MMT: gluconeogenesis Flashcards

1
Q

Describe the physiological significance of gluconeogenesis. List the primary precursors of gluconeogenesis

A

Helps us generate glucose to use for energy from non-carbohydrate sources, namely pyruvate, lactate, glucogenic amino acids, and glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Gluconeogenesis starts in the ___ and ends in the ___

A

Mitochondria; endoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the major organs that carry out gluconeogenesis. Locate the various enzymes of gluconeogenesis in cell compartments

A

Liver and kidney cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

High glucagon stimulates ___ (gluconeogenesis vs glycolysis)

A

Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

high insulin stimulates ___ (gluconeogenesis vs glycolysis)

A

glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

High cortisol stimulates ___ (gluconeogenesis vs glycolysis)

A

Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Generally, diabetes type 1 or 2 stimulates ___ (gluconeogenesis vs glycolysis)

A

gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Specify how we can make DHAP, oxaloacetate, and pyruvate to act as starters in gluconeogenesis

A

DHAP: glycerol
Oxaloacetate: some amino acids
Pyruvate: lactate and some amino acids; whole pathway will be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

discuss how alcoholism can inhibit gluconeogenesis and lead to hypoglycemia

A

sustained ethanol concentration requires constant use of NAD+ to process it, forming a lot of NADH and not much NAD+. The lack of NAD+ and abundance of NADH drives formation of lactate as opposed to pyruvate, and makes alanine convert to lactate instead of pyruvate. As a result, these cannot enter gluconeogenesis and hypoglycemia can happen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe how glycerol becomes DHAP

A

Glycerol uses glycerol kinase > glycerol phosphate, uses glycerol phosphate dehydrogenase > DHAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe how asparagine enters gluconeogenesis

A

Asn uses asparaginase > aspartate, uses transaminase > oxaloacetate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe how lactate enters gluconeogenesis

A

Lactate uses lactate dehydrogenase to form pyruvate, or alanine uses alanine aminotransferase to become pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name the enzymes and reactions that replace pyruvate kinase in gluconeogenesis

A

Pyruvate +Pyruvate carboxylase (uses biotin) > OAA
OAA + PEP carboxykinase (decarboxylation and phosphorylation) > PEP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PEP carboxykinase: reaction is catalyzes, glycolytic enzyme it replaces, energy source,

A

OAA > phosphoenol pyruvate

replaces
Pyruvate kinase

Decarboxylation and phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name the enzyme and reaction that replaces PFK. does it produce ATP?

A

F1,6BP + fructose 1,6 phosphatase > F6P

Allosterically regulated
Does not produce ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

___ drives unfavorable reactions

A

Decarboxylation

17
Q

Name the enzyme and traction that replaces hexokinase

A

G6P + glucose-6-phosphatase > glucose

Does not produce ATP

18
Q

Pyruvate carboxylase is a ___ enzyme

A

Mitochondrial

19
Q

Specify the source of energy used for gluconeogenesis.

A

ATP from fatty acid beta oxidation, TCA and oxidative phosphorylation

20
Q

Describe the coordinated control of the enzymes in glycolysis and gluconeogenesis.

A

-High fructose 2,6 biphosphate can activate PFK (glycolysis) and inhibit fructose 1,6 bisphosphatase (gluconeogenesis)

-largely regulated by high vs low energy charge; things like ATP, acetyl CoA, and citrate signal high energy charge (less glycolysis, more gluconeogenesis) and low energy charge signals glycolysis

21
Q

what would happen if we ran glycolysis and gluconeogenesis at the same time

A

Cells in the muscle may run glycolysis at the same time as gluconeogenesis runs in the liver. Glucose enters the muscle form the blood, converts to pyruvate then lactate. Lactate enters the blood then the liver, then becomes pyruvate and then glucose. Cycle starts again.

22
Q

describe hypolactasia

A

lack of lactose. discomfort, bloating, diarrhea

23
Q

what is galactosemia? what is the treatment?

A

Unable to break down galactose

treatment is avoiding lactose

24
Q

describe classic galactosemia: deficiency type, symptoms

A

type 1; GALT deficiency. Delayed growth, jaundice, lethargy, eventual cataracts, renal failure, developmental delays

25
Q

describe non-classic galactosemia: deficiency type and symptoms

A

type 2; GALK deficiency. Cataracts and risk of E coli sepsis. Less severe as it is the first enzyme used in galactose processing.

26
Q

what is deficient in type 3 galactosemia

A

GALE

27
Q

describe fructoseria: what enzyme is deficient and what are the symptoms

A

fructokinase deficiency; fructose in the urine but otherwise asymptomatic

28
Q

describe Hereditary fructose intolerance: what is deficient, what is happening, what are the symptoms, treatment

A

aldolase B deficiency. More severe because the phosphate is trapped on the molecule. Poor feeding, jaundice, hyperglycemia. Avoid fructose or sucrose.