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Biochem 2 > Starvation Well fed state > Flashcards

Starvation Well fed state Flashcards

1
Q

Mechanisms that Consume Energy at Synapses

A

The brain
2% of total body weight
20% of total oxygen and energy consumption

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2
Q

Compare Km of GLUT3 to that of GLUT1

A

Km GLUT3 < Km GLUT1

(Km is the concentration of substrate which permits the enzyme to achieve half Vmax)

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3
Q

Carbohydrate metabolism with neuron

A

Glycogen synthase
is inactive
(GS is hyperphosphorylated by GSK3 ➔ubiquitin-dependent proteasomal degradation )

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4
Q

LIPID METABOLISM
-> Name the structures in red circles

A
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5
Q

Carbohydrate metabolism with LDH1

A

decreased affinity for pyruvat
➔ enters into the citric acid cycle

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6
Q

Carbohydrate metabolism with PPP

A

pentose phosphate pathway
(➔ NADPH
➔ fatty acid synthesis, free radical protection)

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7
Q

Name of this cycle

A

glutamate-glutamin cycle

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8
Q

astrocyte-neuron network
-> Identify the substances

A
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9
Q

astrocyte-neuron network
-> Name these substances

A
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10
Q

Metabolism of intestinal epithelial cells
-> What is happening in the gut?

A

2 urea cycle enzyme:

  1. Carbamoylphosphate synthetase I (CPS1)
  2. Ornithine transcarbamylase (OTC) ➔ citrulline is produced
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11
Q

Metabolism of intestinal epithelial cells
-> What is happening in the kidney?

A

2 urea cycle enzyme:
1/ Argininosuccinate synthetase (ASS)
2/ Argininosuccinate lyase (ASL) ➔ from citrulline, arginine is produced

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12
Q

Role of glutamin in proliferating cells

A

The rates of utilization of both glucose and glutamine are high in rapidly dividing cells (enterocytes, lymphocytes, tumor cells)

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13
Q

What are “Brite” cells?

A

brown adipocytes surrounded by white fat tissue

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14
Q

Sites of de novo fatty acid synthesis

A

liver, adipose tissue

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15
Q

Schematic drawing of Adipose tissue metabolism in well fed state

A
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16
Q

Schematic drawing of Adipose tissue metabolism in starvation

A
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17
Q

Schematic drawing Triacylglycerol lipolysis

A

1) MAGL: Monoacylglycerol lipase
2) ATGL: Adipose triglyceride lipase
3) HSL: hormone sensitive lipase
4) CGI-58: comparative gene identification 58 (ATGL co-lipase)
5) PKA: protein kinase A

18
Q

Overview of acylglycerol biosynthesis
-> Name this substance

A

Glycerol-3-phosphate

19
Q

Is Glycerol kinase present in liver and adipose tissue?

A

Glycerol kinase present in liver but not in adipose tissue

20
Q

Conversion of glycerol
to the glycolytic intermediate dihydroxyacetone phosphate in liver
-> Name of this enzyme

A

Glycerol kinase

21
Q

Glyceroneogenesis Is Important for which process?

A

Triacylglycerol Biosynthesis

22
Q

The dihydroxyacetone phosphate used to make glycerol-3-phosphate for triacylglycerol synthesis comes ___ (2 sources)

A

1l/ Glucose via the glycolytic pathway
2/ Oxaloacetate via an abbreviated version of gluconeogenesis termed glyceroneogenesis

23
Q

How many phases does glucose homeostasis have?

A

5

24
Q

When is Glyceroneogenesis necessary?

A

Glyceroneogenesis
is necessary in times of starvation,
(when glycolysis is inhibited) since approximately
30% of the fatty acids that enter the liver during a
fast are reesterified to triacylglycerol and exported as VLDL.

25
Q

Can Adipocytes carry out glyceroneogenesis or glucogenesis in times of starvation?

A

Adipocytes also carry out glyceroneogenesis in times of starvation. They do not carry out gluconeogenesis

26
Q

Adipocytes do not carry out gluconeogenesis but contain ___

A

the gluconeogenic enzyme
phosphoenolpyruvate carboxykinase (PEPCK)

27
Q

Adipocytes do not carry out gluconeogenesis but contain the gluconeogenic enzyme
phosphoenolpyruvate carboxykinase (PEPCK)
-> What is the role of this enzyme?

A

This enzyme is upregulated when glucose concentration is low, and participates in the glyceroneogenesis required for triacylglycerol biosynthesis.

28
Q

Glucose homeostasis
-> Characteristics of phase I (Origin of blood glucose; tissues using glucose; major fuel of brain)

A

Origin of blood glucose: Exogenous
Tissues using glucose: All
Major fuel of brain: Glucose

29
Q

Glucose homeostasis
-> Characteristics of phase II (Origin of blood glucose; tissues using glucose; major fuel of brain)

A

Origin of blood glucose: Glycogen - Hepatic gluconeogenesis

Tissues using glucose: All except liver (muscle and adipose tissues at diminished rates)

Major fuel of brain: Glucose

30
Q

Glucose homeostasis
-> Characteristics of phase III (Origin of blood glucose; tissues using glucose; major fuel of brain)

A

Origin of blood glucose: Hepatic glucogenesis; Glycogen

Tissues using glucose: All except liver (muscle and adipose tissue at rates between II and IV)

Major fuel of brain: Glucose

31
Q

Glucose homeostasis
-> Characteristics of phase IV (Origin of blood glucose; tissues using glucose; major fuel of brain)

A

Origin of blood glucose: Gluconeogensis; glycogen

Tissues using glucose: Brains, RBCs, renal medulla, small amount by muscle

Major fuel of brain: Glucose, ketone bodies

32
Q

Glucose homeostasis
-> Characteristics of phase V (Origin of blood glucose; tissues using glucose; major fuel of brain)

A

Origin of blood glucose: Gluconeogensis, hepatic and renal

Tissues using glucose: Brain at diminished rate, RBCs, renal medulla

Major fuel of brain: Glucose, ketone bodies

33
Q

What does this slide indicate?

A

The fasting state: the glucogenic liver

34
Q

What does this slide indicate?

A

Fuel metabolism in the liver during prolonged fasting or in uncontrolled diabetes mellitus

35
Q

Metabolic characteristics of starvation in hepatocytes
-> What are the substance and adrenergic receptors being used?

A

Glucagon

adrenergic receptors: beta2 alpha 1

36
Q

Metabolic characteristics of starvation in hepatocytes
-> The role of pyruvate- carboxylase

A

anaplerotic carboxylation of pyruvate to oxaloacetate during starvation: gluconeogesis

37
Q

Metabolic characteristics of starvation in hepatocytes
-> acetyl-CoA carboxylase is inhibited by __?

A

Inhibited by phosphorylation, high level of palmitil-CoA, low level of citrate

38
Q

Long term starvation➔ glucokinase expression is low or high?

A

Low

39
Q

Long term starvation ➔ glucokinase expression is low
-> what are the 2 consequences?

A

Refeeding➔glucose will not taken up by liver cells because glucokinase expression is low

Consequences 1:
➔ glucose is used by extrahepatic tissue and lactate is produced (pyruvate dehydrogenase is inhibited, the source of acetyl-CoA is fatty acid breakdown during starvation)
➔ lactate enters liver cells

  • Consequences 2:
    ➔ sudden elevation of glucose level in blood
    ➔ Insulin level elevates➔glycogen synthesis
40
Q

Metabolic characteristics of well- fed state in hepatocytes
-> Which substance is prominent?

A

Insulin

Biochem 2 (38 decks)

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