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Metabolic Control Flashcards

1
Q

Major fuels, energy molecules & storage molecules found within the human body

A

Major fuels: Carbohydrate, Lipids & Amino Acids
Energy molecules: Glucose, Fatty acids & Amino acids
Storage molecule: Glycogen, Triglycerides & Proteins

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2
Q

Steps in the TCA Cycle

A

NOTION 1.1

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3
Q

Key features in the regulation of metabolic pathways

A
  1. Tight and separate regulation
  2. Competing metabolic pathways are often localised within
    different cellular compartments, e.g.
    - fatty oxidation in mitochondria
    - fatty acid biosynthesis in cytosol
  3. Regulated by ratio of ATP:AMP in order to sense energy status
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4
Q

What do some regulatory enzymes respond directly to?
Give an example

A

Some regulatory enzymes respond directly to sense adenine nucleotides e.g. PFK (phosphofructokinase)

Phosphofructokinase (Key enzyme in glycolysis):
• Stimulated by AMP
• Inhibited by ATP

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5
Q

What does AMP Kinase act as?

A

AMP kinase acts as a critical sensor of cellular energy
status and regulates multiple pathways in the cell.

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6
Q

Structure of AMP Kinase

A

Different modules:
- Catalytic module
- Carbohydrate binding molecule
- Nucleotide binding molecule

Different subunits:
- Alpha subunit
- Beta subunit
- Gamma subunit

NOTION 1.2

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7
Q

Role of AMPK in regulating ATP metabolism

A

AMPK regulates anabolic and catabolic pathways by phosphorylating key enzymes:

NOTION 1.3/ 1.4

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8
Q

Use of energy in the:
1. Liver
2. Skeletal muscle
3. Adipose Tissue
4. Brain
5. Endocrine tissues
6. Kidneys
7. Blood

A
  1. Liver
    • Central processing and distribution role
    • Provides all other organs with an appropriate mix of
    nutrients via the bloodstream
  2. Skeletal muscle
    • Directed motion
  3. Adipose tissue
    • Nutrient storage (lipid and glucose) and regulated release
    • Endocrine factors
  4. Brain
    • Pumps ions to generate electrical signals
  5. Endocrine tissues (eg pancreas)
    • Energy to synthesise hormones and control regulated release
  6. Kidneys
    • Controlled filtration/pumping of metabolites
  7. Blood
    • Distribution of nutrients
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9
Q

Entry and exit of blood from the liver

A

The liver receives 20-30% highly oxygenated blood from
the hepatic artery, 70-80% blood from the portal vein.

All blood leaves the liver via the hepatic vein.

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10
Q

Benefit of the position of the liver

A

The position of the liver in the circulation gives it first access
to nutrients from the gut.

Similarly the liver can supplement the circulation with nutrients not provided from the digestive tract (glucose, fatty acids, amino acids).

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11
Q

Levels of supply by the following glucose transporters:
- Glut-1
- Glut-2
- Glut-3
- Glut-4
What tissues display these transporters?
What is the Km value?

A

Glut-1:
- Continuous supply regardless of plasma levels
- Found in erythrocytes, and the brain
- Km = 1-2mM

Glut-2:
- “Glucose sensing”. Increased uptake as plasma glucose rises
- Found in liver, kidneys, pancreatic Beta cells
- Km = 7-20mM

Glut-3:
- Continuous supply regardless of plasma levels
- Found in the brain
- Km = 1.6mM

Glut-4:
- Insulin sensitive = selective uptake stimulated by insulin
- Found in muscle, and adipose tissue
- Km = 5mM

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12
Q

What is the effect of the high Km value of Glut-2?

A

Low affinity allows glucose sensing. Thus glucose concentration in the hepatocyte equilibrates with the plasma and reflects that in the blood.

