101 Flashcards
(234 cards)
1
Q
eukaryote cell structure important parts
A
plasma membrane, nucleus and organelles
2
Q
functions of the plasma membrane
A
regulates movement of substances in and out of the cell, detects chemical signals (intercellular comms), identify the cell to other cells and can links adjacent cells to each other for comms.
3
Q
cholesterol in plasma membrane
A
stabilizes the membrane
4
Q
glycocalyx
A
arrangement of glycolipids + glycoproteins on the outside of the membrane for cell recognition
5
Q
ion channel
A
on plasma membrane allows movement of specific ions thru
6
Q
carrier on plasma membrane
A
transports specific substance across membrane by undergoing change in shape (bind then turn around idK)
7
Q
receptor (intergral)
A
on plasma membrane, recognizes specific ligand and alters cell function.
8
Q
enzyme (integral and peripheral)
A
catalyses reaction on inside or out of cell.
9
Q
linker (intergral and peripheral)
A
anchors filaments inside and out plasma membrane
10
Q
cell identity marker (glycoprotein)
A
distinguishes cells from other cells.
11
Q
nucleus functions
A
stores genetic info (DNA) to direct cell activities, ensures transmission of genetic info to next gen (cell division). Contains the nucleolus which assembles ribosomes. Surrounded by it own membrane which contains nuclear pores.
12
Q
gene
A
segment of DNA containing the code for how to make a protein
13
Q
transcription brief
A
DNA sequence/ template from one gene which is copied by mRNA which exits the nucleus
14
Q
gene expression has
A
two steps: translation and transcription
15
Q
translation brief
A
ribosomes use the mRNA sequence to assemble amino acids in the correct order to make protein
16
Q
ribosomes
A
amino acids are assembled in different combinations to form diverse range of proteins and can be found floating in cytosol or attached to the rough ER.
17
Q
ER
A
rough and smooth ER
18
Q
Rough ER
A
extends from nuclear membrane and contains ribosomes. Manufactures, folds and processes proteins to be distributed to other organelles. The plasma membrane or secreted out the cell.
19
Q
smooth ER
A
no ribosomes, enzymes for fatty acid and steroid synthesis. In the liver -> enzymes help release glucose into blood and others detoxify. In muscle lumen is store for Ca ioins.
20
Q
Smooth ER in muscle cells
A
lumen is a store for calcium ions
21
Q
smooth ER in liver
A
enzymes help release glucose into the blood while other enzymes detoxify harmful substances
22
Q
Where do proteins made in the rough ER go
A
either distributed to other organelles within the cell, or secreted out the cell or goes to the plasma membrane.
23
Q
cytoskeleton
A
variety of protein filaments that provide movement and scaffolding of organelles and whole cells.
23
Q
Golgi complex
A
consists of curved/flattened membranous sacs which transports proteins recieved from the rough ER and forms secretory vesicles -> organelles/plasma membrane or out cell (EXOCYTOSIS)
24
Secretory vesicles contain proteins that
either are transported to the plasma membrane, organelles or exit the cell via exocytosis.
25
lysosomes
organelle sacs containing powerful digestive enzymes with acidic pH, abundant in macrophages to breakdown bacteria. Breaks down worn out organelles and cellular debris and can also undergo autolysis.
26
microfilaments
muscle contraction, changes in cell shape during movement and cell division
27
intermediate filaments
resist mechanical stress and can attach cells to each other
28
microtubule
hollow tubes of proteins that determine cell shape, movement of organelles such as vesicles and cell extensions
29
mitochondria
outer membrane separates mitochondria from surrounding cytosol, inner membrane folded into cristae for SA (enzymes and chem reactions).
30
reaction to make food into energy
glucose + oxygen -> carbon dioxide + water + ATP.
31
chem reaction def
whenever chemical bonds are formed, rearranged or broken -> molecules are converted
32
metabolism def
all biochemical reactions occurring in the body which are intra or extracellular.
33
coupled reaction
two reactions that occur concurrently. Eg exothermic energy released used to drive endothermic reactions
34
exothermic reactions
release energy, bonds of reactants greater than products -> catabolic/digestion
35
endothermic reactions
absorb energy = products energy> anabolic and synthesis reactions.
36
redox reactions are always
coupled. OILRIG
37
Co enymes -> REDOX
when nutrients are catabolized for energy, hydrogens can be transferred ton carrier molecules (CO ENZYMES NAD+ AND FAD).
38
ATP hydrolysis
quick release of energy that can be coupled to drive biochemical activities that need energy
39
ATP AND PC
small amount of ATP stored in muscle cells. Phosphocreatine in muscle cells can donate a phosphate to ADP to form ATP again.
