long half life
  • Receptors: Intracellular
  • Mech: Stimulate protein synthesis
  • Slow effect
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6
Q

(1) Why are different proteins formed from the same preprohormone?

A

Different cleaving enzymes are located in different cells (that cleave different sites on the DNA)

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7
Q

(1) 5 Hormones derived from Tyrosine

A
  • Dopamine
  • Noradrenaline
  • Adrenaline
  • T3
  • T4
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8
Q

(1) Structure of Pregnenolone

A

LOOK AT IT

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9
Q

(1) Pregnenolone is the precursor to which 3 hormones?

A
  • Cortisol
  • Testosterone
  • Aldosterone (Used in water-reabsorption)
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10
Q

(2) HPA stand for?

A
  • Hypothalamus
  • Pituitary
  • Adrenals
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11
Q

(2) Features of Posterior Lobe

A
  • 1 Inferior hypophyseal vein feeds into P lobe
  • Releasing hormones from the Supraoptic and paraventricular nuclei travel to P lobe
  • Releases hormones into blood
  • Less cell mass, has axon tracts, vesicles of hormone (made in hypothalamus)
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12
Q

(2) Features of Anterior Lobe

A
  • 2 Superior hypophyseal vein feeds into A lobe (via Infundibulum)
  • Releasing hormones from Neurosecretory neurones travel to A lobe
  • Cell rich
  • Cells in clumps with gaps called signocoids (where trophic hormones collect)
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13
Q

(2) P lobe hormones

A
  • Oxytocin (Unterus contractions + milk ejections)

- Vasopressin (ADH/AVP) (Water reabsorption)

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14
Q

(2) What is Neurophysin and how’s it used?

A
  • Carrier proteins: Transport hormones from PVN and supraoptic nucleus.
  • Neurophysin 1: Oxytocin
  • Neurophysin 2: Vasopressin
  • The carrier protein is secreted from hypothalamus as a part of the hormone precursor molecule (then cleaved as they reach the P lobe)
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15
Q

(2) How does AVP increase water reabsorption and decrease urine output?

A
  • AVP binds to V2 receptors (GPCR) and increases aquaporin presentation on collecting duct and increase Na+ transport into cell.
  • ALSO causes arteriole restriction and increased pressur
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16
Q

(2) How does Alderstone increase H20 reabsorption?

A
  • Binds to nuclear mineralcorticoid receptor (MR)

- Up regulates and activates Na+/K+ pumps

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17
Q

(2) How is water levels detected?

A
  • Plasma osmolarity

- Hypothalamic osmoreceptors

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18
Q

(2) Disease released to inability to respond to AVP

A

Diabetes Insipidus

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19
Q

(2) 6 Major Trophic Hormones : 5 cell types

A

1) Corticotrope (cAMP): Adrenocorticotrophin (ACTH)
2) Somatotrope (JAK/STAT): GH
3) Lactotrope (JAK/STAT): Prolactin (PRL)
4) Gonadotrope (cAMP): Lutenising hormone (LH)
+ Follicle-stimulating hormone (FSH)
5) Thyrotrope (cAMP): Thyroid-stimulating hormone (TSH)

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20
Q

(2) Name the gap between the P and A lobe

A

Pars intermedia (fetal site of melanocyte-stimulating hormone)

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21
Q

(3) 3 Direct effects of GH

A

1) Antagonises insulin
2) Synergises with cortisol
3) Promotes growth of bone, soft tissue and viscera (enhances fibroblast differentiation)
Facilitates insulin in fed state, promotes growth

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22
Q

(3) Indirect effect of GH

A

1) (via IGF-1/2) Antagonised by cortisol

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23
Q

(3) 3 primary controllers of GH secretion

A

1) Receptors on somatotrophs
2) Hypothalmic hormones
(GHRH: Growth hormone releasing hormones, peptide +ve)
(Somatostatin: Growth hormone inhibiting hormone)
3) Stomach hormones (Ghrelin: Influences A lobe)

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24
Q

(3) GH metabolic effects

A
  • Suppresses the ability of insulin to stimulate glucose uptake in peripheral tissues
  • Enhances glucose synthesised in liver
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25
Q

(3) What is GH hypersecretion called? Symptoms

A

Acromegaly: Can cause reduced peripheral eye vision

  • Increased hand sizes
  • Weight gain and headaches
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26
Q

(3) Types of hormones produced from Cortex and medulla

A

Cortex: Steroid hormones
Medulla: Tyrosine hormones

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27
Q

(3) Whats required in the last step of catecholamine production in medulla?