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13
Q

Glucokinase vs Hexokinase

A

Glucokinase (liver) vs Hexokinase (muscle):
- Both phosphorylate glucose to generate Glucose 6-P
- Glucokinase has a much higher Km than hexokinase
- Unlike hexokinase it is not inhibited by the product (Glucose-6-Phosphate)
- Glucokinase also has a much higher Vmax = higher capacity

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14
Q

Pathways of glucose-6-phosphate within the cell

A
  1. Conversion to glycogen (glucose storage)
  2. Dephosphorylation to glucose (systemic energy supply)
  3. Pyruvate generation by glycolysis (multiple fates)
    - Acetyl CoA generation for fatty acid synthesis (liver and systemic fuel and lipid storage)
    - TCA cycle for energy production
    - Lactate production (energy)
  4. Pentose phosphate pathway to generate NADPH and
    substrates for nucleic acid, nucleotide and amino acid synthesis

NOTION 1.5/ 1.6/ 1.7

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15
Q

The liver acts as a “sink” for glucose. What does this mean?

A

Liver effectively acts as a “sink” for glucose: The liver takes up glucose from blood and stores it after meal and releases it as required. The critical role of the liver is to generate substrates required by other tissue or store the molecules it can use to do so later.

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16
Q

Energy source for the liver

A

Most of energy required by the liver comes from fatty acid (FA) and amino acid breakdown.

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17
Q

When is insulin vs glucagon secreted?

A

Insulin – secreted in fed state
Glucagon – secreted in fasted state
Secreted by islets of Langerhans in the pancreas.

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18
Q

Sections of the pancreas
How many islet cells are there in a pancreas?

A

Pancreas has both endocrine and exocrine cells.
About 1 million islets in healthy pancreas.

NOTION 1.8

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19
Q

Graph displaying insulin release vs glucose concentration

A

NOTION 1.9

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20
Q

The effect of high plasma glucose on pancreatic beta cells

A
  • Glut-2 transports glucose into cell
  • Glucose is metabolised rapidly
  • ATP levels increase rapidly
  • The ATP is sensed by K_ATP channels
  • The K_ATP channels then close
  • The cell depolarises
  • The calcium channels then open
  • Insulin is signalled for release

NOTION 1.10

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21
Q

Regulation of carbohydrate metabolism in the liver

A
  1. In fed state high blood glucose stimulates insulin secretion
  2. Insulin stimulates Glc 6-P to glycogen via activation of glycogen synthase and also inhibits the breakdown of glycogen
  3. When blood glucose levels drop glucagon is released
  4. Glucagon stimulates glycogen breakdown to generate
    Glc 1-P which is converted to Glc 6-P
  5. Glucose 6 phosphatase can convert Glc 6-P to glucose which is released back into blood as required
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22
Q

Diagram displaying effect of insulin and glucagon on glucose-6-phosphate pathways in the liver

A

NOTION 1.11

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23
Q

What are normal levels of glucose?
Why is it essential to maintain glucose homeostasis?
Effects of low vs high plasma glucose

A

Glucose homeostasis is a process whereby plasma glucose levels are maintained within very narrow range (4-5 mM). Essential to keep glucose available as the major fuel source for the brain.

Low plasma glucose:
- < 4 mM (hypoglycaemia)
- Sweating, hunger, dizziness, fainting, irritability

High plasma glucose:
- > 7 mM fasting levels (diabetes)
- Headache, thirst, excessive urination, blurred vision

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24
Q

What is glucose homeostasis achieved through?

A

Achieved through:
1. Balance between uptake from blood into tissues (storage) and release from tissues into blood
2. Preferred utilisation of other fuels e.g. fatty acids (FAs) by
muscle