40
ATP-PC system
provides rapid burst of energy and can sustain physical activity for 10 sec.
41
ATP AND NUTRIENT METABOLISM
Need other sources of fuel to sustain ATP levels required to run the bodys activities at rest and exercise. Glucose energy breakdown cascade.
42
Energy is contained within chem bonds of
dietary macronutrients
43
Nutrient metabolism
digestive system via the GI tract breaks down macronutrients to their smallest absorbable units.
44
CARBS
simple sugars: monosaccharides, disaccharides and complex carbs: polysaccharides.
45
Humans/animals store carbs as
glycogen when glucose is plentiful in the skeletal muscle and liver
46
Glucose energy source from carbs
good energy and digestive system breaks down complex carbs and disaccharides to monosaccharides which is absorbed into the blood from small intestine -> liver -> cells
47
Lipids include
triglycerides,phospholipids and sterols. 95% in food and 99% in body are triglycerides.
48
Triglycerides are stored
in adipose tissue, liver and skeletal muscles. Excellent source of energy. More energy dense with slower extraction.
49
Proteins
primarily build body structures and preform essential body functions. can provide energy but not preferred.
49
20 amino acids
humans can produce 11 and 9 are required in diet as essential amino acids.
50
All the ways we can receive and use glucose.
Gluconeogenesis in the liver, glycogenolysis in the liver and blood glucose from the digestion and absorption of carbs in food.
51
gluconeogenesis
When glucose, and glycogen stores are low, the liver can convert non-carb substrates into glucose (lactate, amino acids).
52
glycogenolysis
skeletal muscle glycogen can be broken down to glucose, ON SITE Source of glucose to fuel contracting muscles. Liver glycogen can be broken down to provide blood glucose to fuel all body cells.
53
glycogen
storage form of carbs in muscle and liver
54
glycogenolysis and gluconeogenesis reaction
glycogen -> glycogenolysis -> glucose-6-P -> glucose (gluconeogenesis).
54
Carbohydrate metabolism equation
C6H12O6 + 6O2 → 6CO2 + 6H2O + 36 ATP
55
Carbohydrate metabolism
1) glycolysis (cytoplasm and O2 not needed)
2) krebs cycle, matrix of mito
3) oxidative phosphorylation/ETC -> oxygen needed, inner membrane of mito.
56
Glycolysis
Anaerobic, in cytoplasm:
- glucose (C6) enters glycolysis
- 2 pyruvate made (C3)
- 2 ATP used
- 4 ATP made and 2 NADH made (net 2 ATP)
- rate limiting step: PFK
57
RATE LIMITING STEP OF GLYCOLYSIS
PFK: phosphofructokinase
stimulated by high ADP and Pi during exercise and inhibited by high ATP, high citrate and a low pH.
58
Fate of pyruvic acid (O2 LACK)
anaerobic metabolism:
when energy demands exceed oxygen supply, pyruvic acid reduced to lactic acid and NAD+ is regenerated.
NET: 2 ATP per glucose.
59
lactic acid in exercise
when oxygen is low during exercise, lactic acid is product from pyruvic acid and accumulates in active skeletal muscle fibres and bloodstream -> muscle fatigue.
60
fate of pyruvic acid ( ABUNDANT O2)
when O2 is plentiful, pyruvic acid enters the mitochondrion for complete breakdown via aerobic metabolism (KREBS AND ETC)
61
KREBS CYCLE (CITRIC ACID CYCLE)
PYRUVIC ACID (C3) -> Acetyl CoA (C2) = 1 NADH and CO2 produced.
Acetyl CoA enters krebs and combines with oxaloacetic acid (C4) to form citric acid (C6)
Each turn of the cycle creates 3 NADH, 1 FADH2, 1 ATP and 2CO2.
Removal of 2CO2 ensures that after each turn of the cycle, oxaloacetic acid is regenerated.
RATE LIMITING ENZYME: isocitrate dehydrogenase
- 2 Pyruvic acid molecules generated from glycolysis -> krebs turns twice for each glucose molecule.
62
Removal of what ensures the krebs cycle is continuous
2CO2, to regenerate the oxaloacetic acid (C4).
63
What is the rate limiting step of the krebs cycle and how can it be affected?
ISOCITRATE DEHYDROGENASE is the rate limiting enzyme and it is stimulated by high ADP, Pi (during exercise) and Ca2+. Inhibited by high ATP.
64
NAD AND FAD CARRIERS
glycolysis and krebs cycle involve redox reactions -> Oxidation = removal of hydrogens & high-energy electrons from glucose/pyruvic acid. This needs an acceptor/carrier.
