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1
Q

What are the precursors of steroid hormones?

A

Cholesterol

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2
Q

What is the precursor of prostaglandins?

A

arachidonic acid (C20)

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3
Q

What are the typical body stores in a 70kg adult?

A

11Kg of fat (TG)
150g glycogen
10g glucose

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4
Q

What is the energy efficiency of 1g of fat, protein and carbohydrate?

A 
fat = 38kj 
protein = 21kj 
carbohydrate = 17kj
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5
Q

How is glycerol metabolised in most tissues?

A

enters glycolysis pathway

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6
Q

How is glycerol metabolised in the liver during starvation?

A

undergoes gluconeogenesis

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7
Q

Where does beta-oxidation occur?

A

mitochondrial membrane

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8
Q

How do free fatty acids travel in the blood?

A

bound to albumin

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9
Q

What enzyme breaks down triacylglycerol?

A

lipase

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10
Q

What are the intermediates of the beta-oxidation pathway?

A

CoA thioesters

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11
Q

What is the overall process of beta-oxidation?

A

removal of 2C from fatty acid as acetyl CoA

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12
Q

What is the first step of the beta-oxidation pathway?

A

activation of long chain fatty acids

  • occurs in the cytosol via activating enzyme
  • adds CoA to the fatty acid
  • requires ATP -> AMP
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13
Q

How are fatty acids transported into the mitochondrial matrix?

A

via the carnitine shuttle

  • carnitine acyl-transferase I adds carnitine (+ removes CoA)
  • carnitine acyl-transferase II replaces carnitine with CoA in matrix
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14
Q

What are the 4 enzyme reactions of beta-oxidation in the mitochondria matrix?

A
  1. Removal of 2H
    • by acyl-CoA dehydrogenase
    • requires FAD
    • C=C formation
  2. Addition of water
    • by enoyl-CoA hydratase
    • produces 3-L-hydroxyacyl-
      CoA
  3. Removal of 2H
    • by 3-L-hydroxyacyl-CoA
      dehydrogenase
    • requires NAD+
    • produces B-ketoacyl CoA
  4. Removal of 2C
    • by b-ketoacyl-CoA thiolase
    • addition of CoASH
    • prodcues fatty acyl-CoA
      (-2C), and acetyl CoA
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15
Q

What happens to the products of beta-oxidaiton?

A

actyl-CoA enters the TCA cycle

the fatty acyl CoA undergoes the pathway again

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16
Q

What are the 3 levels of regulation of beta oxidation?

A
  1. adrenaline/glucagon activate lipase for FA activation
  2. rate of mitochondria entry regulated by carnitine shuttle
  3. regulation of rate of NADH and FADH2 reoxidation
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17
Q

What are the main tissues where beta-ox takes place?

A

heart, skeletal muscle and liver

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18
Q

What are the natural sources or carnitine?

A
  • animal and plant sources (diet)

- synthesised in the liver by lysine methylation

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19
Q

How does the beta-oxidation pathway generate ATP?

A

reoxidation of NADH and FADH2 by the electron transport chain

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20
Q

How much ATP is generated from NADH reoxidation?

A

2.5 ATP

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21
Q

How much ATP is generated from FADH2 reoxidation?

A

1.5 ATP

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22
Q

Roughly how many molecules of ATP does acetyl CoA produce in the TCA cycle?

A

10

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23
Q

What vitamin is required for beta-ox of odd-chain fatty acids?

A

cobalamin (B12)

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24
Q

How much glucose is stored in the body?

