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Biochemistry Flashcards

1
Q

What is glycogen used for in human

A

Storage of carbohydrates

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2
Q

What is glycogenesis

A

Synthesis of glycogen from glucose

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3
Q

What is gluconeogenesis

A

Formation of glucose from non-carbohydrate sources such as lactate and glycerol

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4
Q

Where does glycogen occur

A

Liver and muscle cells, same structure different function

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5
Q

Use of glycogen in liver

A

Broken down between meal to keep up blood glucose levels for RBC and brain

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6
Q

Use of glycogen in muscle

A

Can’t be broken down for blood glucose levels, used to provide energy via glycolysis during physical activity

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7
Q

What is glycogenolysis

A

Breakdown of glycogen to glucose

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8
Q

What organ helps to keep blood sugar levels constant between meal times

A

Liver via glycogenolysis

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9
Q

Primary source of glucose overnight

A

Gluconeogenesis, only when hepatic glycogen depleted

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10
Q

First step in glycogen synthesis

A

Glucose - (hexokinase) to Glucose-6-phosphate

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11
Q

How is glycogen chain elongated

A

Glycogen consists of branches and sticks one glucose from UDP-glucose molecules onto this chain to increases size of glycogen.

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12
Q

What is the activated form of glucose

A

UDP-glucose, glucose transfer molecule

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13
Q

What catalyzes glycogen from UDP-glucose

A

Glycogen synthase

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14
Q

Significance of Glycogenin

A

Substrate involved in converting glucose to glycogen, acts as a primer by polymerising first few glucose molecules. Important as Gycogen synthase can extend existing chains of glycogen, not start new molecules

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15
Q

Rate limiting enzyme for glycogenesis

A

Glycogen synthase

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16
Q

Function of transglycosylase

A

Introduce alpha 1-6 glycosidic branches in glycogen

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17
Q

Enzyme used in Glycogenolysis

A

Glycogen phosphorylase, rate limiting step

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18
Q

End product of glycogenolysis

A

Glucose - 1 - Phosphate

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19
Q

Which cells can dephosphorylate glucose-6-phosphate

A

Liver and not skeletal muscle cells

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20
Q

Hormone stimulating synthesis of Glycogen formation

A

Insulin stimulate Glycogenesis, Glycogen synthase

Occurs when lots of carbohydrates are in blood stream

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21
Q

Hormone of starving state

A

Glucagon, signal lack of glucose in blood stream. Stimulate glycogenolysis, glycogen phosphorylase

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22
Q

What hormones other than Glucagon stimulate glycogen phosphorylase

A

Adrenaline and Cortisol, existing carbohydrate stores broken down into glucose

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23
Q

Precursors for gluconeogenesis

A

Lactate - By skeletal muscle under anaerobic condition
Amino acids - From muscle protein by proteolysis
Glycerol - From triglycerides by lipolysis

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24
Q

Where does gluconeogenesis occur

A

Liver and small amounts in kidney

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25
Q

First substrate of gluconeogenesis

A

Pyruvate, 2 to make one glucose

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26
Q

Glycolysis vs gluconeogenesis energetically

A

Gluconeogenesis requires 6 ATP (4 ATP + 2 GTP) to make a Glucose, energetically expensive. Glycolysis generates 2 ATP for each glucose. Hence our body should conduct gluconeogenesis only required

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27
Q

How can lactate enter gluconeogenesis

A

Lactate is a polar molecule. It’s produced by the cori cycle as part of anaerobic skeletal muscle respiration from glucose - pyruvate - lactate. This is transported via blood to the liver to enter gluconeogenesis

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28
Q

Which amino acids can be used to make glucose, Ketogenic or Glucogenic

A

Glucogenic amino acids can enter gluconeogenesis via TCA cycle substrates or converted to pyruvate