A

Cortisol (from cortex) stimulates PNMT to convert NA to A.

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28
Q

(3) Effects of catecholamines (medulla)

A
  • Heart rate and force
  • Increase BP
  • Pupil dilation
  • Hepatic glycogenolysis (A)
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29
Q

(3) Categories of corticosteroids

A 
1) Mineralcorticoids: Aldosterone 
Regulates Na+ and blood pressure (water homeostasis)
2) Glucocorticoids: Cortisol 
Glucose homeostasis 
3) Sex steroid precursors 
Final maturation of hormone in gonads
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30
Q

(3) How ACTH receptor induces cAMP and promotes steroidogensis

A

1) ACTH binds to ACTH-R (GPCR)
2) cAMP then activates StAR
3) StAR (Steroidogenic Acute Regulatory Protein) allows Cholesterol into mitochondrion
4) Converted to Prognenolone
5) Enters ER and becomes Deoxycorticosterone
6) Back to Mito and converted to Aldosterone

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31
Q

(3) Adrenal diseases

A

1) Glucocorticoid OVER production: Cushing’s syndrome (Accumulation of abdominal fat. Thin skin reveals blood flow through underlying vessels)
2) Insufficient Glucocorticoid production: Addison’s
(Caused by destruction of adrenal cortex due to autoimmune diseases, symptoms are weight loss weakness and depression)

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32
Q

(4) Cell type that secretes zymogens and main exocrine functions of pancreas

A

Acinar cells

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33
Q

(4) Synchrony of B-cells is key to increase insulin secretion

A

JOHN CENA

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34
Q

(4) Specific gap-junctional uncoupler of B-cell

A

Connexin-36
TRIVIA
Carbenoxolone (uncoupling agent): Prevents gap junction from staying open. Uncouples cells and decreases insulin secretion

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35
Q

(4) Steps how glucose makes insulin secretion happen

A

1) Increased blood glucose
2) Glucose enters cell (by GLUT 2 transporter)
3) Increases glycolysis and CAC
4) Increased ATP
5) ATP closes K(ATP) channel so less K+ leaves the cells
6) Cell depolarises
7) Voltage-gated Ca2+ channel opens
8) Ca2+ entry triggers exocytosis and insulin is secreted.

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36
Q

(4) Conc of K, Na, Ca in and out of cell

A

OUTSIDE
[K]: 5 mM
[Na]: 140 mM
[Ca]: 1.2mM

INSIDE
[K]: 140 mM
[Na]: 5mM
[Ca]: 100 mM

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37
Q

(4) K(ATP) channel important drug target, which drugs and what do they bind to?

A

Sulphonylureas: Binds to SUR1 and increases insulin secretion
Diazoxide/Cromakalin: Binds Kir6.2 (potassium inward rectifier) allows K+ through both ways, decreases insulin secretion

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38
Q

(4) What is incretin effect?

A

Insulin secretion is more potent when food is taken orally and not glucose directly into blood (glucose infusion injection)
-Diabetics have a lower incretin effect

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39
Q

(4) Causation of insulin secretion: Early phase and late phase

A

Early phase: Neurological input and incretin hormones

Late phase: Gut response controlled by readily available pool of insulin and reserve pool of vesicles

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40
Q

(4) Differences between Human, Porcine and Bovine insulin structures

A

H: Thr, Thr, Thr
P: Ala, Thr, Thr
B: Ala, Ala, Val –> original source of insulin for treatment

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41
Q

(5) What happens when insulin binds to IGF-1 receptors?`

A

1) Increase in GLUT4 transporter on membrane via GLUT4 vesicles. (Transporter then gets broken down)
2) If signal is projected long enough, gene expression alteration and growth occurs.
3) Glucose metabolism, protein synthesis

42
Q

(5) IGF-1 receptor binding and clustering

A

1) Ligand binds
2) Dimerises
3) Auto-phosphorylates
4) Receptors bind together (each dimer can bind 2 insulin molecules)
- Affinity for 2nd insulin molecule is lower than 1st
- Negative cooperativity
- Increases response speed

43
Q

(5) Consequences of IGF-1 receptor activation

A
  • Changes in membrane potential
  • Receptor kinase activation
  • Generation of 2nd messengers
  • GLUT4, increased membrane insertion
44
Q

(5) What occurs after IGF-1 receptor activation?