A

around 10g in plasma

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25
How much glycogen is stored in the body
around 400g
26
What is the function of glycogen in the liver?
source of blood glucose
27
What is the effect of insulin on glycogen?
encourages storage and synthesis
28
What is the effect of glucagon on glycogen?
encourages breakdown
29
How much glycogen is stored in the liver?
100-120g
30
How much glycogen is stored in muscles?
250-300g
31
What is glycogen in muscles used for?
energy for muscle contraction only
32
What substances affect glycogen in muscle?
adrenaline, calcium, AMP, ATP
33
What type of bonds are in glycogen?
a-1,4 glycosidic linkages | a-1,6 links at branches
34
What is the purpose of having branched glycogen?
More efficient as allows several enzymes to attack at once
35
What are the steps of glycogen synthesis?
1. glucose -> glucose 6-phosphate 2. glucose 6-p -> glucose 1-p 3. glucose 1-p -> UDP-glucose + PPi 4. glucose is added to glycogen chain
36
What enzyme converts glucose to glucose 6- phosphate?
Hexokinase in muscle | glucokinase in liver
37
What is the difference between hexokinase and glucokinase?
Glucokinase has a high km for glucose, so only works when glucose conc is high - prevents taking glucose from the brain in starvation
38
what enzyme adds glucose to the glycogen chain?
glycogen synthase
39
What enzyme adds branches to glycogen?
branching enzyme
40
How is glycogen synthase regulated?
inactivated by phosphorylation (kinase) | - activated by phosphatase
41
What enzyme breaks down glycogen?
glycogen phosphorylase | - debranching enzyme for branches
42
What does glycogen phosphorylase produce?
glucose 1-phosphate
43
Why can the liver break glycogen down to glucose and not muscle?
only the liver has the enzyme glucose 6-phosphatase which breaks glucose 6-p to glucose
44
How is glycogen phosphorylase regulated?
activated by kinase (phosphorylated) | inactivated by phosphatase
45
What additional control of glycogen regulation exists in the liver?
in high conc, glucose binds glycogen phosphorylase and inactivates it
46
What additional control of glycogen regulation exists in muscle?
Ca2+ from contraction binds calmodulin domain of glycogen phosphorylase -> activated AMP activates phosphorylase, ATP inhibits it
47
What is the coordinated regulation of glycogen?
Adrenaline/glucagon activate kinase -> synthetase is inactive, phosphorylase is active = glycogen breakdown Insulin activates phosphatase -> synthetase is active, phosphorylase is inactive = glycogen storage and synthesis
48
What enzyme is affected in Von Gierke's disease and the effects?
glucose 6-phosphatase - enlarged liver - hypoglycaemia - no muscle effects (lacks enzyme)
49
What enzyme is affected in Pompe's disease and its effects?
lysosomal glycosidase - muscle weakness - cardiac failure
50
What enzyme is affected in McArdle's disease, and its effects?
glycogen phosphorylase | - exercise intolerance
51
What is the fate of glucose 6-phosphate in the liver?
- free glucose released into blood - oxidation to CO2 - conversion to acetyl CoA then to fat
52
What is the fate of glucose 6-phosphate in fast muscle fibres?
anareobic glycolysis -> lactate
53
What is the fate of glucose 6-phosphate in slow muscle fibres?
glycolysis -> pyruvate -> TCA cycle
54
Where is protein stored in the body?
only in muscle
55
How much protein is required daily?
50-70g
56
What happens to excess protein intake?
it is excreted as urea
57
What are the essential amino acids?
``` valine histamine lysine threonine leucine isoleucline methinonine phenylalanine arginine tryptophan ```
58
What are the forms nitrogen is excreted as?
urea, uric acid, creatinine and ammonia (NH4+)
59
In what situations is nitrogen intake greater than excretion?
growth in childood illness or trauma recovery pregnancy
60
In what situations is nitrogen intake less than excretion?
starvation serious illness e.g. cancer injury or trauma
61
How are cellular proteins degradated?
by the ubiquitin breakdown system
62
How are exogenous proteins degraded?
by lysosomes
63