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29
Q

First reaction in gluconeogenesis

A

Pyruvate to Oxaloacetate

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30
Q

What is glycoysis

A

Breakdown of glucose into pyruvate

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31
Q

Glucagon on glycolysis

A

Glucagon stimulates gluconeogenesis and inhibit glycolysis

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32
Q

Insulin on gluconeogenesis

A

Insulin stimulates gluconeogenesis as plenty of glucose is around

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33
Q

High ADP and AMP in cells and gluconeogenesis

A

High AMP/ADP in cells signals low energy and hence glucose breakdown should be started. This stimulates glycolysis and inhibits gluconeogenesis which is energetically expensive

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34
Q

Concentration of fructose 2,6-bisphosphate on gluconeogenesis

A

High concentrations of fructose 2,6-bisphosphate is found in a fed state, hence glycolysis is favoured at high concentrations

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35
Q

High concentrations of citrate, alanine and acetyl-CoA

A

Precursor molecules of biosynthetic processes, present at high concentration when intermediates for building blocks are abundant. Inhibit glycolysis and stimulate gluconeogenesis

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36
Q

How are lipids digested

A

lingual phase in mouth - Quantitatively unimportant
Gastric phase in stomach - Most importance
Small intestine - Most important, emulsification by bile synthesis by liver, pancreatic lipase, hydrolyses TAGs to monoglyceride and free fatty acids.

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37
Q

What helps emulsify lipids

A

It is the breakdown of large fat globules into smaller, uniformly distributed particles. Helped by bile

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38
Q

How are lipid droplets avoided from coming back together after emulsification

A

Droplets are stabilised by addition of amyopathic coat consisting of - certain products of lipid digestion, monoacylglycerols, cholesterol and bile salts

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39
Q

What are triacylglycerols converted to

A

Diglycerols and fatty acids

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40
Q

Function of free fatty acids produced as a result of emulsification in the stomach

A

Free fatty acids stimluate CCK release from duodenum and secretion of pancreatic lipase

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41
Q

Function of HCO3- in succus entericous

A

Neutralize stomach acid and provide suitable pH for optimal enzyme action

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42
Q

Where does main lipid digestion occur

A

At the duodenum by pancreatic lipase, main digestive enzyme in adults

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43
Q

What can failure to secrete bile cause

A

Lipid malabsorption (steatorrhoea) and secondary vitamin deficiency (A,D,E,K)

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44
Q

Function of co-lipase

A

Bile salts inhibit access of pancreatic lipase to triglycerides. Co-lipase binds to bile salts and brings lipase in close contact with tri and diglycerids, where lipase can break it down.

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45
Q

Gastric lipase breakdown of lipase

A

Triglyceride = Diglyceride + Free fatty acids

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46
Q

Pancreatic lipase breakdown of lipase

A

Triglyceride = 2-monoglyceride + 2 fatty acids

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47
Q

How are short (<6) and medium (8-12) fatty acids absorbed

A

Diffused through enterocyte, exit basolateral membrane and enter the villus capillaries

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48
Q

How are long (> 12) fatty acids and monoglycerides absorbed

A

They enter the apical membrane of enteroctyes by passive diffusion and are resyntheized to triglycerides in the endoplasmic reticulum. They are incorporated into chylomicrons subsequently and carried in lymph vessels to systemic circulation via thoracic duct.

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49
Q

What happens to the chylomicron after entering systemic circulation

A

Chylomicron triglycerides metabolised in capillaries (muscle and adipose mostly) by lipoprotein lipase on endothelial cells. Free fatty acids and glycerol released bind to albumen and taken up by tissue

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50
Q

What enzyme on epithelial cells of capillaries metabolises chylomicrons

A

Lipoprotein lipase

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51
Q

Where does chylomicron remnant undergo endocytosis

A

Hepatocytes to be stored, secreted unaltered in bile and oxidised to bile salts

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52
Q

What aides in cholesterol absorption

A

Transport by endocytosis in clathrin coated pits by Neimann-Pick C1 like 1 (NPC1L) protein

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53
Q

Mechanism of Ezetimibe

A

Binds to NPC1L1 protein, prevents internalization and absorption of cholesterol. Used in conjunction with statins in hypercholesterolaemia

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54
Q

How is calcium absorbed

A

Passive paracellular along the length of small intestine.

Active transcellular mainly duodenum and jejunum.