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25
Summary of the effects of hormones on glucose homeostasis: - Effects of insulin - Effects of glucagon - Other hormones involved
1. Minute by minute adjustment maintains blood glucose at around 4.5 - 5 mM 2. Involves combined actions of insulin and glucagon 3. Insulin – secreted when blood glucose is high and stimulate glucose uptake and storage as glycogen production and triacylglycerol synthesis (TG or fat) 4. Glucagon is secreted when blood glucose levels are low - Tissues respond by glycogen breakdown to generate glucose - Increased gluconeogenesis by the liver - Increase fat oxidation to reduce the use of glucose 5. Counter-regulatory mechanism: glucagon, adrenaline, noradrenaline, cortisol, and growth hormone to protect against hypoglycemia
26
Where does the liver take up amino acids from?
Liver takes up amino acids (via transporter) from the hepatic portal vein. Some amino acids arrive intermittently from other tissues following tissue protein breakdown.
27
How much of the livers energy requirement is provided by amino acids?
Amino acid catabolism provides about 50% of liver’s energy requirement
28
What are amino acids substrates for?
Amino acids are substrates for synthesis of glucose, fatty acids and ketone bodies.
29
Liver amino acid metabolism
NOTION 2.1/ 2.2
30
Glucogenic vs ketogenic amino acids
NOTION 2.3
31
Where does the liver take fatty acids from?
Liver takes up (via transporter) non-esterified fatty acids (NEFAs) from plasma.
32
What are the 2 major fates of fatty acids in the liver?
There are two major fates: 1. Oxidation - Energy source for liver - Production of ketone bodies 2. Triacylglycerol formation - Local store for liver energy needs - Distributed to other tissues as VLDL
33
Liver Lipid Metabolism
NOTION 2.4
34
How does insulin & glucagon regulate lipid metabolism in the liver?
NOTION 2.5
35
How does AMP kinase regulate lipid metabolism in the liver?
NOTION 2.6
36
Summary of the regulation of fat metabolism in the liver by insulin and glucagon
Fed state – insulin is elevated and stimulates Acetyl CoA carboxylase (ACC) to covert acetyl CoA to malonyl CoA – high levels of malonyl CoA inhibits CPT-1 – fatty acids accumulate and are esterified to TGs (cytosol) Fasting state - glucagon elevated - stimulates CPT-1 expression increasing FA transport to mitochondria - FA oxidation is favoured
37
White vs brown adipocytes
White adipocytes are very large (up to 100um) and contain a single lipid droplet. Other organelles, eg nucleus, mitochondria and secretory vesicles are constrained in a very thin cytoplasmic layer. In brown adipose cells, multiple fat droplets are present along with abundant mitochondria to permit high levels of lipid oxidation linked to thermogenesis. NOTION 2.7
38
What happens to glucose in adipocytes, during the fed state?
In fed state: Glucose converted via pyruvate and acetyl-CoA into fatty acids which are stored as droplets of triacylglycerol (TG)
39
In humans, where do most fatty acids get synthesised?
In humans most FA synthesis occurs in the liver. Adipocytes store FAs arriving from liver which are delivered as very low density lipoproteins (VLDL) and directly from intestine.
40
Adipose tissue lipid metabolism
NOTION 2.8
41
What is adipose tissue location and (dys)function central to?
Adipose tissue location and (dys)function is central to the development of metabolic disease in obesity. By exceeding the storage capacity of fat tissue, this can lead to: - Lipotoxicity - Hepatic steatosis - Insulin resistance - Beta-cell dysfunction - Cardiovascular disease - Reduce lipid oxidation NOTION 2.9
42
How are triglycerides synthesised in adipocytes?
NOTION 2.10
43
What happens to triglycerides in adipocytes, during a fasting state?
In fasting state – Triglycerides (TGs) are hydrolysed by lipases to release free FAs, which are delivered in bloodstream to skeletal muscle and heart.
44
What is the release of TGs as FAs by the adipocytes regulated by?
