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Biochemistry II > Fat Synthesis > Flashcards

Fat Synthesis Flashcards

1
Q

What are the two transport mechanisms for glucose in a cell?

A

Sodium independent facilitated transport system and Sodium-monosaccharide co-transport system (SGLT)

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2
Q

This glucose transport mechanism utilizes GLUT and moves glucose down a concentration gradient.

A

Sodium independent facilitated transport system

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3
Q

This glucose transport mechanism is ATP dependent, transports glucose against a concentration gradient and is found in the epithelial cells of intestines, renal tubules, and choroid plexus.

A

Sodium-monosaccharide co-transport system (SGLT)

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4
Q

This glucose transporter transports glucose, galactose, and fructose into the liver, kidney, and pancreas beta-cells and is insulin independent

A

GLUT 2

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5
Q

This glucose transporter transports glucose into muscle and adipose tissue, is stimulated by insulin and low energy charges (AMPkinase), and deals with facilitated diffusion

A

GLUT4

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6
Q

As long as the concentration of glucose is lower in muscle (and transporters are available) where will glucose go?

A

Glucose will move from the blood to the muscle

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7
Q

By adding a ____ to glucose, the glucose concentration in muscle remains low and glucose keeps coming in.

A

Phosphate

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8
Q

When muscle ____ is low, glucose 6 phosphate runs through glycolysis, prep step and Krebs to make more ATP.

A

Energy charge

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9
Q

When muscle glycogen is low, _____ is converted into glycogen.

A

Glucose 6 phosphate

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10
Q

About 90% of insulin-stimulated glucose uptake occurs where?

A

Skeletal muscle

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11
Q

Exercise increases the number of what glucose transporter in skeletal muscle?

A

GLUT4

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12
Q

When glucose is consumed and transported to muscle, if the muscle is full of glycogen what happens?

A

The glucose goes to the liver

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13
Q

When glucose is consumed and transported to muscle, if the muscle is not full of glycogen what happens?

A

Glucose is stored as glycogen

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14
Q

How do muscles say “no” to incoming glucose?

A
  • High energy charge will inhibit PFK
  • Glucose 6 phosphate accumulates
  • Hexokinase is inhibited
  • Inhibition of glucose 6 phosphate causes glucose to accumulate, which stops the flow of glucose from blood to muscle
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15
Q

This enzyme has a lower affinity for glucose, is not inhibited by its product, stimulated by insulin, and is stimulated by fructose.

A

Glucokinase

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16
Q

What primary tissues are involved with the synthesis of fatty acids?

A
  • Liver
  • To a lesser extend adipose tissue and kidneys
  • Mammary glands during lactation
17
Q

Where does the synthesis of fatty acids occur?

A

Cytosol

18
Q

What are the “ingredients” for the synthesis of fatty acids?

A
  • Two carbon pieces (acetyl)
  • Electrons (NADPH)
  • Energy (ATP)
19
Q

What are the steps of fatty acid synthesis?

A

-Sugar runs through glycolysis
-Prep step to make acetyl CoA
-Kreb’s cycle
-Citrate is made
-Too much ATP causes Kreb’s cycle to slow
Citrate is kicked out of the mitochondria
-Two carbon acetyl CoA is given back to start fat synthesis
-Acetyl CoA is converted to malonyl CoA
-Malonyl CoA is given to fatty acid synthase (FAS), which adds them to a growing fatty acid

20
Q

What enzyme in the Kreb’s cycle is inhibited by ATP, resulting in citrate accumulating?

A

Isocitrate dehydrogenase

21
Q

What enzyme converts acetyl CoA to malonyl CoA?

A

Acetyl CoA carboxylase

Coenzyme: Biotin

22
Q

What is the rate limiting step of fatty acid synthesis?

A

Acetyl CoA carboxylase

23
Q

What is acetyl CoA carboxylase activated by? Deactivated by?

A

Citrate; Long chain fatty acyl CoA

24
Q

Short term regulation of acyl CoA carboxylase involves what type of process? What are some examples?

A

Reversible phosphorylation

  • AMPK phosphorylates and inactivates acyl CoA carboxylase (ACC)
  • Epinephrine and glucagon increase cAMP, which phosphorylates and inactivates ACC
  • Insulin dephophorylates and activates ACC
25
Q

What are some ways acyl CoA carbocylase (ACC) is regulated over the long term?

A
  • High calorie/high carb diet increases ACC synthesis which increases fatty acid synthesis. Low calorie/low carb diet does the opposite
  • Upregulated by insulin: increased response/increased receptors (sterol regulatory element-binding protein (SREBP-1))
26
Q

What stimulates acetyl CoA carboxylase?

A

Citrate and Insulin

27
Q

What inhibits acetyl CoA carboxylase?

A
  • Malonyl CoA
  • Palmitoyl CoA
  • Epinephrine
  • Glucagon
28
Q

This substance is involved in type II diabetes and inhibits ACC leading to activation of AMPK, a decrease of SREBP-1, and a lowering of blood glucose.

A

Metformin

29
Q

This multienzyme complex contains an acyl carrier protein, is similar to coenzyme A, and has a terminal thiol group at the end of an “arm”.

A

Fatty acid synthase

30
Q

What are the first three reactions that set the stage for fatty acid synthesis?

A

1) Acetyl group (2C) is transferred to the thiol group on ACP by acetyl CoA-ACP acetyl transacylase
2) Acetyl group moved to a temporary holding site on a cysteine residue on the enzyme
3) Malonyl group (3C) transferred to the thiol group on ACP by malonyl-CoA-ACP transacylase

31
Q

What are the last four reactions of fatty acid synthsis?

A
  • Condensation: Acetyl ACP and Malonyl ACP are converted to Acetoacetyl-ACP by beta-ketoacyl-ACP synthase
  • Reduction: Acetoacetyl-ACP is converted to D-3-hydroxybutyryl-ACP by beta-ketoacyl-ACP reductase
  • Dehydration: D-3-hydroxybutyryl-ACP is converted to crotonyl-ACP by beta-hydroxyacyl-ACP dehydratase
  • Reduction: crotonyl-ACP is converted to butyryl-ACP by enoyl-ACP reductase
32
Q

After the last four reactions of fatty acid synthesis (condensation, reduction, dehydration, reduction) we have a four carbon molecule (butyryl). What happens to this molecule?

A

It is transferred to a holding site (cysteine), another malonyl is added, and the steps are repeated until it is 16 carbons long (Palmitate, 16:0)

33
Q

Release of the fatty acid is the last step in fatty acid synthesis. How is this accomplished?

A

The thioester bond of palmitoyl-S-ACP is cleaved by palmitoyl thioesterase releasing the saturated palmitate.

34
Q

Where does the NADPH needed for fatty acid synthesis come from?

A
  • Pentose phosphate pathway

- Malate–>pyruvate in the cytosol

35
Q

How is palmitate elongated?

A

Elongases. NADPH is required

36
Q

How is palmitate desaturated?

A

Desaturases (adds double bonds)

37
Q

Can humans create double bonds beyond the 9th-10th carbon?

A

No

38
Q

What is the primary site for fructose disposal?

A

Liver

39
Q

What enzymes are essential for fructose metabolism and are highly expressed in the liver?

A

Fructokinase and triokinase

Biochemistry II (16 decks)

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