What is oxidative deamination?
removal of an amino group from an AA: | AA + H20 + coenzyme -> keto acid + ammonia + coenzyme-2H
64
What is transamination?
Transfer of an amino group to another molecule: AA 1 + keto acid 2 -> keto acid 1 + AA 2 - often first step in AA breakdown
65
What is the purpose of transamination?
production of non-essential AAs | intermediate for removing amino group from AAs
66
What is transdeamination?
When transdeamination of an AA produces glutamate | - glutamate can then be degraded to produce ammonia which enters the urea cycle -
67
What are glucogenic amino acids?
amino acids that can be converted to glucose by the liver
68
What are ketogenic amino acids?
amino acids that are degraded to acetyl CoA (fats)
69
Which amino acids are exclusively ketogenic?
lysine and leucine
70
Which amino acids are ketogenic and glucogenic?
phenylalanine and tyrosine
71
Where does degradation of proteins occur?
in liver and muscle | - but only liver can degrade amino acids to urea
72
How are amino acids transported to the liver?
- mainly glutamine from muscle | - also alanine, glutamate and aspartate
73
What is the order of the urea/ornithine cycle:
ammonia + Co2 -> carbonyl phosphate carbonyl phosphate + ornithine -> citrulline citrulline + carbonyl phosphate -> arginosuccinate arginosuccinate -> fumerate + arginine arginine -> urea + ornithine
74
why does ammonia need to be excreted?
it is neurotoxic
75
What is the concentration of circulating glucose?
3.9-6.7mM
76
What is the normal fasting glucose concentration?
4.4-4.5mM
77
What glucose concentration causes coma/death?
<2.5.>
78
What are the advantages of glucose as a fuel?
- water soluble (travels unbound) - crosses the blood brain barrier - can be oxidised anaerobically
79
What are the disadvantages of glucose as a fuel?
- relatively low ATP yield - osmotically active - high concentrations can damage cells
80
What are the sources of blood glucose?
diet glycogen gluconeogenesis
81
When does gluconeogenesis occur?
in carbohydrate deprivation
82
Can fatty acids be used for gluconeogenesis?
no
83
What sources can be used for gluconeogenesis?
lactate, glycerol, monosaccharides, glucagonic amino acids
84
What 3 steps of glycolysis need to be bypassed in gluconeogenesis?
1. glucose -> glucose 6-p - via hexokinase 2. fructose 6-p -> fructose 1,6- bisp - via phosphofructokinase 3. phosphoenolpyruvate -> pyruvate - via pyruvate kinase
85
Where do the irreversible steps of glycolysis happen?
in the cytosol
86
What enzymes are used to bypass irreversible steps in gluconeogenesis?
glucose 6-phosphatase fructose 1,6-bisphosphatase pyruvate carboxylase PEP carboacylkinase
87
What 2 levels is gluconeogenesis regulated at?
mobilisation of substrate | enzyme activation
88
What activates gluconeogenesis enzymes?
low insulin/glucagon
89
What activates pyruvate carboxylase for gluconeogenesis?
acetyl CoA
90
What is the glucose-alanine cycle?
glucose is made by gluconeogensis in the liver glucose undergoes glycolysis in muscle produces alanine and lactate alanine and lactate travel to liver and produce pyruvate pyruvate is then used in liver to undergo glucogenogenesis
91
What enzymes maintain blood glucose?
insulin, glycogen and adrenaline
92
What are the effects of insulin on the liver?
inhibits gluconeogenesis | increases glycogen, fatty acid and protein synthesis
93
What are the effects of insulin on muscle?
increases glucose uptake via GLUT4 | increases protein and glycogen synthesis
94
What are the effects of glucagon?
increases glycogen breakdown and gluconeogenesis = increases blood glucose - increases circulating fatty acids and ketone bodies increases amino acid uptake by the liver
95
what is the estimated average requirement (EAR)?
intake that will be sufficient for 50% of the population | - mid point in bell graph
96
What is the reference nutrient intake (RNI):
intake that is sufficient for the majority of the population = EAR + 2SD
97
What is the lower RNI?
intake that is inadequate for the majority of people | = EAR - 2SD
98
What is the EAR, RNI and LRNI for vitamin C?
