Gluconeogenesis Flashcards

1
Q

What are the two pathways that form “free” glucose

A

gluconeogenesis

glycogen degradation

convert glucose-6-P-phosphate to glucose.

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2
Q

Describe what occurs after carbohydrate consumption

A

insulin dependent glucose transport into adipose tissue, heart, and skeletal muscle.

insulin dependent glucose transport into liver and other tissues

glycolytic pathway activated

PDH is active in tissues that have mitochondria forms AcCoA

AcCoA metabolized by CAC

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3
Q

What occurs in the liver in the fed state

A

insulin cuases genes for glycolytic enzymes to be expressed. produce glucokinase, PFK1 and pyruvate kinase

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4
Q

Effects of glucagon and epi during the fasting state

A

block glycolysis. inhibit PFK2 which in hibits PFK1. inhibit pyruvate kinase.

decrease gene transcription glucokinase, PFK1, pyruvate kinase

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5
Q

Changes in the body from fed to fasting

A

during the fed state these are high: insulin, blood glucose, liver glycogen,

During fed state these are low: glucagon, free fatty acids, blood ketone bodies

during fasting these are high: glucagon, free fatty acids, blood ketone bodies

during fasting these are low: insulin, BGL, liver glycogen

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6
Q

What would occur of the glucose-6-phosphatase enzymes was not working properly?

A

gluconeogenesis and glycogen degradation could not occur. you cannot maintain normal blood glucose levels without eating for long periods of time.

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7
Q

How many ATPs does gluconeogenesis require

A

6 ATP

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8
Q

Synthesis of glucose from non-carb precursors

A

pyruvate, lactate, glycerol, glucogenic amino acids.

pyruvte is converted to oxaloacetate in a two step process

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9
Q

gluconeogenic precursors

A

lactate- general metabolism, RBC metabolism, muscle metabolism

glucogenic amino acids (alanine)- overnight degradation of muscle amino acids.

glycerol-degradation of adipose tissue and TAGs.

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10
Q

why are neonates at risk for hypoglycemia?

A

neonates brains are very dependent on glucose from glycogen degradationand gluconeogenesis. PEP carboxykinase is needed to make glucose from lactate or alanine, but it takes a few hours to induce its activity.

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11
Q

What 4 enzymes are required to reverse the three irrevesible steps of glycolysis

A

Mitochondial: Pyruvate carboxylase

Cytoplasmic- Phosphoenol pyruvate (PEP) carboxy kinase

Fructose 1,6 bisphosphate

Glucose 6 phosphate

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12
Q

Pyruvate carboxylase

A

mitochondrial enzyme that carboxylates pyruvate to form oxaloacetate. ATP provides the energy to add the carboxyl group to biotin, the carrier of the activated CO2 group. **acetyl CoA is an allosteric activator of this enzyme. **

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13
Q

Pyruvate carboxylase deficiency

A

Cannot convery pyruvate to oxaloacetate. causes accumulation of pyruvate in the plasma. the pyruvate gets converted to lactate by lactate dehydrogenase. This causes lactic acid build up. high alanine in the serum. cannot participate in gluconeogenesis or the ureas cycle.

causes failure to thrive, developmental delay, recurrent seizures, and metabolic acidosis

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14
Q

Glucose-6-phosphotase

A

essential enzyme required to releae glucose from the liver and into the circulaiton. required for gluconeogenesis ans glucogenolysis

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15
Q

Why can’t skeletal muscle synthesize glucose.

A

glucose-6-phosphatase is absent. make lactate instead.

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16
Q

Allosteric regulation of Glucokinase

A

Glucokinase: activated by insulin and glucose

17
Q

Allosteric regulation of glucose-6-phosphatase

A

G-6-phosphotase: ihibited by insulin and glucose. Activated by glucagon.

18
Q

Allosteric regulation of phosphofructo kinase

A

Phosphofructokinase: activated by F2,6BP and AMP. Inhibited by ATP and citrate

19
Q

Allosteric regulation of Fructose1,6bisphosphatase

A

inhibted by F2,6BP and AMP

20
Q

Allosteric regulation of pyruvate kinase

A

activated by: F1,6BP and glucose

inhibited by: glucagon and ATP

21
Q

alloteric regulation of phosphoenolpyruvate carboxykinase (PEPCK)

A

activated by: glucagon

inhibited by: insulin

22
Q

Allosteric regulation of pyruvate carboxylase

A

activated by acetyl CoA

23
Q

Regulation for the synthesis of glycolytic enzymes

A

increased insulin and glucose. decreased cAMP (as a result of decreased glucagon or epi) a need for more ATP

glucokinase

PFK-1

pyruvate kinase

24
Q

regulation for the synthesis of gluconeogenic enzymes

A

increased glucagon or epinephrine. starvation or fasted state. increased cAMP. resulting from less available energy (ATP)

glucose-6-phosphotase

Fructose-1,6-bisphosphotase

PEP carboxykinase

pyruvate carboxylase

25
Q

How does ethanol metabolism cause hypoglycemia

A

ethanol dehydrogenase causes high NADH which opposes gluconeogenesis.

this removes pyruvate and oxaloacetate from the pool of gluconeogenic precursors by converting them to lactate and malate.

increased NADH leads to increased lactate formation. decreased NADH leads to decreased lactate formation.

26
Q

Glucose-6-phosphotase deficiency

A

located in the ER. autosomal recessive disease.

interferes with gluconeogenesis and causes build up of glycogen in the liver

causes fasting intolerance, growth retardation, enlarged liver (accumulation of glycogen and fat), elevated serum uric acid and lactate.