What hormone controls fatty acid levels?

[Jbarrie]

Is it

A)cortisol
B)epinephrine
C)Insulin
D)Glucagon

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[Czarcasm]

Is it

A)cortisol
B)epinephrine
C)Insulin
D)Glucagon

C: Insulin (acts via metabotropic receptor to increase GLUT4 in fat cells).

 

[mcloaf]

You could make a case for at least three of those answers. Where is this question from?

 

[Czarcasm]

You could make a case for at least three of those answers. Where is this question from?

Yeah, I was thinking cortisol too but decided against it since it's only active during periods of chronic stress while insulin, which is regularly secreted, seemed like the better answer choice. Just wondering, what's the third though? Glucagon and epinephrine both mobilize energy.

 

[Czarcasm]

Ah nevermind. I read that as increase fatty acid levels, not controls. Changes the whole approach to the question.

 

[mcloaf]

Yeah, I was thinking cortisol too but decided against it since it's only active during periods of chronic stress while insulin, which is regularly secreted, seemed like the better answer choice. Just wondering, what's the third though? Glucagon and epinephrine both mobilize energy.

If I had to pick just one answer I'd choose epi via hormone sensitive lipase, but it's reasonable to say that insulin and glucagon have significant effects on blood fatty acids (I guess some quibble about whether glucagon has its own effects or if these are just the effects of low insulin, but I'm not an expert).

I left cortisol open since it has such wide ranging effects on metabolism.

 

[Jbarrie]

I got it from a TPR workbook I borrowed from a friend. The correct answer was cortisol.
Explanation: cortisol influences carbohydrate, protein, and fat metabolism. One effect of cortisol is to stimulate gluconeogenesis . Increased gluconeogenesis in turn causes an increased formation of glycogen in the liver. In addition cortisol causes an increased release of fatty acids from fat cells. I feel like this question was super tricky.

 

[mcloaf]

I feel like this question was super tricky.

It's not really tricky so much as simply wrong. Honestly, I'd proceed with caution in any resource that gives you questions as bad as this.

 

[justadream]

@Czarcasm
@mcloaf
So is the answer both insulin and cortisol?

What about glucagon? Would it do the opposite of what insulin does (promote fatty acid uptake)?

Also, wouldn't epinephrine work as well?

"However, when hormones such as epinephrine are secreted, or when insulin levels drop in response to low blood glucose levels, this triggers an intracellular secondary messenger cascade that phosphorylates hormone-sensitive lipase to break triglycerides into glycerol and free fatty acids for use in metabolism, a process called lipolysis"

http://en.wikipedia.org/wiki/Fatty_acid_metabolism

 

[Czarcasm]

@Czarcasm
@mcloaf
So is the answer both insulin and cortisol?

What about glucagon? Would it do the opposite of what insulin does (promote fatty acid uptake)?

Also, wouldn't epinephrine work as well?

"However, when hormones such as epinephrine are secreted, or when insulin levels drop in response to low blood glucose levels, this triggers an intracellular secondary messenger cascade that phosphorylates hormone-sensitive lipase to break triglycerides into glycerol and free fatty acids for use in metabolism, a process called lipolysis"

http://en.wikipedia.org/wiki/Fatty_acid_metabolism

From what I can remember, adipose cells do not synthesize their own FA. After a fatty meal, chylomicrons from the small intestines travel through lacteals, through lymph vessels and eventually into blood via the jugular vein. Various cells have a type of lipase on their surface that allows them to take up these FA. Whatever FA remains (chylomicron remnants) is taken up by the liver and repackaged into lipoproteins (along with cholesterol and TAG's synthesized by the liver). A little more detail from wikipedia:

Chylomicrons carry triglycerides (fat) from the intestines to the liver, to skeletal muscle, and to adipose tissue.
Very-low-density lipoproteins (VLDL) carry (newly synthesised) triglycerides from the liver to adipose tissue.
Intermediate-density lipoproteins (IDL) are intermediate between VLDL and LDL. They are not usually detectable in the blood when fasting.
Low-density lipoproteins (LDL) carry 3,000 to 6,000 fat molecules (phospholipids, cholesterol, triglycerides, etc.) around the body. LDL particles are sometimes referred to as "bad" lipoprotein because concentrations, dose related, correlate with atherosclerosis progression.