``` EAR = 25mg RNI = 40mg LRNI = 10mg ```
99
How is BMI calculated?
weight/height^2
100
what are the categories of bmi?
``` normal = 18.5-24.9 overweight = 25-29.9 obesity grade 1 = 30-34.9 obesity grade 2 = 25-29.9 obesity grade 3 = >40 ```
101
What is the recommended daily salt intake?
6g
102
What methods can be used to measure body composition?
``` body density, body water total body potassium creatinine excretion skinfold measurements mid-arm circumference bioelectrical impedence ```
103
How much energy is derived from 1 gram of carbohydrate?
4kcal
104
How much energy is derived from 1 gram of fat?
9.2kcal
105
How much energy is derived from 1 gram of protein?
5.4kcal
106
How much energy is derived from 1 gram of alcohol?
7kcal
107
What is the metabolisable energy?
Digestible energy - energy lost in urine and sweat
108
What does energy requirements depend on?
``` metabolic rate diet induced thermogenesis physical activity temperature of environment growth, pregnancy, lactation age ```
109
What does leptin signal in appetite?
signals the state of fat stores | increases satiety via hypothalamus
110
What does insulin signal in appetite?
signals the state of carbohydrate stores | increases satiety via hypothalamus
111
What signals stimulate hunger?
NPY and ghrelin
112
What does POMC signal?
suppresses appetite
113
Where do short term signals for satiety come from?
GI, hepatic portal vein and liver
114
What are genetic causes of obesity?
leptin deficiency
115
What are endocrinological causes of obesity?
adrenal hyperactivity | hypothyroidism
116
What drug is licensed for treating obesity in the UK?
orlistat | - decreases fat absorption
117
What is the problem with treating obestiy with leptin?
obese people often have leptin resistance
118
What surgical options can treat obesity?
liposuction, intestine resection, stomach banding and stapling
119
What is the average daily intake of fat?
88g
120
What percentage of the average diet is fat?
40% of energy intake
121
What are 2 essential fatty acids?
linolenic acid and linoleic acid
122
What are essential fatty acids required for?
membrane phospholipids and eicosanoid precursors
123
What percentage of the average diet is carbohydrate?
40% of energy intake
124
What are common monosaccharides in the diet?
glucose, fructose, sorbitol, inositol
125
How much sucrose is consumed on average?
105g/day
126
What percentage of the average diet is protein?
10-15%
127
How much protein is recommended daily?
0. 75g per kg of body weight - 55g for men - 44g for women
128
How much protein do newborns require?
2.4g/kg
129
What can happen with excess protein consumption?
Renal damage and bone demineralisation
130
What are the different forms of PEM?
growth failure marasmus kwashiorkor marasmic kwashiorkor
131
What disease has no oedema and 60-80% of expected weight?
underweight
132
What disease has oedema and 60-80% of expected weight?
kwashiorkor
133
What disease has no oedema and <60% of expected body weight?
marasmus
134
What disease has oedema and <60% of expected body weight?
marasmic kwashiorkor
135
What are the features of marasmus?
``` emaciation muscle wasting, fat loss, loss of protein from organs impaired immunity and absorption diarrhoea apathy ```
136
What additional features to marasmus does kwashiorkor have?
``` oedema enlarged and fatty liver hair changes dermatitis mental retardation (possible) ```
137
What causes kwashiorkor?
usually food deficiency + infection
138
What vitamins are water soluble?
B and C
139
What vitamins are fat soluble?
A, D, E, K
140
What are differences between water and fat soluble vitamins?
water - not stored, generally not toxic | fat - stored, not easily absorbed or excreted, can be toxic in excess
141
What are the functions of B vitamins
coenzymes in metabolic pathways
142
What is vitamin B1 known as?
thiamin
143
What does thiamin/B1 deficiency result in?
Beri-Beri: - infantile, wet (oedema, cardiac) and dry (chronic, neuropathy) Werniche-Korsahoff syndrome - in alcoholics, memory loss/dememtia
144
What foods are anti-thiamin factors?
