Biosynthetic Pathways Flashcards

1
Q

Anabolic Pathways

A

forming of precursors (catabolic eg amino acids, fatty acids and sugar molecules), form complex molecules together and joining of complex molecules together (RNA and DNA)

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2
Q

Food Stores in Fed State

A

Plenty of nutrients, build up of food stores. Increase of insulin secretion and nutrient uptake. Glucose is made into glycogen, fatty acids form triglycerides and amino acids make protein

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3
Q

Food Stores in Starvation State

A

Lack of nutrients, food store broken down. Glycogenolysis, glucogenesis, lipolysis, proteolysis and ketogenesis

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4
Q

Glucogenesis Def

A

Formation of glucose from non-carbohydrate (lipid/protein) precursors when glycogen is depleted. Mix of reversible and irreversible steps. Need enzyme to undo irreversible processes, thus path requires energy

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4
Q

Examples of glucogenesis irreversible steps

A

PEP to pyruvate by pyruvate kinase and pyruvate to acetyl co A by pyruvate dehydrogenase

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5
Q

Substrates of Glucogenesis

A

Lactate, Glycerol and Amino Acids

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6
Q

Glucogenesis from Glycerol Substrate

A

Glycerol released from adipose tissues into blood by triglyceride hydrolysis. Glycerol is phosphorylated by glycerol phosphate by glycerol kinase (taken from ATP). Glycerol kinase exists in liver, kidney and intestines. Glycerol phosphate oxidised to DHAP

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7
Q

Acetyl Co A relation to glucogenesis

A

Acetyl Co A created in lipolysis and not used in glucogenesis (and can’t reform a lipid as pyruvate dehydrogenase is irreversible). High Acetyl Co A stimulates glucogenesis. Inhibits pyruvate dehydrogenase (inhibiting glycolysis)

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8
Q

High AMP relation to glucogenesis

A

inhibits 1,6-biphosphate (glucogenesis) and activates phosphofructase (glycolysis)

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9
Q

Glucogenesis from amino acid substrate

A

Converts to TCA cycle intermediate and ultimately form oxaloacetate (pyruvate carboxylase converted to Acetyl Co A) converted to PEP (PEP carboxykinase) and then glucose

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10
Q

Glucogenesis fructose 1,6-biphosphatase

A

Inhibited by AMP and by 2,6 biphosphate (which is increased by insulin)

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11
Q

Pyruvate kinase (glycolysis) balanced out by what in glucogenesis

A

pyruvate carboxylase and PEP carboxylase

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12
Q

Phosphofructokinase (glycolysis) is balanced out by what in glucogenesis

A

fructose 2, 6 - biphosphate

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13
Q

hexokinase/glucokinase (glycolysis) is balanced out by what in glucogenesis

A

Glucose 6 phosphate and glucose 6 phosphate translocase (adding phosphate from 6th C from ER)

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14
Q

Fatty Acid Oxidation

A

Forms ATP and NADH for glucogenesis

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15
Q

Pentose Phosphate (Hexose Monophosphate) Pathways Outline

A

Generates NADPH and 5 Carbon sugars for nucleic acids (DNA and RNA). More anabolic and catabolic. 2 Phases oxidative (NADPH) and cyclic (nucleic acids)

16
Q

2 Irreversible Phases of Oxidative Pentose Phosphate Pathways

A

Glucose-6-P catalysed by glucose-6-phosphate dehydrogenase to ribulose -5-P, CO2 and NADH & 6-phosphogluconolacetone htdrolase

17
Q

3 Reversible, Non-oxidative Phases

A

Catalyse interconversion of 3,4,5,6,7 carbon sugars, Ribose-5-P for DNA and RNA synthesis

18
Q

NADPH Outline

A

Electron carrier for pathways. Acts as coenzyme for enzymes in antioxidants - detoxifying

18
Q

Regulation of pentose phosphate pathway

A

Rate determined by concentration of substrate, rate determining step (glucose-6-P dehydrogenase). NADPH acts as inhibitor, Insulin acts as a stimulant

19
Q

G6PD Deficiency

A

Caused by inheriting mutated G6PD (presents aminly in RBC). Results in insufficient production of NADPH causing Glutathione to not be regenerated resulting in oxadative damage

20
Q

Oxidising Factors

A

Oxidant drugs (eg antibiotics), favism (fava beans), inflammatory response and neonatal jaundice

20
Q

Results of oxidation of RBCs

A

Proteins are denatures (forming Heinz body’s). Happens most commonly in erythrocytes due to pentose phosphate pathway being only source of NADPH. Results in haemolytic anaemia

21
Q

Amino Acid Biosynthesis

A

Amino acids aren’t stored and essential amino acids can’t be made in body. essential amino acids can be broken down into alpha-keto acids and rejoined to differnt ones to form non-essential amino acids. Excess is used as TCA cycle intermediates. excreted as urea

22
Q

Glucogenic Amino Acids

A

Breakdown yields TCA cycle intermediates to make glucose

23
Q

Ketogenic Amino Acids

A

Breakdown acetyl Co A

24
Q

Aminotransferase

A

Move an amine group from alpha keto acid and alpha keto glutamate to alpha amino acids and glutamate

25
Q

Alanine aminotransferase

A

Alanine + alpha keto glutarate to pyruvate + glutamate

26
Q

Aspartate Aminotransferase

A

Oxaloacetate + glutamate to aspartate + alpha-ketoglutarate

27
Q

Urea Cycle

A

Occurs in liver. 3 ATP/urea molecule. Water soluble transported in circulationand excreted in kidney

28
Q

Purine Synthesis

A

De Novo and salvaging pre-existing molecules

29
Q

Pyrimidine synthesis

A

De Novo

30
Q

Relationship between ATP and GTP

A

Of equal energy. Both are needed in equal amounts for some reactions

31
Q

Thymidylate synthase Outline

A

dUridine Diphosphate to dTMP by enzyme thymidylate synthase with cofactor tetrahydrofolate. Chemotherapy drugs target thymidylate synthase as it inhibits DNA production. Inhibited by 5- FU. Dihydrofolate reductase damages cofactors which also inhibits thmidylate synthase

32
Q

Result of excess purine breaksown

A

Gout - excess of uric acid percipiatates as urate crystals. Causes inflammation of joints in pain