NAD derived from niacin and FAD from riboflavin
NAD+ and FAD are the oxidised forms. NADH + H+ is REDUCED
FADH2 IS REDUCED
65
reduced form of NAD+
NADH + H+
66
Reduced form of FAD
FADH2
67
Where is NAD+ derived from
niacin
68
Where is FAD derived from
riboflavin
69
Electron transport chain
NADH+ H+ and FADH2 pass their hydrogens and high energy electrons to the protein complexes in the membrane then to O2 as the final ACCEPTOR (producing metabolic water) in aerobic metabolism.
This process is coupled to ATP production
EACH NADH+ H+ carrier leads to 2.5 ATP formed
each FADH2 leads to 1.5 ATP Formed
At the same time NAD+ and FAD is regenerated to accept electrons in the glycolysis and krebs cycle.
70
How many ATP per NADH + H+ carrier
2.5 ATP
70
How many ATP per FADH2 carrier
1.5 ATP
71
Electron transport chain and proton gradient
electrons are transferred from complex to complex and some of their energy is used to pump protons into the intermembrane space to create a proton gradient
72
CHEMIOSMOSIS
ATP synthesis is powered by the flow of H+ back across from the inner membrane (proton gradient) of the mitochondria through ATP synthase. H+ combines with O2 the final acceptor to make H2O
73
RATE LIMITING ENZYME OF THE ETC
cytochrome oxidase (IV), stimulated by high ADP and Pi (during exercise) and limited by high ATP and cyanide.
74
Aerobic metabolism of triglycerides
Lipids go through lipolysis -> glycerol and fatty acids.
- glycerol component converted to pyruvic acid to go into krebs and ETC.
- Each of 3 fatty acids has 16-18C
2C fragments are split off thru a series of enzymatic reactions in the mitochondria called beta-oxidation
each 2C fragment is converted to acetyl CoA-> krebs and ETC
one 16C fatty acid can make 129 ATP!!
75
Can proteins make energy?
Amino acids can be catabolized for energy but not preferred compared to fat.
76
Acetyl CoA
is an important key metabolite linking different metabolic pathways
77
Energy Metabolism in Skeletal Muscle During Exercise: ATP stores
ATP stores provide only a few seconds of energy
78
ATP-PC (phosphocreatine) system (Energy Metabolism in Skeletal Muscle During Exercise)
provides rapid burst of energy sustaining physical activity for about 10 Seconds and is anaerobic
79
Anaerobic glycolysis system (Energy Metabolism in Skeletal Muscle During Exercise)
slower than ATP-PC but faster than aerobic system, provides energy for intense/short duration (~2min) activity plus lactic acid
80
Aerobic metabolism (Energy Metabolism in Skeletal Muscle During Exercise)
aerobic metabolism of glucose and fats is slower but provides high ATP for rest/sustained activity
81
diffusion
due to random thermal motion, passive movement of solutes from an area of high conc to low until equilibrium is reached
82
dynamic equilibrium
at equilibrium, solute molecules continue to cross membrane but there is no net flow or movement of the number of molecules from one area to another.
83
ficks 1st law of diffusion
J= PA (C0 -Ci)
84
J= PA (C0 -Ci)
ficks 1st law of diffusion
85
what does J stand for in ficks 1st law of diffusion
flux (the rate of solute movement)
86
what does P stand for in ficks 1st law of diffusion
permeability coefficient (how permeable the membrane is to that solute)
87
A in ficks 1st law of diffusion
area (surface area of the membrane)
88
C0 in ficks 1st law of diffusion
conc outside cell
89
Ci and C0 in ficks 1st law of diffusion
the chemical conc gradient
89
Ci in ficks 1st law of diffusion
conc in cell
90
flux/ rate of diffusion is dependent on
the size of particles
permeability of the membrane to solute
sa of membrane
the chemical conc difference across the membrane
91
other factors that affect diffusion
temp
electrochemical gradient and pressure gradient
92
simple diffusion
passive transport
- move freely through phospholipid bilayer
- high to low conc till eq
- move by kinetic energy no ATP
- small, lipid soluble, non polar substances can pass through the hydrophobic interior
-
93
examples of small molecules that undergo simple diffusion
oxygen, CO2 and alcohol, small enough to pass
94
is channel mediated facilitated diffusion passive or active?
passive as substances use a protein channel to cross the membrane
95
channel mediated facilitated diffusion
passive, substances use protein channel to cross membrane
kinetic energy diffusion
- polar, hydrophilic molecules/ions, cannot pass through phospholipid by itself
96
example molecules for channel mediated facilitated diffusion
water, Na+, Cl-, K+
97
can channel mediated facilitated diffusion be gated
yes some channels can be gated
-voltage-gated
-ligand gated
and mechanically gated
98
what facilitated diffusion can reach saturation
carrier mediated facilitated diffusion
98
carrier mediated facilitated diffusion
substances need protein transporter/carrier to cross membrane - highly selective for solute
- once solute attaches to binding site, there is a conformational change of the protein to allow solute across. Kinetic diffusion (passive). for polar, larger solutes like glucose, hydrophillic.