Regulated by: - Adrenaline, which stimulates activity of TG lipase (fasting state) - Insulin, which inhibits the activity of TG lipase (fed state)
45
Break down of triglycerides in the adipocytes
NOTION 2.11
46
Structure of a muscle fibre
NOTION 2.12
47
Insulin stimulated glucose uptake in the skeletal muscle
NOTION 2.13
48
Muscle carbohydrate storage
NOTION 2.14
49
What are mutations in glycogenin associated with?
Mutations in glycogenin are associated with glycogen storage disease type IV (Andersen’s disease).
50
Effect of Akt2 phosphorylation on glycogen synthase
NOTION 2.15
51
Effect of AMPK on recycling of the GLUT4 transporter
NOTION 2.16
52
Summary of effect of Insulin & AMPK on GLUT4 translocation
- Insulin via Akt signalling increases GLUT4 translocation - AMPK inhibits GLUT4 recycling away from the membrane - Both increase glucose uptake but by different mechanisms
53
What are the primary fuels of resting muscle?
In resting muscle primary fuels are: - free fatty acids from adipose tissue - ketones from liver - oxidised via acetyl-CoA to produce ATP and CO2 NOTION 2.17
54
Muscle energy metabolism during intense exercise
NOTION 2.18
55
Summary of fuel metabolism in skeletal muscle, during moderate vs intense exercise
Moderate exercise – utilises FAs and ketone bodies (also some glucose) Maximally active muscle: – glycogen breakdown is stimulated by adrenaline – no Glc 6Pase so Glc 6-P is channelled to energy production – Glc 6-P is broken down to lactate (2 ATP) – involves glycolysis and lactate dehydrogenase (LDH)
56
What is the role of creatine during intense exercise?
Acts as a buffer store of ATP: - during heavy activity phosphocreatine is converted to creatine and ATP - during recovery period the reverse reaction generates phosphocreatine
57
What is involved in the cori cycle?
NOTION 2.19
58
Fuel metabolism in the Brain
1. Normally uses only glucose as fuel 2. Very active respiratory metabolism – accounts for 20% of total O2 consumption at rest. 3. ATP generated is required to create and maintain an electrical potential across plasma membrane of neurons 4. Cannot use free FAs – but can metabolise Beta- hydroxybutyrate (a ketone body) – important during prolonged fasting or starvation.
59
Summary of fuels, products & storage in the liver, adipose tissue, skeletal muscle & the brain
NOTION 3.1
60
What amount of fuel is stored in the following forms: - Free glucose - Glycogen - Protein - Triglyceride Therefore, how much energy does this amount to? How many days can it supply?
NOTION 3.2
61
How many kcal/g can be found in lard, sugar and glycogen?
Lard = 9kcal / g Sugar = 4kcal / g Glycogen = 1kcal / g
62
What is involved in the early phases of starvation?
1. Glucose enters blood from breakdown of liver glycogen and from hepatic gluconeogenesis 2. Fatty acids are released from adipose tissue - lack of inhibition of hormone sensitive lipase by insulin - FAs taken up by liver and oxidised to acetyl CoA - acetyl CoA enters TCA cycle and ATP formed drives gluconeogenesis - as acetyl CoA accumulates ketone bodies are formed 3. Muscle utilises FAs (insulin low) 4. Net breakdown of protein in muscle (insulin low) - alanine taken up liver to form glucose - amino acids are major fuel for gluconeogenesis
63
What is involved in glycogenolysis?
NOTION 3.3
64
What is involved in adapted phase of starvation?
1. From about 3 weeks onwards – steady state 2. Up to now, depletion of body’s protein mass and fat stores 3. Loss of protein is then minimised (inefficient and life threatening) – 1.75 g protein provides 1g glucose – if no adaptation then could lose 150g protein per day. 4. Ketone bodies (from FA breakdown) reach about 6-8 mM in blood – provide 75% of fuel for brain –lactate cycling provides some glucose
65
What are ketone bodies?
• Ketone bodies can be oxidized in the mitochondria to yield 2 GTP and 22 ATP. • Ketone bodies are transported from the liver to other tissues reconverted to acetyl-CoA. • Ketone bodies cannot be used as fuel by the liver, because the liver lacks the enzyme β-ketoacyl-CoA transferase