coffee and tea
145
What reaction does thiamin act on?
pyruvate -> acetyl CoA | pyryvate dehydrogenase complex
146
What is vitamin B2 known as?
riboflavin
147
What is riboflavin found in?
milk
148
What is the function of riboflavin?
FAD and FMN
149
What is B3 known as?
Niacin, nicotinic acid nicotinamide
150
What is a vitamer?
different structural forms of a vitamin
151
Why do alcoholics get vitamin B deficiencies?
empty calories from alcohol - inadequete level of vitamins and nutrients GI tract malfuncitons Cirrhosis affects storage, transport and metabolism of vitamins
152
What is the function of niacin (B3)?
NAD and NADP
153
What are the sources of niacin?
cereals, can be formed from tryptophan
154
What does deficiency of niacin (B3) result in?
Pellagra Casal's necklace (photosensitive dermatitis) diarrhoea dementia
155
What is vitamin B6 known as?
pyridoxine
156
What is the function of pyridoxine (b6)?
amino acid metabolism and haem synthesis
157
What is pyridoxine (B6) deficiency?
usually secondary | in isoniazid treatment for TB
158
What are some theraputic uses of B6 (pyridoxine)?
siezures, Down's syndrome, autism, PMS
159
What is vitamin B12 known as?
cobalamin
160
What is the function of cobalamin (b12)?
carrier of methyl groups
161
What defect does b12 deficiency cause?
pernicious anemia
162
what are the sources of b12?
animal tissues
163
How is vitamin b12/cobalmin transported?
by intrinsic factor
164
What is the function of folate (b9)?
carries 1C units | - active form = tetrahydrofolate
165
Where is folate found?
green vegetables liver, whole grains
166
What do folate and B12 do?
involved in amino acid metabolism
167
What does folate/B12 deficiencies cause?
megaloblastosis inadequate myelin synthesis neural tube defects
168
What can cause folate/B12 deficiency?
``` low intake coeliac disease Crohn's drugs/alchol lack of intrinsic factor ```
169
What is B5 known as?
pantothenic acid
170
what is the function of pantothenic acid (B5)?
component of coenzyme-A (CoASH)
171
What is B7 known as?
biotin
172
Where is biotin (B7) found?
in most food and gut flora synthesis
173
What is the function of biotin (B7)?
prosthetic group for carboxylations
174
When can biotin/B7 deficiency occur?
eating raw egg whites | long term antibiotic use
175
What is vitamin C also called?
ascorbic acid
176
What is the function of vitamin C?
antioxidant collagen formation iron absorption
177
What disease results from vitamin C deficiency?
scurvy | - impaired wound healing, haemorrhage and anemia
178
What people are likely to have vitamin C deficiency?
elderly, alcoholics, adolescents that eat junk food
179
What is the RNI for vitamin C?
40mg | - smokers is 80mg
180
What sources does vitamin A come from?
in form of retinol | - liver, fish liver oils, milk, eggs, green yellow & orange fruit and vegetables
181
What are the active forms of vitamin A?
retinoic acid - hormone retinal - vision B-carotene - antioxidant
182
What are the risks of vitamin C megadoses?
kidney stones diarrhoea systemic conditioning
183
How is potency of vitamin A expressed?
retinol equivalents | 1 RE = 1 microgram of retinol
184
What are the functions of vitamin A?
binding chromatin to control protein synthesis | conversion of light energy in retina
185
How is vitamin A transported?
From gut to liver = chylomircons | from liver to tissues = retinol bindng protein and pre-albumin
186
What happens in vitamin A deficiency?
night blindness -> xerophthalmia -> keratomalacia -> irreversible blindness
187
What happens in vitamin A toxicity?
teratogenic (in pregnancy) | dermatitis, hair loss, liver dysfunction, bone thinning
188
What are the sources of vitamin E?
vegetable oils, nuts, green vegetables
189
What type of molecules are vitamin E (and the most potent)?
tocapherols | most potent is alpha-tocepherol
190
What is the function of vitamin E?
antioxidant for PUFAs and circulating lipoproteins
191
What is vitamin E deficiency in humans?
haemolytic anaemia in premature infants
192
What are the 2 main types of vitamin D?
D3 - cholecalciferol (from UV on skin) | D2 - ergocalciferol (from plants)