99
carrier mediated facilitated diffusion molecule example
for hydrophilic, larger solutes like glucose.
99
saturation of carrier mediated facilitated diffusion
if all transporters are occupied the flux will reach a plateau
100
osmosis
diffusion of water through a semipermeable membrane from an area that is more dilute to an area that is more concentrated (less water- high solute conc/osmolarity), cell membranes sometimes have aquaporins to assist this process. No ATP.
101
primary active transport
solute transported uphill against conc gradient, need ATP hydrolysis for energy, protein carriers are highly selective and require conformational change.
102
primary active transport example
Na+ and K+ ATPase pump, pumps out 3 Na+ out and 2 K+ in. Used to maintain electrical gradient across cell membrane
103
secondary active transport, counter transport and co transport
makes use of electrochemical gradient set up by a different protein (eg. Na/K+ ATPase pump) to drive other solutes across membrane against their own gradients. highly selective, these proteins themselves do not hydrolyse ATP.
104
secondary active transport, counter transport and co transport examples
sodium hydrogen counter transporter and sodium glucose cotransporter (SGLT)
105
antiporters
counter transport, secondary active transport -> sodium hydrogen counter transporter
106
symporters
co transport, secondary active transport, sodium glucose co transporter (SGLT)
107
vesicular transport
membrane changes shape and uses vesicles to move substances, requires ATP and two main types: exocytosis and endocytosis (phagocytosis).
108
DIRECT COMMUNICATION (INTERCELLULAR COMMS)
VIA GAP JUNCTIONS,IONS SMALL SOLUTES, LIPID SOLUBLE MATS, USUALLY LIMITED TO SAME CELL TYPE (ADJACENT) INTERCONNECTED BY CONNEXONS
108
TPYES OF INTERCELLULAR COMMS
PARACRINE COMMUNICATION, DIRECT COMMS, ENDOCRINE AND SYNAPTIC
108
SYNAPTIC COMMS
ACROSS SYNAPTIC CLEFTS LOCAL, NEUROTRANSMITTERS TARGET CELLS MUST HAVE APPROPRIATE RECEPTORS
109
PARACRINE COMMS
THROUGH EXTRACELLULAR FLUID, CHEMICAL MEDIATORS; PARACRINE FACTORS, LIMITED TO LOCAL WHERE PARACRINE FACTOR CONC HIGH -> TARGET CCELL MUST HAVE RECEPTORS
110
ENDOCRINE COMMS
BLOOD, HORMONES, TARGET CELLS PRIMARILY IN OTHER TISSUES/ORGANS MUST HAVE APPROPRIATE RECEPTORS
111
Cell signalling involves:
1. RECEPTION
2. SIGNAL TRANSDUCTION
3. CELLULAR RESPONSE
112
RECEPTION (CELL SIGNALING)
CAPTURING SIGNAL/STIMULUS BY BINDING PROTEIN RECEPTORS
113
2. SIGNAL TRANSDUCTION
PROCESS INVOLVED IN TRANSFORMING THE STIMULUS TO A RESPONSE, (CHANGES IN RECEPTOR SHAPE INTRACELLULAR SIGNALLING PATHWAYS)
114
CELLULAR RESPONSE (CELL SIGNALING)
END RESULT OF SIGNAL TRANSDUCTION -> ADVANTAGE TO THE CELL/HUMAN IN MAINTAINING HOMEOSTASIS
115
Ligand-receptor interactions are characterised by:
SPECIFICITY, AFFINITY, SATURATION AND COMPETITION
116
Specificity IN LIGAND RECEPTOR INTERACTIONS
the ability of a receptor to bind only to one type or a limited number of structurally similar
chemical messengers. Only cells that express the correct receptor can bind a particular ligand.
117
Saturation IN LIGAND RECEPTOR INTERACTIONS
the degree to which receptors are occupied by chemical messengers. If all are occupied,
the receptors are fully saturated; if half are occupied then the saturation is 50%.
118
Affinity IN LIGAND RECEPTOR INTERACTIONS
the strength with which a chemical messenger binds to a receptor.