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55
Q

Under what amount is Ca absorption active

A

< 5 mM of Ca

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56
Q

What regulates active Ca absorption

A

1,25-dihydroxyvitamin D3 (calcitriol) and parathyroid hormone which increases synthesis of former

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57
Q

Storage form of Iron

A

Ferratin

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58
Q

Major control of Iron absorption

A

Ferroportin aka SLC40

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59
Q

What regulates ferroportin

A

Hormone hepcidin released from liver when body iron levels are high

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60
Q

How is cobalamin absorbed

A

Cobalamin (B12) is ingested in food. Haptocorin released from salivary glands. Stomach acid releases B12 from food. Haptocorin binds with B12 in stomach. Parietal cells release intrinsic factor. Pancreatic protease digest haptocorin in small intestine releasing B12. B12 binds to intrinsic factor in small intestine. This complex is absorbed in ileum by endocytosis.

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61
Q

How are fat soluble vitamins absorbed

A

A, D, E and K are incorporated into mixed micelles. Passively transported into enterocytes. Incorporated into chylomicrons or VLDL which are distributed by intestinal lymphatics.

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62
Q

How are water soluble vitamins transported

A

In apical membrane similar to monosaccharides, amino acids and di- and tripeptides

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63
Q

How is vitamin B9 transported

A

Folic acid by Na-independant proton-couple folate transporter 1

64
Q

How is vitamin C transported

A

Ascorbic acid by Na-dependant vitamin C transporter

65
Q

How is vitamin H transported

A

Biotin by Na dependant multivitamin transporter

66
Q

Can fatty acids be used for gluconeogenesis

A

No

67
Q

Main storage form of lipids in the body

A

Triglycerides

68
Q

Lipids are mostly

A

Hydrocarbon and water-insoluble

69
Q

First step of fat catabolism is

A

Lipolysis

70
Q

What is lipolysis

A

Catabolism of triglycerides to fatty acids and glycerol

71
Q

What is activation of fatty acids

A

Conversion of fatty acids to fatty acyl-CoA

72
Q

Where does lipolysis and activation occur

A

In the cytoplasm

73
Q

What is beta-oxidation

A

Conversion of fatty acyl-CoA to acetyl-CoA

74
Q

Formula for how many oxidations occur for even numbered saturated fat

A

Ex: C16
16/2 - 1 = 7
7 oxidation cycles occur

75
Q

Products of one beta-oxidation cycle

A

1 acetyl-CoA, 1 FADH2, 1 NADH + H+, 1 fatty acyl-CoA shortened by 2 carbon atoms

76
Q

What is formed in the liver under fasting conditions

A

Ketone bodies from acetyl-CoA by beta-oxidation

77
Q

Function of ketone bodies

A

Diffuse into the blood stream and to peripheral tissue. Important molecules of energy metabolism for brain, heart muscle and renal cortex, it’s converted back to acetyl-CoA which enters TCA cycle

78
Q

Major fatty acid precursor

A

Malonyl-CoA

79
Q

What regulates acetyl-CoA carboxylase activity

A

Nutrient and energy status

80
Q

What converts acetyl-CoA to malonyl-CoA

A

Acetyl-CoA carboxylase

81
Q

What stimulates acetyl-CoA conversion by acetyl-CoA carboxylase to malonyl-CoA

A

Citrate, levels of this are high when acetly-CoA and ATP are abundant. Insulin signals fed state hence stimulates storage of fuels and synthesis of proteins

82
Q

What signals the starved state

A

Glucagon

83
Q

Is fatty acid synthesis oxidative or reductive?

A

Reductive

84
Q

What transports acetyl groups from mitochondria to cytoplasm

A

Citrate

85
Q

What donates carbon atoms to a growing fatty acid

A

Malonyl-CoA

86
Q

Where is urea synthesized

A

Liver via urea/ornithine cycle

87
Q

One nitrogen of urea is derived from

A

Aspartate and other from free ammonium

88
Q

Rate limiting step in glycolysis

A

Glycogen phosphorylase mediated glycogen to glucose-1-phosphate breakdown

89
Q

What converts glucose-1-phosphate to glucose-6-phosphate

A

Phosphoglucomutase

90
Q

Fate of glucose-6-phosphate

A

Glycolysis or transport into blood via GLUT2 in liver as glucose, mediated conversion by glucose-6-phosphatase

91
Q

How does gluconeogenesis proceed

A

Synthesis of oxaloacetate in mitochondria, TCA cycle intermediate that accepts acetyl groups from fat breakdown

92
Q

What is glycogenin

A

Protein that sits at the center of glycogen polymer.