66
Formation of ketone bodies
NOTION 3.4
67
Conversion of ketone bodies to Acetyl-CoA
NOTION 3.5
68
Role of the liver in response to prolonged starvation
NOTION 3.6
69
Role of adipose tissue in response to prolonged starvation
NOTION 3.7
70
Role of skeletal muscle in response to prolonged starvation
NOTION 3.8
71
Irish Republican hunger strikes
Irish Republican hunger strikers (1981) Survival 46-73 days Length of survival a result of starting body fat mass
72
Why does death usually occur due to starvation?
Eventually when fat stores are exhausted, a final phase of protein breakdown leads to death from respiratory failure.
73
Blood glucose concentration is held in a narrow range by insulin. What range of [blood glucose] is maintained?
3.5 - 7.0 mmol/l
74
WHO Classification of Diabetes Mellitus
Fasting glucose > 7 mmol/l 2-hour glucose > 11.1 mmol/l
75
Where does the term “diabetes mellitus” come from?
• Term diabetes introduced by Greek means “to siphon” referring to excessive urination • Mellitus from Latin word meaning “sweet like honey”
76
What is diabetes mellitus?
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
77
What is diabetes insipidus caused by?
Diabetes Insipidus is caused by defect in vasopressin the antidiuretic hormone that also controls levels of salt.
78
Classification of Diabetes Mellitus
- Type 1 - Type 2 - Gestational Diabetes Mellitus
79
What is T1D primarily due to? What is a typical presentation?
Primarily due to pancreatic islet ß-cell destruction Associated with ketoacidosis and islet cell antibodies. Type 1 Diabetes: Typical Presentation • Under 25 Years • Lean • Weight Loss • Ketonuria
80
Metabolic consequences of insulin deficiency
1. Hyperglycaemia resulting from: a.) decreased glucose uptake into tissues b.) decreased utilisation of glucose c.) increased hepatic glucose output 2. Polyuria, polydipsia, weight loss: a.) above ~6 mM glucose is excreted in urine b.) urine volume increases causing dehydration and thirst c.) glycosuria – calorie loss leading to weight loss 3. Antilipolytic effect of insulin is lost – plasma fatty acids increase 4. Circulating ketone bodies increase 5. Severe metabolic acidosis – coma and death
81
Ketone bodies & diabetes
• Normal Metabolites Of Fat • Energy Source When Fasting • Excess Production If No Insulin • Impaired Use If No Insulin • Leads To Diabetic Ketoacidosis
82
Symptoms & Diagnosis of T1DM
Symptoms: Lethargy, Thirst, Excessive Urination, Weight loss Diagnosis: Simple blood glucose test
83
Treatment of T1D: Discovery of Insulin
1889: Minkowski and von Mering • removed the pancreas from a dog 1921: Banting, Best and Macleod • Made an extract of the pancreas and injected into diabetic dogs
84
Sections of the pancreas
NOTION 3.9
85
Therapy for T1D
Fast –acting and long-acting insulin (analogues) Insulin pumps Artificial pancreas (closed loop) Islet transplantation: - Direct transplantation - Stem cells for regeneration of Beta-cells
86
Prevelance of T2D
Most prevalent form of diabetes (90%)
87
Who is primarily affected by T2D?
Affects people primarily after age 40, many of whom are overweight.
88
What causes T2D?
Results from insulin resistance and an insulin secretory (Beta cell) defect.
89
Evolution of T2DM
NOTION 3.10
90
Treatment of T2D
1. Diet & Exercise 2. Anti-hypertensive drugs 3. Insulin 4. Stimulation of insulin secretion - Sulphonylureas 5. Lipid lowering drugs 6. Stimulation of insulin action - Metformin - Thiazolidinediones
91
Statistics of T2D/ Obesity
NOTION 3.11
92
What is BMI?
- BMI – Body Mass Index - The most practical measure of body composition - Used most widely to ‘estimate’ the prevalence of obesity
93
BMI values
< 20 = underweight 20 – 25 = normal weight 25 – 30 = overweight > 30 = obese
94
BMI equation
BMI = Weight (kg)/ Height^2 (m)
95
Limitations of BMI
- Does not take into consideration ethnic differences in body composition - Does not take into account muscle mass