119
Competition IN LIGAND RECEPTOR INTERACTIONS
the ability of different chemical messengers to compete for the limited binding sites of
receptors. Competing messengers generally have a similar structure to the natural ligand (e.g., drugs)
(ligand)
120
DIFFERENT TYPES OF RECEPTORS
CELL SURFACE RECEPTOR OR INTRACELLULAR RECEPTORS
121
CELL SURFACE RECEPTOR
TYPICALLY MEMBRANE-ANCHORED PROTEINS THAT BIND HYDROPHILIC MOLECULES (e.g., hormones such as insulin, or neurotransmitters such as acetylcholine)
122
INTRACELLULAR RECEPTORS
FOR HYDROPHOBIC MOLECULES TYPICALLY FOUND IN CYTOPLASM OR NUCLEUS: (e.g., steroid hormones such as oestrogen/testosterone)
123
Kinases- PHOSPHORYLATION CASCADE
add a phosphate group to other proteins thereby activating the protein. That phosphate is “plucked” from ATP!
124
Phosphatases
remove phosphate group from proteins thereby deactivating the protein
125
HOW DO Lipid-soluble messengers MOVE THRU CELL+BIND
PENETRATE THE PLASMA MEMBRANE AND BIND TO NUCLEAR CYTOPLASMIC RECEPTORS FORMING THE RECEPTOR HORMONE COMPLEX
126
RECEPTOR-HORMONE COMPLEX (HOW IT FORMED)
LIPID SOLUBLE CHEMICAL MESSENGERS PENETRATE THE PLASMA MEMBRANE AND BIND TO CYTOPLASMIC/NUCLEAR RECEPTORS IN THE CELL TO FORM A RECEPTOR-HORMONE COMPLEX
127
WHAT DOES RECEPTOR HORMONE COMPLEX DO
TRANSLOCATES TO NUCLEUS AND REGULATES GENE EXPRESSION (1ST STEP TRANSCRIPTION) -> IF GENE EXPRESSION UPREGULATED THE RESULTING MRNA MIGRATES THROUGH NUCLEAR PORES TO RIBOSOMES FOR TRANSLATION (2ND) -> PROTEINS
128
LIPID SOLUBLE MESSENGERS PROCESS OF PROTEIN FORMATION
1. PENETRATE PM
2. BIND TO NUCLEAR/CYTOPLASMIC RECEPTOR -> RECEPTOR HORMONE COMPLEX
3. TRANSLOCATES TO NUCLEUS TO REGULATE GENE EXP (1ST STEP TRANSCRIPTION)
4. IF GENE EXP UPREGULATED, RESULTING MRNA MIGRATES THRU NUCLEAR PORES TO RIBOSOMES FOR TRANSLATION
5. PROTEIN! THAT CONDUCTS CELLULAR WORK
129
Water-soluble messengers – Ligand-gated channels
1. Water-soluble chemical messengers bind
to a cell-surface receptor → ligand-gated
channel
2. The 3D structure of the channel
undergoes a conformational change
3. The channel may open allowing a specific
solute to move across the membrane
➢ This can cause changes to the electrochemical gradient if the solute is an ion
130
TYPES OF WATER SOLUBLE MESSENGERS
LIGAND GATED CHANNELS, GPCRS (ADENYLYL OR PHOSPHOLIPASE C) AND RECEPTOR TYROSINE KINASES
131
Water-soluble messengers – 2) G-protein coupled receptors (enzyme adenylyl)
1. Water-soluble/large chemical messengers
bind to a G-protein coupled receptor
(GPCR)
2. GPCR activates the G protein
3. G protein activates the enzyme Adenylate Cyclase – leading to cyclic AMP (cAMP) forming from ATP * cAMP is the “2nd messenger”
4. cAMP activates Protein Kinase A (PKA)
5. Activated PKA alters cellular activity
* E.g., glycogen → glucose (glycogenolysis)
triglycerides → fatty acids (lipolysis)
132
Phosphodiesterase
inactivates cAMP. Caffeine acts to inhibit phosphodiesterase, leading to elevated cAMP in cells
133
CAFFEINE INHIBITS
PHOSPHODIESTERASE WHICH USUALLY INHIBITS cAMP -> elevated cAMP in cells
134
Water-soluble messengers –3) G-protein coupled receptors - phospholipase C
1. Water-soluble/large chemical messengers bind to a G-
protein coupled receptor (GPCR)
2. GPCR activates the G protein
3. G protein activates the enzyme Phospholipase C (PLC)
4. PLC generates inositol triphosphate (IP3) and
diacylglycerol (DAG) from phosphatidylinositol (PIP2)
5. IP3 stimulates the smooth ER to release Ca2+ into the
cytosol
6. Ca2+ binds to and activates calmodulin (which alters
cellular activity)