So that explains how adipose cells receive FA's to begin with (they don't synthesize it).

The action of insulin is to promote anabolic (biosynthetic) processes. It therefore activates glycogenesis (formation of glycogen), promotes the formation of lipids and aminoacids, but inhibits gluconeogenesis and glycolysis.

Epinephrine is released during times of immediate stress via activation of sympathetic nervous system. The SNS stimulates the adrenal medulla (chromaffin) cells to release epinephrine into the blood. This allows quick mobilization of energy for the "fight or flight" response. It promotes glycolysis and glycogenolysis (breakdown of glycogen) to increase blood glucose so cells that are in dire need of nutrition get it (brain, skeletal muscle, heart).

Cortisol is released in times of chronic stress (prolonged stress) and it's primary function is to ensure there is a steady reserve of energy so we don't run out. So, to back up the actions of epinephrine, it promotes glyconeogenesis (formation of glycogen), gluconeogenesis (formation of glucose from non-glucose sources including proteins and FA), and glycolysis.

Finally, glucagon acts in an antagonistic fashion to insulin. Beta cells are stimulated to release insulin when blood glucose levels are high (particularly after a meal). As insulin levels drop, glucagon levels increase to increase blood glucose to maintain a constant flow of glucose in blood.

With all that in mind, I still think the most appropriate answer to this question is insulin. Earlier I said insulin activates GLUT4 synthesis for uptake of glucose in fat cells (adipose cells store some glycogen), but the primary source of TAGs that are stored in adipose cells come from the lipoproteins floating in the blood. These lipoproteins are produced and packaged under appropriate conditions, particularly when blood glucose levels are high.

 

[Jbarrie]

It's not really tricky so much as simply wrong. Honestly, I'd proceed with caution in any resource that gives you questions as bad as this.

Thanks I basically threw this source out. Its littered with errors.

 

[Jbarrie]

From what I can remember, adipose cells do not synthesize their own FA. After a fatty meal, chylomicrons from the small intestines travel through lacteals, through lymph vessels and eventually into blood via the jugular vein. Various cells have a type of lipase on their surface that allows them to take up these FA. Whatever FA remains (chylomicron remnants) is taken up by the liver and repackaged into lipoproteins (along with cholesterol and TAG's synthesized by the liver). A little more detail from wikipedia:



So that explains how adipose cells receive FA's to begin with (they don't synthesize it).

The action of insulin is to promote anabolic (biosynthetic) processes. It therefore activates glycogenesis (formation of glycogen), promotes the formation of lipids and aminoacids, but inhibits gluconeogenesis and glycolysis.

Epinephrine is released during times of immediate stress via activation of sympathetic nervous system. The SNS stimulates the adrenal medulla (chromaffin) cells to release epinephrine into the blood. This allows quick mobilization of energy for the "fight or flight" response. It promotes glycolysis and glycogenolysis (breakdown of glycogen) to increase blood glucose so cells that are in dire need of nutrition get it (brain, skeletal muscle, heart).

Cortisol is released in times of chronic stress (prolonged stress) and it's primary function is to ensure there is a steady reserve of energy so we don't run out. So, to back up the actions of epinephrine, it promotes glyconeogenesis (formation of glycogen), gluconeogenesis (formation of glucose from non-glucose sources including proteins and FA), and glycolysis.

Finally, glucagon acts in an antagonistic fashion to insulin. Beta cells are stimulated to release insulin when blood glucose levels are high (particularly after a meal). As insulin levels drop, glucagon levels increase to increase blood glucose to maintain a constant flow of glucose in blood.

With all that in mind, I still think the most appropriate answer to this question is insulin. Earlier I said insulin activates GLUT4 synthesis for uptake of glucose in fat cells (adipose cells store some glycogen), but the primary source of TAGs that are stored in adipose cells come from the lipoproteins floating in the blood. These lipoproteins are produced and packaged under appropriate conditions, particularly when blood glucose levels are high.

Thanks for setting time aside to explain all the answer choices. Very Helpful.