93
Q

Function of glycogenin

A

Catalytic activity, covalently binds four glucose molecules to itself, forming starting point of glycogen polymer.

94
Q

Why is glycogenin significant

A

Glycogen synthase can only add glucose residues to existing glycogen chains. Glycogenin provides this chain for glycogenesis to occur

95
Q

What forms can pyruvate enter the TCA cycle

A

As acetyl-CoA or oxaloacetate

96
Q

Can amino acids be synthesized in the TCA cycle

A

Yes

97
Q

Can muscle glycogen be used as blood glucose

A

No, only liver glycogen can

98
Q

What does glucose have to be bound to before it can be transferred onto glycogen

A

Uridine diphosphate glucose (UDP)

99
Q

Precursors for gluconeogenesis

A

Lactate, glycerol and glucogenic amino acids

100
Q

Glucagon and gluconeogenesis

A

Glucagon stimulates it, insulin inhibits

101
Q

What do catabolic pathways do

A

Breakdown reduced substrates for energy generation

102
Q

What provides reducing force in anabolism

A

NADPH

103
Q

Is catabolism oxidative

A

Catabolism is oxidative whereas anabolism is reductive

104
Q

Which pathway generates cofactors which can drive oxidative phosphorylation

A

Catabolic pathways

105
Q

How many ATP and NADH + H+ produced per glucose molecule in glycolysis

A

2 ATP and 2 NADH+ per glucose molecule broken down

106
Q

What is glycolysis

A

Breakdown of glucose to pyruvate

107
Q

What does pyruvate have to be converted to before it enters the TCA cycle

A

Acetyl-CoA

108
Q

Does TCA cycle consume NADH and FADH2

A

No

109
Q

Does the TCA cycle provide precursors for gluconeogenesis

A

Yes

110
Q

First substrate of gluconeogenic pathway

A

Pyruvate, converted in the cori cycle from lactate

111
Q

TCA cycle overview

A

Two carbon unit (from acetyl-CoA) condenses with four carbon unit. This six carbon unit is decarboxylated twice, yielding CO2. 4 oxidation reactions occur yielding 3 NADH + H+, 1 FADH2 and 1 GTP

112
Q

Electron transport chain is located at

A

Inner mitochondrial membrane

113
Q

Where are electrons gotten from to reduce O2 to H2O in oxidative phosphorylation

A

NADH and FADH2

114
Q

What is energy of reduction used for in oxidative phosphorylation

A

To pump protons from mitochondrial matrix to intermembrane space. This creates a proton concentration gradient. Protons flow back across the membrane. This energy of proton flow is used to phosphorylate ADP to ATP

115
Q

What is the P/O ratio

A

Number of ATP formed per oxygen atom reduced

116
Q

What relates to the free energy change of a reaction

A

Difference in redox potentials between substrate and product of a redox reaction

117
Q

What does a more negative redox potential mean

A

More likely to donate an electron

118
Q

What has a lower redox potential, NADH or FADH2

A

FADH2, hence NADH likes to donate electrons more

119
Q

Transferring electrons from negative to positive redox does?