7. DAG activates Protein Kinase C (PKC) which also
alters cellular activity
8. IP3 and Ca2+ are the 2nd messengers!
135
IP3 and Ca2+
2nd messengers
136
enzyme Phospholipase C (PLC)
PLC generates inositol triphosphate (IP3) and diacylglycerol (DAG) from phosphatidylinositol (PIP2) -> IP3 stimulates the smooth ER to release Ca2+ into the cytosol. Ca2+ binds to and activates calmodulin (which alters
cellular activity), DAG activates Protein Kinase C (PKC) which also alters cellular activity
137
enzyme Adenylate Cyclase
leading to cyclic AMP (cAMP) forming from ATP * cAMP is the “2nd messenger”
4. cAMP activates Protein Kinase A (PKA)
5. Activated PKA alters cellular activity
* E.g., glycogen → glucose (glycogenolysis)
triglycerides → fatty acids (lipolysis)
138
Water-soluble messengers – 4) Receptor Tyrosine Kinases (INSULIN)
1. Insulin binds to Insulin Receptor (subunits located outside and inside).
2. Conformational changes cause subunits located inside the cell to self-
phosphorylate each other.
3. Activated Receptor Tyrosine Kinase phosphorylates Insulin Response
(IRS) Proteins
4. Phosphorylated IRS proteins in turn activate glycogen synthase which
causes glycogen production.
5. Phosphorylated IRS protein also stimulates GLUT4 translocation to the
membrane so glucose can enter the cell.
138
is there a second messenger for the Receptor Tyrosine Kinases
no
138
second messenger for GPCR (Adenylyl cyclase)
cAMP
139
second messenger for GPCR (phospholipase C)
IP3 and Ca2+
140
Receptor Tyrosine Kinase
activated by insulin -> Activated Receptor Tyrosine Kinase phosphorylates Insulin Response
(IRS) Proteins -> Phosphorylated IRS proteins in turn activate glycogen synthase which
causes glycogen production -> Phosphorylated IRS protein also stimulates GLUT4 translocation to the
membrane so glucose can enter the cell
141
Homeostasis
Homeostasis is the maintenance of a relatively constant internal environment for optimum body function (“dynamic constant”), during rest/unstressed conditions. The body uses feedback systems to detect and respond to stimuli - therefore maintaining homeostasis
142
neg feedback
corrects stimulus -> Body temperature, blood glucose, hormone
levels etc.
143
pos feedback
stimulus amplification Fewer examples in the body: Childbirth, blood clotting, lactation
144
Body Temperature Homeostasis
“Normal” core body temperature ~ 37◦C
However, there is cyclical variation even at rest
145
Heat Transfer
Heat can be transferred between the body and the environment in four ways
1.conduction (gain or lose)
2. convection (gain or lose)
3. radiation (gain or lose)
and evaporation (only to lose)
146
the endocrine system
system of ductless glands found throughout body which secret chemical signals (hormones) which contribute to homeostasis by regulating activity of target cells in body/metabolism
147
a system of ductless glands throughout body -> secrete chemical signals
endocrine system
148
function of hormones
help regulate chemical composition and volume of internal environment (interstitial fluid), metabolism and energy balance, contraction of smooth/cardiac muscle fibres, glandular secretions/immune system. Control growth/development, regulate operation of reproductive systems and help establish circadian rhythms
149
endocrine glands (what are they?)
cells secrete their products (hormone) into interstitial fluid (extracellular fluid around cells) which can then enter blood capillaries to be transported around the body.
150
exocrine glands
secrete their products using ducts that carry secretions to the lumen of an organ or to the outer surface of the body (sweat glands, oil, mucous or digestive glands).
151
the endocrine system includes
endocrine glands, endocrine tissue and small pockets of endocrine cells.
152
endocrine glands in the endocrine system are organs...
organs whose primary purpose is to produce hormones, eg pituitary and thyroid glands
153
endocrine tissue
in organs which have other functions eg. pancreas and hypothalamus
154
small pockets of endocrine cells in the endocrine system
found in other organs such as the kidney and heart, enteroendocrine cells of the stomach and intestine.
155
Lipid soluble hormone examples
steroid hormones - adolsterone, cortisol, testosterone and oestrogen. Thyroid hormones T3 and T4.
155
movement of lipid soluble hormones
travel in blood plasma bound to transport proteins, diffuse through target cells plasma membrane and b ind to intracellular receptors inside cytosol/nucleus
156
neural stimulus (control of hormone secretion)
preganglionic sympathetic fibers stimulate adrenal medulla cells to secrete catecholamines (epinephrine and norepinephrine).
156
water soluble hormones examples
amine hormones- epinephrine (adrenaline) and norepinephrine (noradrenaline), peptide hormones: antidiuretic hormone (ADH) Oxytocin, protein hormones: growth hormone, insulin and glucagon.
