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Biochemistry 2300 > Lectures 29/30: Integration of Metabolism > Flashcards

Lectures 29/30: Integration of Metabolism Flashcards

1
Q

Location of pyruvate transporter

A

Mitochondrial membrane

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2
Q

Location of cartinite/acyl carnitine transporter

A

Mitochondrial membrane

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3
Q

Location of citrate transporter

A

Mitochondrial membrane

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4
Q

Location of aspartate transporter

A

Mitochondrial membrane

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5
Q

Location of malate transporter

A

Mitochondrial membrane

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6
Q

Location of adenine nucleotide translocase

A

Mitochondrial membrane

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7
Q

Location of P-H symport proteins

A

Mitochondrial membrane

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8
Q

Location of citrulline transporter

A

Mitochondrial membrane

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9
Q

Location of ornithine transporter

A

Mitochondrial membrane

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10
Q

Location of citric acid cycle

A

Mitochondrial matrix

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11
Q

Location of oxidative phosphorylation

A

Mitochondrial matrix

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12
Q

Location of beta-oxidation

A

Mitochondrial matrix

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13
Q

Location of ketogenesis

A

Mitochondrial matrix

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14
Q

Location of amino acid synthesis and degradation

A

Mitochondrial matrix and cytosol

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15
Q

Location of urea cycle

A

Mitochondrial matrix and cytosol

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16
Q

Location of glycolysis

A

Cytosol

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17
Q

Location of gluconeogenesis

A

Cytosol

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18
Q

Location of pentose phosphate pathway

A

Cytosol

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19
Q

Location of fatty acid synthesis

A

Cytosol

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20
Q

Location of nucleotide synthesis

A

Cytosol

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21
Q

Metabolic control through compartmentation

A

Transport can control the activity of pathways
Transport is not always direct: converted
In general: synthetic pathways are cytosolic and oxidative pathways are in mitochondria (glycolysis and gluconeogenesis are exceptions as they share enzymes and are both mostly cytosolic)

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22
Q

Mitochondrial steps of gluconeogenesis

A

Pyruvate converted into oxaloacetate by pyruvate carboxylase: occurs in mitochondria
Oxaloacetate must leave mitochondria: indirectly transported into cytosol as malate using the malate transporter to enter glyconeogenesis

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23
Q

Malate transporter

A

Transports oxaloacetate in form of malate from mitochondrial matrix to cytosol, where it is oxidized to oxaloacetate

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24
Q

Malate dehydrogenase

A

Converts oxaloacetate to malate to be transported via malate transporter to cytosol to be used in gluconeogenesis

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25
Q

Alcohol intoxication and hypoglycemia

A

Ethanol is metabolized in cytosol to acetyl-CoA, generating NADH
Malate dehyrodgenase reaction is prevented from proceeding from matte and NAD+ to oxaloacetate and NADH: inhibition of gluconeogenesis in the liver
When this occurs in fasting period, blood glucose levels can drop leading to hypoglycaemia and unconsciousness

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26
Q

Maintenance of cellular homeostasis

A
  1. Regulation of energy levels in the cell (ATP, AMP)
  2. Regulation to avoid build-up or scarcity of metabolites: regulation through allosteric effectors and substrate availability
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27
Q

Maintenance of homeostasis in whole organism

A

Coordination of metabolism in different cell types/different tissues regarding energy and metabolite levels
Regulation through hormone signalling leading to changes in enzyme activity through covalent modification and changes in expression
1. Each tissue must recieve suffice energy in a form it can use
2. Build up of metabolites in body must be prevented
3. Xenobiotics must be degraded

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28
Q

Fatty acids

A

Highest caloric value per carbon
Most abundant stored energy in human body (triacylglycerol)
Last longest during fasting periods
No fatty acid oxidation in absence of oxygen or mitochondria
No fatty acid oxidation i brain
Cannot be converted to glucose

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29
Q

Glucose

A 
Used by all tissues
Limited storage in form of glycogen
Can generate ATP even when oxygen is low
Precursor for all other metabolites
Also needed in pentose phosphate pathway
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30
Q