193
What is the function of vitamin D?
rickets in children | osteomalacia in adults
194
What are the toxic effects of vitamin D?
hypercalcaemia, calcification of soft tissue
195
What are the sources of vitamin K?
green leafy vegetables, eggs, milk, meat , cereal, gut flora
196
Why are babies susceptible to vitamin K deficiency?
- levels in human milk are low - vitamin K doesn't cross placenta easily - neonatal gut is sterile = haemorrhage disease of the new born
197
what happens in vitamin K deficiency?
defective blood clotting | - in long term antibiotic therapy
198
What hormone stimulates fatty acid synthesis?
insulin in the fed state
199
How are fatty acids synthesised?
1. acetyl CoA + bicarbonate -> Malonyl CoA - requires biotin 2. chain is extended by fatty acid synthetase - adds 3C and removes 1 each time - requires NADPH
200
Where is TAG synthesised?
the liver
201
How is TAG synthesised?
3 fatty acids are joined to glycerol phosphate (from glycolysis) phosphate disappears
202
What is the structure of lipoproteins?
inner core of TAG and cholesterol esters | outer shell of phospholipids, cholesterol and apoproteins
203
Why are lipoproteins needed?
to transport lipids as they are not water soluble
204
What do chylomicrons transport?
dietary TAG
205
What does VLDL transport?
endogenous TAG
206
What does LDL transport?
cholesterol to tissues
207
What does HDL transport?
cholesterol to the liver
208
How is exogenous fat transported?
1. Packaged with ApoB in small intestine 2. Form chylomicrons with addition of ApoC-11 and ApoE in blood 3. lipoprotetin lipase removes free fatty acids from TAG 4. FFAs enter adipocytes and are re-esterifed to TAG 5. Remaining glycerol goes to liver and chylomicron remenant is taken up by ApoE receptors on liver
209
How is endogenous fat transported?
1. Packaged with ApoB-100 in the liver 2. Becomes VLDL in blood with apoC-II and apoE 3. lipoprotein lipase takes free fatty acids, leaving IDL 4. IDL is converted to LDL which transports cholesterol to tissues 5. cholesterol is taken up by B-100 receptors
210
Where is HDL synthesised?
in the liver and small intestine
211
What enzyme converts cholesterol to cholesterol esters?
LCAT
212
How is the number of LDL receptors regulated?
by cholesterol | - receptor mediated enodcytosis
213
What are the steps in cholesterol synthesis?
acetyl CoA + acetoacetyl CoA -> HMG-CoA | -> mevalonate -> cholesterol
214
What enzyme do statins inhibit?
HMG-CoA reducatse
215
What do LDL receptors recognise?
B-100
216
What is the purpose of LDL receptors?
to remove LDL from circulation
217
What is familial hypercholesterolaemia?
defective LDL receptors
218
How does atherosclerosis develop?
foam cell accumulation -> fatty streak formation -> plaque
219
What are foam cells?
macrophages filled with lipid
220
How do foam cells develop?
oxidised LDL is taken up by scavenger receptors on macrophages as they are not down-regulated
221
what are the essential minerals?
Na, Mg, Ca, K
222
What are the normal Na+ concentrations?
inside cell = 12mM | outside cell = 140mM
223
What are the normal K+ concentrations?
inside cell = 140mM | outside cell = 5mM
224
What is Mg2+ required for?
cofactor for ATP and enzyme complexes
225
What is cobalt used in the body for?
component of B12/cobalamin
226
What is molybdenum (Mo) used for?
cofactor for molybdopeterin
227
What does manganese overload cause?
form of parkinson's disease
228
What is the daily requirement of iron?
18mg
229
WHat is the daily requirement of copper?
2mg
230
What is the daily requirement of zinc?
15mg
231
What controls iron export?
ferroportin | - regulated by hepcidin
232
What is the distribution of iron in the body?
``` muscle - 300mg bone marrow - 300mg liver - 1000mg RBCs - 1800mg -> lost in blood loss ```
233
How is iron taken up by cells
in Fe2+ form | bu DMT1
234
How is iron stored in cells?
as Fe3+ in ferretin
235
How is iron transported?
by transferrin
236
What is HFE1?
genetic iron overload | treated by phlebotomy
237
How can iron overload be treated?
with deferoxamine | - chelating agent