96
Syndromes featuring lipodystrophy
NOTION 3.12
97
Physiological control of food intake
NOTION 3.13
98
What was the prescription given for diabetes, in the olden days?
Prescription includes bones, wheat grains, fresh grits, green lead earth and water. “Let stand moist, strain it, take it for four days”.
99
What are macrophages?
Macrophages = WBC that digests anything that does not have, on its surface, proteins that are specific to healthy body cells, including cancer cells, microbes, cellular debris, and foreign substances. This process is called phagocytosis.
100
With regard to neutrophils, basophils, eosinophils, monocytes, macrophages and erythrocytes: - What is their Histology like? - What is their diameter? - How many nuclear lobes do they contain? - Do they contain granules? - What is their mode of action?
NOTION 4.1
101
What is the function of a phagocytic cell?
Clearance of microbes, apoptotic cells and foreign particles
102
What are the 3 different types of macrophages?
Macrophage polarisation: - M0 Macrophage (naïve) - M1 Macrophage (“Fight” mode) - M2 Macrophage (“Heal” mode)
103
When are M1 macrophages activated?
They are classically activated. They are pro-inflammatory and microbicidal.
104
When are M2 Macrophages activated?
They are alternatively activated. They are anti-inflammatory and involved in tissue repair.
105
What are the “SHIP” functions?
Sample: Monitor using chemical signals Heal: Most signals are benign: remove from tissue (M2) Inhibit: Chemicals to kill pathogens (switch to M1) Present: Antigen to other immune cells
106
What are some characteristics of M0 macrophages metabolism?
M0 macrophages metabolism: - Low catabolic and anabolic activities - Low glucose flow through glycolysis, PPP and TCA - Mitochondrial oxidative phosphorylation (OXPHOS) is the predominant source of ATP (36 ATP/ glucose) NOTION 4.2
107
What are some characteristics of M2 macrophage metabolism?
M2 macrophage metabolism: - Glycolytic and PPP activity is decreased - TCA is intact and mitochondrial oxidative phosphorylation (OXPHOS) is the predominant source of ATP (36 ATP/ glucose) - Increased Beta - oxidation - Increased glutamine metabolism NOTION 4.3
108
What can fructose-6-phosphate be converted to?
It can be converted to Fructose-1,6-bisphosphate by phosphofructokinase. This reaction is irreversible, and to convert Fructose-1,6-bisphosphate back to Fructose-6-phosphate, another enzyme is required, Fructose-1,6-bisphosphatase. In addition, fructose-6-phosphate can be converted to fructose-2,6-bisphosphate, by phosphofructokinase-2. This reaction is irreversible, and to convert fructose-2,6-bisphosphate back to fructose-6-phosphate, another enzyme is required, Fructose-2,6-bisphosphatase. NOTION 4.4/4.5
109
What is the effect of fructose-2,6-bisphosphate on phosphofructokinase, and fructose-1,6-bisphosphatase?
NOTION 4.6
110
How is the TCA cycle fuelled in M2 macrophages, with low levels of glycolysis?
Either beta-oxidation, or glutamine metabolism NOTION 4.7/ 4.8
111
Arginine metabolism in M2 macrophages vs M1 macrophages
NOTION 4.9
112
What are some characteristics of M1 macrophage metabolism?
- Increased glucose uptake - Glycolysis as main ATP source (2 ATPper glucose) - Activation PPP and fatty acid synthesis - TCA broken at 2 points; no OXPHO - Arginine is metabolised by inducible nitric oxide synthase NOTION 4.10
113
What is involved in PPP in M1 metabolism?
By forming NADPH via the PPP, this can trigger the formation of superoxide radicals, using NADPH oxidase. NOTION 4.11
114
TCA Cycle in M1 metabolism What is the effect of itaconate? What about succinate?
Strong upregulation of IRG1 • Production of itaconate • Inhibition succinate dehydrogenase • Accumulation succinate Itaconate: affect bacterial metabolism Succinate: drives production of IL-1β cytokine (fuels inflammation) NOTION 4.12/ 4.13

Energy For Life (BI25M7) (4 decks)

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