A
  • Receptor moves to clatharin coated pits
  • Hormone and receptor internalised
  • Recycled from endosomes, insulin degraded by insulin degrading enzymes.
  • Receptor later degraded in lysosomes
45
Q

(5) The four types of GLUT transporter

A

GLUT-1: Basal + non-insulin mediated glucose uptake (High capacity, low Km)
GLUT-2: B-cell, precursor for glucose-sensing
(High capacity, low affinity high Km)
GLUT-3: Non-insulin mediate glucose uptake in brain
(High capacity, low Km)
GLUT-4: Insulin-stimulated glucose uptake (muscle/adipose)
(Activating by insulin, low Km)

46
Q

(5) Islets of Langerhans, cells and what they secrete

A
  • Alpha cell: Glucagon
  • Beta cell: Insulin
  • Delta cell: somatostatin
  • PP cell: pancreatic polypeptide
  • Epsilon cell: Ghrelin
47
Q

(5) Glucagon synthesis from preprohormone

A

-Processed differently in alpha cells and gut
ALPHA CELLS
(GRPP+Glucagon+IP1+ major proglucagon fragment)
GUT
(Glicentin + GLP-1 + IP-2 + GLP-2)

48
Q

(5) Main circulating form of somatostatin and function

A 
SS-28
Inhibits secretion of insulin via activation of SSTR2/5:
-Inhibit adenylate cyclase + cAMP
-Open K+ATP and hyper polarise membrane
GPCRs = SS receptors
49
Q

(5) Pancreatic polypeptide

A
  • Release stimulated by protein meals
  • Inhibits enzymatic and bicarbonate pancreatic exocrine secretion
  • Affecting GI migrating motor complex and gastric secretions
50
Q

(6) Outline regulation of glycogen synthesis

A 
1) Glycogen synthase
ACT: Dephos by protein phosphatase 
DEACT: Phos by protein kinase A
2) Glycogen phosphorylase 
ACT: Phos by phosphorylase kinase 
INACT: Dephos by protein phosphatase
51
Q

(6) Effects of insulin on metabolism

A

1) Promotes Fat cell lipoprotein lipase: promotes fat synthesis via glucose and breakdown of chylomicrons via lipoprotein lipase
2) Downregs fat to plasma FFA (by hormone sensitive lipase)
2) Downregs Carnitine acyltransferase 1 transport across mito membrane
3) Promotes glycolysis
4) Downregs gluconeogenesis (via promoting pyruvate kinase)

52
Q

(6) Effects of glucagon on metabolism

A

1) Downregs fat cell lipoprotein lipase: decreases fat synthesis by glucose and break down of chylomirons
2) Promotes fat to plasma ffa via hormone sensitive lipase.

53
Q

(6) Effects of lacking insulin

A

1) Increased protein metabolism
2) Increased fat metabolism
3) Diabeetic ketoacidosis

54
Q

(6) What is type 1 diabetes

A

INSULIN DEPENDENT (Insufficent production due to destruction of B cells by immune reaction)

55
Q

(6) What is type 2 diabetes

A

NON-INSULIN DEPENDENT (Insulin resistance)

56
Q

(6) Cause of insulin resistance

A
  • Obesity driven insulin resistance
  • Decrease in receptors /receptor binding
  • 10% of people don’t develop compensatory responses, develop B-cell failure and diabetes
57
Q

(6) What is gestational diabetes mellitus

A
  • Caused by placental hormone interference (GH)

- Progesterone indirect effects via A lobe effect on increasing lactotrophs (increased Prolactin)

58
Q

(6) Symptoms of diabetes

A
  • Elevated blood glucose
  • Dehydration and increased thirst
  • Inability to use glucose energy leading to fatigue, nausa, vomiting
  • Blurred vision
59
Q

(6) Treatment of diabetes

A

Diet: Low cholesterol
Weight reduction and excercise
Increase body’s insulin sensitivity
Insulin

60
Q

(7) Did you know all hormones in the gut are peptides?