238
How is zinc taken up by cells?
ZIP
239
How is zinc exported from cells?
ZNP
240
How is zinc transported?
by metallothioneins
241
What are signs of zinc deficiency?
suppressed immunity, loss of appetite, growth retardation, dermatitis, alopecia, delayed sexual maturation
242
What is acrodermatitis enteropathica?
severe skin lesions caused by zinc deficiency | - ZIP4 mutation
243
What is transient neonatal zinc deficiency
mutation in ZNT2 due to lack of zinc from mother
244
How is zinc deficiency treated?
with zinc
245
How is copper imported?
as Cu+ by crt1
246
How is copper imported to golgi?
ATP7A/B
247
What is Wilson's disease?
Copper accumulation in liver and brain - ATP7B mutation - get kayser-fleischer rings
248
What is Menkes disease?
ATP7A mutation - defective absorption of copper - no cure, 2 year life expectancy
249
How is copper overload (wilson's disease) treated?
chelation therapy - D-penicillanmire and with zinc
250
What are the main hormones that control metabolism?
insulin and glucagon
251
What stimulates insulin secretion?
increased blood glucose and amino acid concentration glucagon secretin
252
What can inhibit insulin secretion?
adrenaline
253
How is insulin secreted from pancreatic beta cells?
stimulus causes closure of K+ channels leads to opening of Ca2+ channels for influx triggers secretion
254
How insulin activated in pancreatic cells?
proinsulin is cleaved to c-peptide and insulin
255
What stimulates glucagon secretion?
low blood glucose high blood amino acid conc adrenaline
256
What are the metabolic effects of insulin?
promotes growth and fuel storage | - glycogen, TAG and protein synthesis
257
What type of receptor is the insulin receptor?
RTK
258
What is the main pathway downstream of insulin receptor activation?
activation of AKT/PKB
259
How does insulin receptor activation affect glucose?
- AKT/PKB increases GLUT4 translocation to membrane | - also inactivates glycogen synthase kinase to promote glycogen synthesis
260
How does insulin receptor activation inhibit lipolysis?
- AKT/PKB activates phosphodiesterase | - inhibits lipase to prevent TAG breakdown
261
How does insulin receptor activation affect gene expression?
SHC causes Ras -> Raf | activates MAPK cascade to activate transcription factors
262
What are the effects of glucagon on metabolism?
- maintains blood glucose in fasting - activates glycogen breakdown and gluconeogenesis - promotes FA oxidation and ketone body formation in the liver
263
What effect does adrenaline have on metabolism?
mobilises fuel during stress
264
What effect does cortisol have on metabolism?
maintains long term requirements
265
What is used as fuel in the fasting state?
1st - glycogen | 2nd - lactate, glycerol and amino acids are used in gluconeogenesis
266
How is conversion to glucose favoured in the fasting state?
pyruvate dehydrogenase is inhibited to prevent pyruvate being converted to acetyl CoA
267
What is released in ketone body formation?
acetoacelate and beta-hydroxybutyrate
268
What change happens in prolonged starvation?
ketone body formation is increased to spare protein | urea production decreases
269
What fuels do the brain and muscle use in prolonged starvation?
brain uses more ketone bodies | muscle uses fatty acids
270
How is protein breakdown reduced in prolonged starvation?
ketone bodies stimulate insulin release
271
How does type 1 diabetes occur?
autoimmune destruction of beta cells -> no insulin production
272
How is type 1 diabetes treated?
insulin administration after meals
273
what are the characteristics of type 1 diabetes?
hyperglycaemia and ketoacidosis
274
How does type 2 diabetes occur?
insulin resistance
275
What is the characteristics of type 2 diabetes?
hyperglycaemia but no ketoacidosis
276
What are the major complications of diabetes?
microangiopathy, retinopathy, nephropathy, neuropathy
277
What is metabolic syndrome?
type 2 diabetes/insulin resistance + any 2 of: - hypertension - dyslipidaemia - central obesity - microalbuminuria

FBS1 (9 decks)

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