Amino acids

A

Glycogenic amino acids are nearly as versatile as glucose

Most amino acid storage is in muscle protein, not beneficial to break this down

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31
Q

Metabolic goal of fed state

A

Remove glucose form blood

Store energy for later

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32
Q

Metabolic goal of post-absorptive state

A

Provide glucose to the tissues that need glucose

Provide energy to other issues, maintain glucose levels in blood

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33
Q

Metabolic goal of fasting

A

Provide glucose to the tissues that need glucose
Provide energy to other issues, maintain glucose levels in blood
Reduce glucose requirements as much as possible

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34
Q

Metabolic goal of exercise

A

Provide energy to muscle

Increase oxygen supply to muscle

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35
Q

Metabolites secreted by adipose tissue

A

Fatty acids and glycerol

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36
Q

Metabolites secreted by muscle

A

Lactate and amino acids

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37
Q

Metabolites secreted by liver

A

Glucose, ketone bodies, lipoproteins

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38
Q

Metabolites secreted by brain

A

None

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39
Q

Brain

A 
Virtually no energy storage
No fatty acid oxidation
Glucose is obligatory fuel
No secretion of energy metabolites
Ketone bodies used when present
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40
Q

Heart

A

Virtually no energy storage
Fatty acids or glucose used
No secretion of energy metabolites
Ketone bodies used when present

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41
Q

Ketone bodies as fuel

A

Ketone bodies only cover 70% of what brain needs, brain will still need glucose

42
Q

Adipose tissue in fed state

A

Uptake of glucose and fatty acids
Synthesis of TG
Removal of blood glucose after a meal
Storage of energy for later

43
Q

Adipose tissue in fasted state

A

Lipolysis of TG
Secretion of fatty acids and glycerol
Provision of energy during fasting

44
Q

Skeletal muscle in fed state

A

Glucose uptake, storage as glycogen

Amino acid uptake for protein synthesis

45
Q

Skeletal muscle in fasting/starvation

A

Protein breakdown
Amino acids (as alanine) to liver
At rest: fatty acid oxidation
Ketone bodies used if present

46
Q

Skeletal muscle in active sate

A

Glycogenolysis
Anaerobic glycolysis
Secretion of lactate
Fatty acid oxidation if sufficient oxygen

47
Q

Kidney

A

Some gluconeogenesis
Glutamine breakdown and excretion of ammonium
Excretion (NOT production) of urea

48
Q

Liver in fed state

A

Glycogen synthesis and storage, but glucose uptake is not unregulated
Glycolysis
Fatty acid synthesis from excess acetyl-CoA
Triacylglycerol synthesis and secretion as VLDL

49
Q

Liver in fasted state

A

Glycogenolysis
Secretion of glucose
Gluconeogenesis
Ketogenesis (when fasting is prolonged
VLDL secretion to provide triacylglycerols/fatty acids and cholesterol to heart and skeletal muscle
Urea cycle (also active when lost of amino acids are degraded)

50
Q

Liver failure

A

Can lead to hypoglycaemia during fasting due to insufficient gluconeogenesis and increased ammonium levels

51
Q

Cori cycle

A

Transport of lactate from muscle to liver where it is converted to pyruvate and then glucose and released

52
Q

Glucose-alanine cycle

A

Pyruvate is produced by muscle glycolysis
Pyruvate is transaminate to make alanine
Alanine is transported from muscle to the liver where ammonium is released to urea cycle and pyruvate is used to make glucose

53
Q

Hormones

A

Convey short and long-range signals
Can be polypeptides, amino acid derivatives, steroids
Signalling through specific receptors: maintenance of homeostasis, integration across organism
Response to external stimuli
Follow cyclic programs: sleep/wake, menstrual
Signalling: bind receptor, mediate response, terminate signal

54
Q

Signal transduction

A

Ligand binds receptor
Intracellular signal propagation: activation of enzymes, formation of second messengers, secondary activation enzymes, protein translocation
Causes: cytoskeleton rearrangement, enzyme modification, gene expression changes