A

You didn’t? Retard

61
Q

(7) Stomach cells and their secretions

A

Parietal cells: HCl
Chief Cells: Pepsinogen
Enteroendocrine cells: Gastrin

62
Q

(7) Drug using proton pump inhibitors to fight indgestion

A

Omeprazole

63
Q

(7) Role of gastrin

A
  • Controls acid secretion directly: CCK-2R Parietal cells
  • Indirectly via ECL cells to secrete Histmine (that binds to H2R on Parietal cells)
  • Drives mucosal growth
64
Q

(7) How is gastrin regulated

A
  • Regulated by pH, somatostatin
  • Neural input: Cholinergic activation of ECL and D cells in lumen body + Inhibition of D cells in lumen of antrum
  • Somatostatin (SS28) via D cells. Uses Somatostain receptor
  • Parasympathetic stimulation of ECL and parietal cells via Ach receptors
65
Q

(7) Gastrin receptors

A

CCK1: Specific for CCK
CCK2: Specific for both CCK and gastrin with high affinity

66
Q

(7) Somatostatin in the stomach

A

Low gastric pH stimulates delta cells to secrete SS and inhibit gastrin release
ALSO stimulated by mechanical stimulation and components of a meal
(Muscarinic stimulation is key neural stim to SS secretion)

67
Q

(7) Somatostatin inhibitory functions in the stomach

A

1) Reduces gastric acid production
2) Inhibits pepsinogen secretion
3) Stops pancreatic enzyme secretion
4) Inhibits gut motility
5) Reduces intestinal transport of nutrients
6) Inhibits tissue growth and proliferation

68
Q

(7) WAT is Zollinger-Ellison syndrome

A

Condition where there is an overproduction of gastrin, too much gastric acid causing peptic ulcers

69
Q

(8) What is entero-insular axis?

A

An axis between gut and the pancreas

Links: Incretins from the gut, neurotransmission, nutrients

70
Q

(8) VAT IS incretin effect

A

This is the increased insulin response produced by taking glucose orally vs Intravenous glucose

71
Q

(8) Role of GLP-1 (glucagon like peptide)

A

1) Stim insulin secretion
2) Increase B-cell mass
3) Inhibits glucagon secretion
4) Delays gastric emptying
PRODUCED BY L-Cells

72
Q

(8) How does Exenatide work

A

This is a GLP-1 agonist, used in type 2 diabetes treatment. Regulator of glucose metabolism and insulin secretion

73
Q

(8) Role of GLP-2

A

Stimulated by Nutrients –> acts in GI mucosal epithelium

  • Increase hexose transport, proliferation
  • Decrease apoptosis, permeability, motility
74
Q

(8) What is and role of GIP (an incretin)

A

Gastric Inhibitory peptide (glucose dependent insulinotropic peptide)

  • Stimulates insulin
  • Inhibits motility and secretion of H+ stomach secretion
  • From K-cells, proximal intestine/duodenum
75
Q

(8) Use of GIP therapeutically

A
  • GIP can get degraded into an antagonist

- Used as a target for treat obesity.

76
Q

(8) VAS IS DAS Ghrelin

A
  • 22 aa peptide from stomach (+ arcuate nucleus in hypothalmus)
  • Stim hunger (controls appetite)
  • Counters leptin (inhibits hunger)
77
Q

(8) Function of Ghrelin

A
  • Stims GH secretion
  • Increases food intake
  • Produces weight gain
  • stims gastric contraction, enhances stomach emptying
  • Ghrelin levels are low after eating and in obesity
78
Q

(8) How Ghrelin affects THE MIND

A

1) Released from stomach, acts on vagus nerve
2) At CNS level, Ghrelin activates NPYin arcuate nucleus of hypothalamus, which involced in regulation of feeding. Balanced by leptin.

79
Q

(8) What is Prader-Willi syndrome

A

A deletion of HBII-85 class of small nucleolar RNAs (snoRNAs) is assocaited with hyperphagia, obesity and hypogonadism.

