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Gluconeogenesis + KB

Biochem and medical genetics

QuestionAnswer
Gluconeogenesis The making of new glucose Substrates - lactate, glycerol and amino acids Occurs in the liver predominantly, with a smaller amount in the kidney cortex Pathway includes both a mitochondrial and a cytosolic section
Why is gluconeogenesis important Daily required glucose - 200g Daily glucose intake - 100g Stored glycogen in the liver liberates 90g for other organs In fasting these stored only last 12 hours, so we need a way to make more glucose
Glycolysis vs gluconeogenesis Some enzymes in glycolysis are irreversible so need different enzymes Energy input for gluconeogenesis exceeds glycolysis reversed (6 v 2 ATP) Different control Involves mitochondria and ER, not just cytosol
Mitochondrial part of gluconeogenesis Pyruvate transported to mitochondria , converted to oxaloacetate by pyruvate decarboxylase (ATP) Then to malate by malate dehydrogenase (NADH) Then exported from mitochondria and turned back to oxaloacetate (NAD) Then to PEP by PEP carboxykinase (GTP)
Cytosolic part of gluconeogenesis From PEP glycolysis reverses until Fructose 1,6 bisphosphate This is converted to fructose 6 phosphate by fructose 1,6 bisphosphatase - different enzyme and PFK is irreversible In ER glucose 6 phosphatases converts glucose 6 phosphate to glucose
Why is glucose formed in the ER Don't want to randomly dephosphorylate glucose as this reduces control in the liver Isolating the enzyme in the ER allows for control of entry and exit of glucose via transporters
Why is gluconeogenesis so energy expensive The steps required to bypass irreversible reactions are energy demanding There has to be a doubling of all substrates prior to glyceraldehyde 3 phosphate as pyruvate only has 3 carbons
Supply of lactate to gluconeogenesis Converted to pyruvate by lactate dehydrogenase This also produces NADH This occurs via the Cori cycle Lactate produced by anaerobically respiring muscle, rbcs, renal medulla etc transported to liver where it undergoes gluconeogenesis
Supply of alanine to gluconeogenesis Converted to pyruvate by alanine aminotransferase, which releases NH3
Supply of glutamine to gluconeogenesis Glutamine supplied from muscles Deaminated to glutamate Deaminated again to alpha ketoglutarate This enters kerbs cycle to form malate
Supply of glycerol to gluconeogenesis Released from TAGs in adipose Converted to glycerol 3 phosphate in liver Converted to DHAP which is fed into gluconeogenesis
Why can't FAs be used to make glucose Input into krebs cycle is Acetyl CoA - 2 carbons Loss of 2 CO2 in krebs cycle - 2 carbons lost No net carbons left once reach oxaloacetate
Control of gluconeogenesis Allosteric control by metabolites - acute Covalent modification by hormones - acute Transcriptional control of gluconeogenic genes/enzymes by hormones - chronic
Allosteric control of gluconeogenesis Citrate activates fructose 1,6 bisphosphatase Acetyl CoA activates pyruvate decarboxylase
Hormonal control of gluconeogenesis Glucagon activates fructose 1,6 bisphosphatase and PEP carboxykinase This inhibits pyruvate kinase - prevents futile cycling
Transcriptional control of gluconeogenesis Glucagon increases - pyruvate carboxylase, PEP carboxykinase, fructose 1,6 bisphosphatase and glucose 6 phosphatase Glycogen decreases - glucokinase and pyruvate kinase Insulin increases - glycogen synthase, hexokinase, PFK, pyruvate kinase
Why does gluconeogenesis decrease with prolonged starvation Cost vs benefit - required breakdown of muscle so leads to rapid wasting Alternative fuel - ketone bodies
Ketone bodies Made in fasting and starvation Alternative fuel to power body in nutrient deprivation Not obtained from the diet Production and use is an adaptation to fasting Cant be stored
What are ketones Small 4 carbon molecules Water soluble Acetoacetate and beta hydroxybutyrate are metabolically active Acetone is volatile and can be smelled on the breath
Ketogenesis Production of ketone bodies Occurs in liver Specifically in mitochondria
Ketolysis Breakdown and utilisation of ketone bodies Occurs in peripheral tissues especially brain and nerve cells Dosent occur in liver Occurs in mitochondria
Role of HSL in ketogenesis Starts in adipose tissue HSL is active in fasting as insulin levels are low so inhibition is reduced TAGs are broken down and released as NEFA bound to albumin in the blood
Pathway of ketogenesis 2 Acetyl CoA - acetoacetyl CoA by acetoacetyl CoA thiolase Add Acetyl CoA via HMG CoA synthase to form HMG-CoA Loss of acetyl CoA to form acetoacetate by HMG CoA lyase This can then convert to b-hydroxybutyrate (dehydrogenase) or acetone
What causes Ketogenesis Oxaloacetate is diverted away from krebs cycle to gluconeogenesis Less available to combine with acetyl CoA so it cant enter krebs cycle This is diverted to ketogenesis This means these processes occur together
Ketolysis in peripheral tissues Released into blood by liver Uptake is proportional to concentration in blood Ketolysis does not occur in liver - does not express 3-ketoacyl CoA transferase needed for ketolysis to prevent futile cycling
Pathway of ketolysis B hydroxybutyrate to acetoacetate by dehydrogenase To Acetoacetyl CoA by addition of succinyl CoA by 3-ketoacyl CoA transferase Acetoacetyl CoA thiolase adds CoASH for form 2 acetyl coA
Why make ketones Used by peripheral tissues in fasting Used by brain - cannot use fatty acids so provides an alternative fuel derived from fatty acids Ketones are glucose sparing - insufficient glucose without them
Ketones in starvation Part of a normal adaptation to fasting They are acids - and concentration normally sits within bloods buffering capacity Without ketones we would not be able to survive so long without food
Diabetic ketoacidosis Ketogenesis is uncontrolled High conc of ketone in blood - drops pH Associated with coma and death Rapid breathing - Kussmaul breathing Smell acetone on breath
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