156
How does the body control all these chemical signals to be released/when to secrete hormone?
humoral stimulus, neural stimulus and hormonal stimulus
157
humoral stimulus (control of hormone secretion)
when there is a change in conc of chemical/chem composition in blood (capillary blood contains low conc of Ca2+ which stimulates secretion of parathyroid hormone by parathyroid glands).
157
water soluble hormones movement into target
travel free in blood plasma, cannot diffuse through target cells plasma membrane, bind to cell surface receptors
157
are endocrine tissues under the influence of more than one type of input
yes, many endocrine tissues are under the direct influence of more than just one type of input which may stimulate or inhibit hormone secretion
158
hypothalamus -posterior pituitary gland
nerve fibres originating in hypothalamus travel through infundibulum to terminate in posterior pituitary (specialised neurosecretory cells) that release hormones from axon terminals. Nerve impulses from the hypothalamus stimulate secretion of these hormones (ADH, oxytocin) into blood from posterior pitutary.
158
hormonal stimulus (control of hormone secretion)
the hypothalamus secretes hormones that stimulate anterior pituitary gland to secrete hormones to stimulate other endocrine glands to secrete hormones (thyroid, adrenal cortex, testis)
159
specialised neurosecretory cells (hypothalamus-posterior pit)
nerve fibres originating in the hypothalamus travel down infundibulum to terminate in posterior pit, can release hormones from axon terminals
159
how is the hypothalamus and posterior pituitary connected
infundibulum
160
tropic hormone
a hormone that stimulates another endocrine gland to secrete its hormone.
160
hypothalamus-anterior pituitary gland
connected via hypophyseal portal veins (BV network), releasing/inhibiting hormones are secreted by hypothalamus, diffuse into blood and travel via portal venous system to target anterior pit cells. Hypothalamic hormones stimulate/inhibit release of anterior pitutary hormones from specific cells (growth hormone, thyroid stimulating hormone etc)
161
how is the hypothalamus and anterior pituitary connected
hypophyseal portal veins, portal venous sytem to target anterior pit cells from hypothalamus
162
hypothalamus-pituitary axis negative feedback regulation
stops hormones when levels r normal -> target gland hormone levels rise and inhibit further tropic hormone release via negative feed back, inhibiting hypothalamus and anterior pituitary release.
162
TRH (cold)
hypothalamic neurone activated -> stimulate release of TRH (Thyrotropin-releasing hormone) -> anterior pit -> TSH -> thyroid -> T3 and T4 -> inc metabolic rate.
163
which pituitary produces/stimulates more hormone release
anterior
163
thyroid hormone release
low levels of T3,T4 or low metabolic relate stimulates TRH in hypothalamus- -> TRH (hypophyseal veins) to anterior -> TSH released into blood stimulate thyroid follicular cells -> into blood by these cells
163
posterior pitutary hormones
neurosecretory cells -> ADH and Oxytocin
164
thyroid hormones
T3 and T4, inc basal metabolic rate, stimulate synthesis of Na+/K+ ATPase, inc body temp, stim protein synthesis, increase use of glucose/fatty acids for ATP production, lipolysis inc, enhance actions of catecholamines
165
negative feedback thyroid hormones
elevated T4 inhibits release of TRH and TSH by hypothalamus and anterior pitutary.
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test function
male pattern of development before birth, enlargement of male sex organs and expression of male secondary sex characteristic, anabolism (protein synthesis).
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FSH
follicle stimulating hormone, together with testosterone, FSH stimulates spermatogenesis -> spermatogeneic cells
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testosterone production
Hypothalamus releases GnRH -> anterior via portal vein -> FSH and LH (LH stimulates test secretion) -> test
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plasma testosterone levels during exercise
plasma testosterone levels are increased during exercise and stimulate muscle protein synthesis and hypertrophy
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LH
luteinising hormone, stimulates test secretion
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exercise and gnrh
exercise is the most potent influencer for secretion of GHRH and thereby growth hormone release
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Growth hormone secretion
hypothalamus -> somatostatin and GHRH (growth hormone releasing hormone) -> anterior pit via portal vein -> growth hormone -> liver and other tissues -> insuline growth factors -> stimulate protein synthesis and growth + other effects
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GH (growth hormone) has an anti-insulin effect
spares plasma glucose promoting fat breakdown for use as fuel
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growth hormone stimulates
protein synthesis and growth, increases gluconeogenesis in liver and blocks glucose entry to adipose cell to favor fat mobilisation.
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cortisol stimulants
exercise, bone break, burns, 'stress' -> higher brain centers.
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What stimulates growth hormone
exercise, sleep, stress and low plasma glucose
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GH and insulin like growth factors
Stimulate amino acid uptake, protein synthesis and growth of long bones
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Cortisol and exercise
exercise promotes release of CRH/ACTH which in turn increases plasma cortisol, cortisol is an important stress hormone.