55
Q

Ionotropic receptors

A

Ion channels

Neurotransmitters

56
Q

G-protein coupled receptors

A

Over 800
Catecholamines
Glucagon
Vision, taste, smell

57
Q

Cytokine receptors

A

Cytokines: inflammatory molecules

58
Q

Receptor tyrosine kinases

A

Insulin

Growth factors

59
Q

Nuclear hormone receptors

A

Membrane-permeable ligands
Steroids
Thyroid hormones
Vitamins A, D

60
Q

Insulin

A

Reduces blood glucose and builds energy stores (anabolic)
Polypeptide hormone made in pancreatic beta cells: secretion trigged by metabolism of glucose and ATP production because of glucose oxidation
Upregulation of glucose uptake in muscle and adipose
Increased glycolysis
Increased fatty acid uptake into adipose
Increased glycogen synthesis, fatty acid synthesis and protein synthesis

61
Q

Glucagon

A

Increases blood glucose and mobilizes energy stores (catabolic)
Polypeptide made in pancreatic alpha cells
Increased gluconeogenesis in liver
Increased glycogenolysis, lipolysis, fatty acid oxidation, proteolysis
Does not act on muscle cells

62
Q

Catecholamines

A

Mobilize energy for muscle activity “Fight or flight” response
Amino acid derivatives
Increased gluconeogenesis in liver
Increased glycogenolysis, lipolysis, fatty acid oxidation and proteolysis

63
Q

Pancreatic islets

A

Produce insulin and glucagon

Pancreas in an endocrine organ and an exocrine organ

64
Q

Regulation of insulin and glucagon secretion

A

Insulin levels rise quickly after a meal and glucagon levels decrease quickly after a meal
Glucose stimulates insulin secretion
Glucose and insulin inhibit glucagon secretion

65
Q

Beta cells

A

Produce insulin
Pancreas
Contain glucokinase (also in liver): isoform of hexokinase

66
Q

Glucokinase

A

In liver and beta cells of pancreas
Isoform of hexokinase
Acts as glucose sensor: activity is dependent on glucose concentration over a wide range
Does not react with other monosaccharides ie. fructose does not cause insulin secretion

67
Q

Insulin action on muscle

A

Promote glucose transport into cells
Stimulates glycogen synthesis
Suppresses glycogen breakdown

68
Q

Insulin action on adipose tissue

A

Activates extracellular lipoprotein lipase
Increases level of acetyl-CoA carboxylase
Stimulates triacylglycerol synthesis
Suppresses lipolysis

69
Q

Insulin action on liver

A

Promotes glycogen synthesis
Promotes triacylglycerol synthesis
Suppressed gluconeogenesis

70
Q

GLUT transporters

A

Takes up glucose

71
Q

GLUT4

A

Only GLUT transporter unregulated by insulin
In muscle and adipose
Expression and localization regulated by insulin: causes translocation into membrane
Other isoforms are present in liver, pancreatic cells, brain, but are not regulated by insulin

72
Q

Lipoprotein lipase

A

Activated by insulin causing increased uptake of fatty acids
Storage of dietary or liver-derived fat in adipocytes by hydrolysis of TG into lipoproteins and uptake of fatty acids for resynthesis to TG
Fatty acids are activated wth CoA to be esterified with glycerol-3-phoshate

73
Q

Glycogen synthase

A

Glycogen synthesis pathway
Upregulated by insulin
Down regulated by glucagon

74
Q

Acetyl-CoA carboxylase

A

Fatty acid synthesis pathway
Upregulated by insulin
Down regulated by glucagon
Inactive by phosphorylation

75
Q

HMG-CoA reductaste

A

Glycogenolysis pathway
Down regulated by insulin
Upregulated by glucagon
Inactive by phosphorylation

76
Q

Hormone sensitive lipase

A

Adipocyte lipolysis pathway
Down regulated by insulin
Upregulated by glucagon
Activated by phosphorylation

77
Q

Phosphofructokinase 2

A

Glycolysis pathway
Upregulated by insulin and down regulated by glucagon
Inactive by phosphorylation

78
Q

Insulin receptor

A

Receptor tyrosine kinase

Insulin signalling activates several phosphatases

79
Q

Glucagon receptor

A

GPCR

  1. Binding
  2. Activation of receptor
  3. Activation of G protein
  4. Activation of adenylate cyclase
  5. Production of cAMP
  6. Activation of PKA
  7. Downstream activation of other protein kinases
80
Q

Glycogen phosphorylase

A

Activated by phosphorylation by phosphorylase kinase: promoted by glucagon and EN signalling
Deactivated by phosphoprotein kinase, which is promoted by insulin