80
Q

(8) WAT is Cholecystokinin (CCK)

A

Peptide produced by I-cells of small intestine

  • Secreted into blood after meal
  • Produced from a single gene by post-translational processing of a pre-prohormone
81
Q

(8) Function of CCK

A

Binds specific CCK1 receptors:

1) Gallbladder: stim contraction
2) Pancreas: Pancreatic secretion
3) Smooth muscle in stomach: Regulate gastirc emptying
4) Peripheral nerves: Bowel motility
5) Inhibits gastric acid secretion by binding to CCK1 receptors on D-cells in antrum.
- Ingested fate and protein are major food components that stimulate CCK release.
- Ghrelin stims release of CCK

82
Q

(8) WAT is motilin

A

22 aa peptide

  • M cells of duodenum, secretion NOT induced by eating
  • Synchronised with interdigestive migrating motor complex (MMC) under fasting conditions.
83
Q

(8) Function of motilin

A
  • Binds to specific receptors on smooth muscle cells of stomach and intestines and enhance propulsive activity
  • Motilin agonists (like erythromycin) useful to treat acute gastroparesis.
84
Q

(8) WAT is secretin

A

First hormone to be discovered

  • A 27 aa peptide
  • Released by S-cells in dueodenum
  • Stims pancreatic fluid and bicarbonate secretion leading to neutralisation
  • Inhibits gastric acid secretion
  • Secretin receptor is a GPCR.
85
Q

(9) Main type if cell in adipose tissue

A

Adipocytes (Preadipocytes become mature adipocytes when stim by glucose, insulin, FFA)

86
Q

(9) WATs the good and bad bits of body fat

A 
Subcutaneous fat (formed from mesodermal SC): Good, fat storage, insulation, secretion of adipokines
Visceral fat: Bad, surrounds organs
87
Q

(9) Name the adipose derived hormones

A

1) Leptin (Increased obesity, fullness feeling)
2) Chemerin
3) Adiponectin (Decreased in obesity)

88
Q

(9) Role of Leptin

A

Signals via RTKs (Receptor tyrosine kinase)

  • Produced from arcuate nucleus of hypothalamus
  • Inhibits hunger
89
Q

(9) Mechanisms of leptin resistance

A

1) Decrease endospanin 1
- More R at membrane, increased leptin signals
- Deliver shRNA via Lentiviruses to arcuate nucleus brain
2) Increase endospanin 1
- Increase degradation of R
- Lack satiety signals
- High circulating levels in obese humans

90
Q

(9) WAT are endospnanins

A

These regulate trafficking of receptors

91
Q

(9) Function of adiponectin

A

244 aa protein

  • Secretion by insulin
  • Reduced by obesity
  • Promotes glucose uptake in muscle
  • Inhibits gluconeogenesis
  • Promotes fatty acid oxidation
  • Complementary and additive effects with leptin
92
Q

What is an anus?

A

Yes

93
Q

(9) Receptors of Adiponectin

A

1) ADIPOR1 (skeletal muscle)
2) ADIPOR2 (liver)
Upside down GPCRs, signal to AMPK
-Adiponectin has several forms where ADIPOR2 has low affinity for the trimer.

94
Q

(9) Adpionectin disorders

A

Leptin KO mice have low adpionectin levels (due to hyperinsulinemia)

  • Adiponectin mutant slightly insulin resistant
  • Adiponectin can protect obese mice.

Adiponectin mutatns, linked to cardiovascular disease and atherosclerosis in humans

95
Q

(9) Other adipokines

A

1) Reistin: Correlates with obesity (118 aa cys-rich)

2) Visfatin: enzyme high levels in obesity and visceral fat. Insulin sensitising

96
Q

(9) What does WAT (white adipose tissue) do

A

In fed state, stores triglycerides

97
Q

(9) Obese adipose tissue changes

A 
INCREASED
-Leptin
-CHemerin
DECREASED
Adiponectin
98
Q

(9) Dysfunctional metabolic states

A

1) Elevated glucose
2) Pro-inflammatory state
3) Atherogenic Dyslipidemia
4) Elevated blood pressure
5) Pro-thrombotic state

99
Q

(9) The 4 disorders from apidocyte derived factors

A

1) Obesity
2) Hyperinsulinemia/ Insulin resistance (Diabetes milletus)
3) Cardiovascular disease
4) Dyslipidemia

100
Q

(9) What does Brown adipose tissue secrete

A

AUTOCRINE: IGF-1 and basement membrane proteins
PARACRINE: Nitric oxide, nerve growth factor
ENDOCRINE: Leptin, adiponectin, FFA

Signalling and Men (6 decks)

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