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BFOM > Metabolic cycle regulation > Flashcards

Metabolic cycle regulation Flashcards

1
Q

Pyruvate Carboxylase modulators

A

Positive: acetyl coa (carb flame), glucagon transcription

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2
Q

G-6-phosphatase modulators

A

Positive: Glucagon transcription

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3
Q

Brain AMPK kinase

A

Ca2+-calmodulin-dependent kinase B - ca2+ stimulant

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4
Q

Epinephrine

A

Positive modulator for glycolysis in the muscle to produce ATP.

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5
Q

Pyruvate Kinase modulators

A

Positive: F-1,6-Bis-P, Insulin via transcription
Negative: ATP, Acetyl CoA, Long Chain FA, Glucagon

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6
Q

Glucagon on metabolic pathways: FA mobilization

A

Adipose tissue

Positive - PKA, Hormone-sensitive lipase

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7
Q

Phosphfructokinase I modulators

A

Positive: ADP, AMP, F-2,6-BisP, Insulin via transcription
Negative: ATP, citrate

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8
Q

Insulin on metabolic pathways: Glycolysis, acetyl CoA production

A

Liver & Muscle

Positive: PFK-1 by PFK2, Pyruvate DH complex, Pyruvate kinase (transcription)

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9
Q

AMPK-P energy producing processes

A

Heart (glycolysis, glucose uptake, b-oxidation), Skeletal muscle (b-oxidation, glucose uptake), brain (feeding)

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10
Q

AMPK Kinase modulators

A

Positive: AMP, leptin, adiponectin

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11
Q

F-1,6-Biphosphatase modulators

A

Negative: F-2,6-bisP

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12
Q

Insulin on metabolic pathways: Triacylglycerol synthesis

A

Adipose

Positive: Lipoprotein lipase (transcription)

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13
Q

PEP Carboxylase modulators

A

Positive: Glucagon and Glucagon transcription

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14
Q

Positive Modulators on most energetic steps of Krebs cycle

A

Ca2+ in the muscle only

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15
Q

Negative Modulators on most energetic steps of Krebs cycle

A

ATP, NADH+H, FADH2

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16
Q

Glucagon on metabolic pathways: Ketogenesis

A

Brain

Negative - acetyl-CoA Carboxylase

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17
Q

Adenylate Kinase

A

Will make AMP from 2 ADPs

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18
Q

Explain why pyruvate carboxylase should be active in fed states

A

Acetyl CoA is a positive modulator for PC.

Liver fed: excess acetyl Coa with OAA from excess pyruvate make citrate, citrate shuttled to cytosol for FA synthesis.

19
Q

Succinyl-CoA and odd chain FAS as a negative modulator and why

A

alpha-ketoglutarate DH and citrate synthase, want to slow down Krebs because we are going faster than ATP synthesis in ETC can occur.

20
Q

Gluconeogenesis enzymes

A

G-6-phosphatase, F-1,6-Bisphosphatase, PEP Carboxylase, Pyruvate carboxylase

21
Q

Explain why hepatocytes express an additional hexokinase isozyme

A

Hexokinase - outside the liver, lower km, energy needed by extrahepatic cell during low glucose
Glucokinase - liver is dominated by its presence, separate isozyme for glucose phosphorylation, storage needed by hepatic cells at high glucose, higher Km

22
Q

Glut 1

A

most important at fasting blood glucose levels

23
Q

Glucagon on metabolic pathways: Glycogen breakdown/synthesis

A

Liver
Breakdown - positive glycogen phosphorylase
Synthesis - negative glycogen synthase

24
Q

AMP

A

positive modulator for AMPK and AMPK kinases

25
Q

Major reactions of glycolysis

A

Hexokinase, Phophofructokinase I, Pyruvate Kinase

26
Q

AMPK-P Energy consuming procceses

A

Pancreas (insulin secretion), Liver (FA, cholesterol synthesis), Adipose (FA syntehsis and lipolysis)

27
Q

Most energetic Steps in Krebs

A

Pyruvate DH, Citrate Synthase, Isocitrate DH, alpha-ketoglutarate DH

28
Q

Glucagon on metabolic pathways: Glycolysis/gluconeogenesis

A

liver
Glycolysis - negative PFK-1
Gluconeogenesis - positive FBPase-2,
negative - PEP carboxykinase (as well as transcription), pyruvate carboxylase, g-6-phosphatase (all transcription

29
Q

Insulin on metabolic pathways: Glucose uptake

A

Muscle, Fat – GLUT 4 positive

Liver - Glucokinase (transcription)

30
Q

Role and modulators of Pyruvate dehydrogenase phosphatase

A

Activate pyruvate DH via positive modulator insulin and Ca2+

31
Q

Glucokinase positive modulators

A

Insulin via transcription

32
Q

FBPase-2 modulator

A

Positive: FBPase-2

33
Q

Glut 4

A

important after a meal when insulin is released. Only depends on insulin in muscle and adipose. Stored in the ER and recruited to surface by insulin for glucose transport. Once insulin signal is gone it is brought back to the ER

34
Q

G-6-Phosphatase expression

A

only expressed in liver and kidneys

35
Q

Explain why pyruvate carboxylase should be active in the fasted states

A

Acetyl CoA is a positive modulator.
Muscle Fasted: Excess acetyl CoA from B-oxidation of FA and ketone bodies from the liver.
Liver Fasted: Excess acetyl CoA from B-oxidation of FA. Alanine from muscle makes pyruvate to OAA (using PC)
OAA can’t react with excess CoA because gluconeogenesis uses OAA to make glucose. Excess acetyl CoA used to make Ketone bodies

36
Q

GLUT 4 modulators

A

Positive: Insulin via transcription

37
Q

Insulin on metabolic pathways: Glycogen Synthesis/breakdown

A

Liver & Muscle – positive glycogen synthase, negative glycogen phosphorylase

38
Q

Modulators for Pyruvate DH

A

Positive: AMP, NAD+, CoA
Negative: ATP, NADH, Acetyl-CoA

39
Q

Hyperglycemic

A

no AMPK-kinases – Liver kianse B1 - stress stimulant

40
Q

Role and modulators of pyruvate dehydrogenase kinase

A

inactivate pyruvate DH via positive modulator ATP

41
Q

PFK-2 modulators

A

insulin positive modulator

42
Q

AMPK modulators

A

Positive: AMPK
negative: Phosphocreatine

43
Q

Insulin on metabolic pathways: Fatty acid synthesis

A

Liver

Positive: Citrate Lyase, acetyl-CoA carboxylase, FAS (transcription)

44
Q

Glut 2

A

important immediately after a meal when glucose levels increase and during gluconeogenesis

BFOM (15 decks)

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