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amount of cortisol released is dependent on
exercise duration and intensity
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adrenal cortex
produces steroid hormones made from cholesterol which are lipid soluble: glucocorticoids (cortisol), mineralcorticoids (aldosterone) and small amounts of sex steroids
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how does cortisol spare blood glucose
promoting breakdown of proteins to make amino acids available for converting to glucose (gluconeogenesis) and allow for injury repair. Mobilising free fatty acids from adipose tissue for use as fuel
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Cortisol secretion
hypothalamus releases CRH -> anterior pit via portal vein -> ACTH to adrenal cortex -> cortisol -> mobilises tissue amino acids, free fatty acids, stimulates gluconeogenesis and blocks entry of glucose into tissue
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epinephrine/norephinephrine (catecholamines) response
wide spread response mobilises body fuels for energy and activates cardiovascular and respiratory systems to ensure immediate response to stressor, non essential activites are inhibited.
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cortisol effects
mobilises tissue amino acids, free fatty acids, sitmulates gluconeogenesis and blocks entry of glucose into tissues.
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what stimulates epinephrine/norephinephrine
acute stress/exercise stimulates hypothalamus to initiate sympathetic nervous system response (fight/flight)
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Epinephrine and norepinephrine secretion
sympathetic nerves stimulate the adrenal medulla to release epinephrine (adrenaline) and norepinephrine (noradrenaline) hormones to further enhance stress response, catecholamines are water soluble chem signals binding to adrenergic receptors on target tissues -> effects using second msg in cell
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catacholamines (adrenaline and noradrenaline) bind to
adrenergic receptors on target tissues (water soluble) and bring about their effects using second messenger systems in cell.
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short term stress response
inc heart rate, blood pressure, liver converts glycogen to glucose and releases glucose into blood, dilation of bronchioles, changes in blood flow patterns leading to decreased digestive activity and reduced urine output, inc metabolic rate
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muscle glycogen utilisation (glycogenolysis)
rate of glycogen breakdown increases with exercise intensity, adrenaline in plasma inc rapidly with inc in exercise intensity and adrenaline increases cAMP production which promotes glycogen breakdwn.
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Dual control (redundant) of glycogenolysis
glycogen breakdown is under the dual control of adrenaline-cAMP and Ca2+-calmodulin pathways
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adrenaline-cAMP pathway vs Ca2+ calmodulin pathway
adrenaline: provides extracellular control of glycogenolysis whereas Ca2+ provides intracellular control of glycogenolysis
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Ca2+ calmodulin pathway
provides intracellular control of glycogenolysis: when a muscle cell is stimulated, calcium ions are released from the smooth ER, some Ca2+ initiate muscle contraction and some bind to calmodulin stimulating glycogen breakdown
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mechanisms which spare plasma glucose include
breaking down liver glycogen, breaking down triglycerides in adipose and mobilising free fatty acids to plasma, producing glucose from glycerol, lactate and aa in liver, reducing glucose uptake into cells
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Fast acting hormones in achieving blood glucose homeostasis in exercise
adrenaline, noradrenaline, glucagon and insulin perform the role of fast acting hormones
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thyroxine cortisol and growth hormone in achieving blood glucose homeostasis in exercise
permissive and slow acting hormones
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blood glucose homeostasis during exercise or starvation
endocrine system acts to maintain homeostasis of blood glucose levels when blood glucose is used rapidly, or when dietary intake of carbs is inadequate, this is important as some cells in the body use glucose as their principal fuel source such as the brain and red blood cells.
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insulin conc during exercise
decreases during exercise, need fuels within blood during exercise.
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how does glucose uptake into skeletal muscle increase during exercise when insulin conc is decreasing
Chemical gradient allows glucose to flood into cell via GLUT4. Contracting muscle stimulates GLUT4 transporters to go into muscle membrane to help glucose come in to be used for energy
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impact of sympathetic nervous system on substrate metabolism (insulin and glucagon)
NE/E can modify the secretion of insulin and glucagon during exercise when there is minimal change in blood glucose levels.
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resting membrane potential
RMP compares polarity of the inside of the cell with respect to outside, does not give any indication of the total amount of charges but only charge difference between inside and outside cell membrane
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resting membrane potential in live human neuron
-70mV
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equilibrium potential for K+ (Ek+) -90mV
membrane potential (voltage) at which K+ flux due to conc gradient and flux due to electrical gradient become equal and opposite
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graded potentials
changes in the membrane potential occur due to a stimulus opening (or closing) a gated ion channel -> amplitude can vary in magnitude depending on strength of stimulus
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