81
Q

Kinases

A

Inhibited by insulin

82
Q

Phosphatases

A

Activated by insulin

83
Q

Type 1 Diabetes

A

Destruction of beta cells: total loss of insulin production
Beta cell destruction is often autoimmune response
Treatment by giving insulin
Untreated Type 1: ketoacidosis can develop

84
Q

Type 2 Diabetes

A

Insulin signalling is less sensitive than normal, causing insulin resistance
Insulin levels are normal or even increased
Strongly linked to obesity
Can be treated with some oral drugs that increase insulin sensitivity and lifestyle changes
AMPK activators promote insulin sensitivity

85
Q

Longterm effects of hyperglycaemia

A

Nerve and kidney damage
Risk of cataract formation
Possible mechanisms: glucose can react with proteins, protein modification impairs function
Glucose converted to sorbitol when glucose concentrations are very high: increases osmotic pressure

86
Q

Lipid metabolism with diabetes

A

Increased circulating triacylglycerol levels: lipoprotein lipase is not activated
Increased fatty acid levels linked to cardiovascular disease

87
Q

Obesity

A

Caused by long-term positive energy balance
Caused by inheritance and lifestyle
Genetics, environment, epigenetics/microbiome

88
Q

Genetics and obesity

A 
Leptin
Leptin receptor
Melanocortin receptor
Neuropeptide Y receptor
Uncoupling protein
Susceptibility genes
89
Q

Environment and obesity

A

Availability of food
High-calorie food
Larger portion size
Lack of physical activity

90
Q

Epigenetics and obesity

A

Micro biome and perinatal influences

91
Q

Leptin

A

Hormone secreted from adipose tissue to regulate long-term energy storage
Signals satiety
Deficiency or impaired signalling can cause obesity: human obesity is often associated with leptin resistance

92
Q

Adiponectin

A

Hormone secreted from adipose tissue to regulate long-term energy storage
Activated AMPK to promote fuel catabolism

93
Q

Characteristics of cancer cells

A
  1. Uncontrolled growth: high proliferation, high need for synthesis of DNA, lipids, proteins
  2. Growth without attachment: metastasis, growth of solid tutors instead of monolayers, inside of tumour can become hypoxic
  3. Growth without external growth factors: changes in signal transduction, mutations, escaping normal regulation mechanisms
  4. Dedifferentiation: support of unlimited growth
94
Q

Positron Emission Tomography Imaging

A

PET visualized the body metabolic activity following injection of 2-deoxy-2-fluoroglucose (fluorodeoxyglucose)
Deoxyglucose is phosphorylated by hexokinase but not further protein down, and accumulates in cell
Dark areas indicate tissues that take up a lot of glucose

95
Q

Warburg Effect

A

1920s
Cancer cells generate high levels of ATP through glycolysis and lactate production even when sufficient oxygen is present
Mitochondria in cancer cells are dysfunctional: not generally confirmed
Later research confirmed that most cancer cells have very high rates of glycolysis even in presence of oxygen: various reasons

96
Q

Metabolic needs of highly proliferating cells

A

More ATP production, synthesis of lipids, nucleotides and proteins
High requirement of NADPH and antioxidants
Metabolic adaptations in different cancers are highly diverse and depend on original cell type

97
Q

Glycolysis in cancer cels

A

Less efficient way to generate ATP, but occurs even in presence of oxygen
Glycolytic intermediates and pyruvate are diverted into biosynthesis reactions

98
Q

Glutamine

A

Major fuel after glucose for cancer cells
Anapldrotic reaction to glutamate and alpha-ketoglutarate
Can be fully oxidized when malic enzyme is active

99
Q

Glucose uptake or hexokinae inhibitors

A

Affect cancer cells more than normal cells

100
Q

PKM2 activators

A

Decreased use of glycolytic intermediates in synthesis

Some cancer cells become dependent on extracellular serine when PKM2 is activated

101
Q

Dichloroacetate

A

Inhibits pyruvate dehydrogenase kinase

Activated pyruvate dehydrogenase: pyruvate is oxidized an not used in synthetic reactions

102
Q

Glutaminase inhibitors

A

Targeting glutamine addiction of cancer cells

Biochemistry 2300 (10 decks)

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