A

Releases energy

120
Q

What can be used to separate immunoglobulins

A

Electrophoresis; separates by size

121
Q

Main function of plasma proteins

A 
Maintain oncotic or colloid osmotic pressure
Transport hydrophobic substances
pH buffering
Enzymatic
Immunity
122
Q

Retinol binding protein

A

Alpha globulin, transport vitamin A which is converted to retinaldehyde. This is part of rhodopsin, a visual pigment

123
Q

Deficiency in what globulin leads to visual impairment

A

Alpha globulin

124
Q

Deficiency in what globulin indicates iron deficiency

A

Beta globulins as it helps transport Iron

125
Q

Globulin in fibrinogen (inactive form of fibrin)

A

Beta globulin

126
Q

Most abundant plasma protein

A

Albumin

127
Q

Main protein determinant of plasma oncotic pressure

A

Albumin

128
Q

What hormone from the pancreas stimulate albumin production

A

Insulin

129
Q

Starvation/ low protein diet causes a decrease in what plasma protein

A

Albumin

130
Q

How can albumin transport hydrophobic substances

A

Albumin has multiple binding sites for hydrophobic molecules. Hydrophobic clefts in globular domains that have low affinity but high capacity due to high concentration.

131
Q

What endogenous lipophilic substances does albumin transport

A

Fatty acids
Bilirubin
Thyroid hormone

132
Q

How is iron transported in the body

A

As ferric iron Fe3+ bound to transferrin

133
Q

How is copper transported in the body

A

Bound to ceruloplasmin

134
Q

Deficiency of copper transport causes

A

Wilson’s disease

135
Q

How are thyroxine and cortisol transported in circulation

A

Thyroid-binding globulin

Cortisol-binding globulin

136
Q

How do transport globulins increase plasma concentration of hormones and their half life

A

Transport globulins allow circulation around the body. Without them, the hormones would be eliminated rapidly by the kidney or liver.

137
Q

What aides fat transport in the body

A

Lipoproteins

138
Q

Structure of lipoproteins

A

Hydrophobic core of lipids - Cholesterol esters and triglycerides. Surrounded by a shell of polar lipids (phospholipids) and apoproteins. Unesterified/free cholesterol dispersed throughout

139
Q

Lipid transport in dietary vs synthesized fat

A

Dietary fat - Chylomicrons whereas synthesized fat is transport via vLDL

140
Q

Receptors on hepatocytes for HDL

A

Scavenger receptors

141
Q

Only organ capable to metabolising and excreting cholesterol

A

Liver

142
Q

How is cholesterol excreted from body

A

As bile salts via biliary system or in faeces

143
Q

What vitamins does the liver store

A

Vitamin D - 3 weeks worth
A - 10 months worth as retinol palmitate
B12 - Few years worth
Iron - From breakdown of haemoglobin, stored associated with ferritin

144
Q

Important compounds made from cholesterol

A

Vitamin D, steroid hormones and bile salts

145
Q

Cholesterol is insoluble in water. How is this solubilised

A

Cholesterol is incorporated into lipoproteins and thereby solubilised.

146
Q

Starting substrate for cholesterol

A

Acetyl-CoA * 2

147
Q

Rate limitng enzyme in synthesis of cholesterol

A

HMG-CoA catalyzing the irreversible formation of mevalonic acid

148
Q

What stimulates activity of HMG-CoA

A

Fasting and starvation

149
Q

What reduces HMG-CoA activity

A

Dietary cholesterol and high intrahepatocyte cholesterol.

150
Q

This compound made from cholesterol has a role in the regulation of Calcium and Phosphorous metabolism

A

VItamin D

151
Q

Most abundant form of vitamin D in the circulatory system

A

Vitamin D3

152
Q

Steroid hormones synthesized from cholesterol and the organs responsible

A

Corticodsteroids - Adrenal cortex
Androgens - Testis
Estrogen - Ovary

153
Q

Can the three steroid organs secrete steroid hormones mainly secreted by the other

A

Yes, upto a small amount

154
Q

Main metabolism product of cholesterol

A

Bile salts

155
Q

How can cholesterol excretion be therapeutically manipulated

A

Anion exchange resins bind bile salts and inhibit reabsorption of bile salts into enterohepatic circulation.
Increase bile salt excretion - increased synthesis of bile salts - concentration of cholesterol in liver decreased as cholesterol is used to synthesize bile salts - number of LDL receptors of hepatic cells increases - uptake of LDL cholesterol from plasma increases

156
Q

Example of anion exchange resin used to bind to bile salts and inhibit reabsorption of bile salts

A

Cholestyramine

GI (32 decks)

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