Ester Production, Acetyl CoA, and Yeast Growth

I was wondering if anyone could help clarify the relationship between ester production and cell growth/Acetyl CoA availability.

Acetate ester production requires Acetyl CoA and Acetyl CoA is also involved in/required for cell growth. I've read, from various sources, that Acetyl CoA is limited in cells and that if cells are actively growing it is mostly tied up in growth (ie. not available for ester formation). Accordingly, more cell growth = less ester formation.

I've also read (on Wyeast's webpage for example), the opposite - that increased cell growth (ie. from under-pitching) results in higher ester formation:

"The pitch rate will have a direct effect on the amount of cell growth during a fermentation. Cell growth decreases as pitch rates increase. Ester production is directly related to yeast growth as are most other flavor and aroma compounds.

A low pitch rate can lead to:
Excess levels of diacetyl
Increase in higher/fusel alcohol formation
Increase in ester formation
Increase in volatile sulfur compounds
High terminal gravities
Stuck fermentations
Increased risk of infection

High pitch rates can lead to:
Very low ester production
Very fast fermentations
Thin or lacking body/mouthfeel
Autolysis (Yeasty flavors due to lysing of cells)

With some beer styles, where a complex ester profile is desirable (German Wheat) it can be beneficial to under pitch...."

This seems contradictory to the limited Acetyl CoA/ester production is negatively correlated with yeast growth theory above. Any thoughts??

Acetyl-CoA is two things: acetate, and Coenzyme A. The Coenzyme is not consumed. It's job is to shuttle around the breakdown product of sugars from metabolism. Sugar is broken down (anaerobically, without oxygen necessary) into pyruvate, which can be reduced to an acetate attached to Coenzyme A to make acetyl-CoA.

Now, the fate from here is variable. If oxygen is present, the acetate can be fully broken down into CO2 and water. If oxygen is not present it needs to be turned into something else so the CoA can be reused. It's these "something elses" that lead to a lot of the byproducts from yeast. The human body turns it into lactic acid when your muscles run out of oxygen, for example.

Now, I don't know much about the specific biochemistry of yeast, and what they choose to do with their sugars. They may very well be so used to working anaerobically that a lot of the acetate from acetyl-CoA goes to making esters and suchlike even before they run out of oxygen, as they rush along trying to reproduce in the most efficient way possible. Once they have finished expanding they have time to sit around and re-digest the less energy-dense chemicals they have created.

phasedweasel: I've been looking tirelessly for a good reference on yeast metabolism that doesn't necessarily require a degree in organic chemistry to understand. You seem knowledgeable, do you have any recommendations? Or anyone else on the board, for that matter?

There were some good Brew Science forum discussions about it. Here's one and here's another (this second one is more general and not just about esters). Stoutaholic seems to know this subject well.

There is conflicting info (or at least appears conflicting) about ester formation. Kaiser made a comment in one of those threads that he was told that ester formation vs. pitch rate is not linear but rather a U-shaped curve, with a minimum in the middle and increased esters on each end.

I have heard the same about the u-curve, and that it's also strain dependent, probably causing the conflict. Neat stuff.

Thanks for all of the input! I found an article that explains the situation quite well. According to the authors, the substrates for acetate ester production, Acetyl CoA and fusel alcohol, are not the limiting factors rather it is the regulation of a pair of genes, alcohol acetyl trasnferases I and II (ATF1 and ATF2). Expression of these genes is repressed (and ester production decreased) by oxygen and unsaturated fatty acids while glucose and nitrogen addition and lowering of fermentor top pressure all serve to increase both yeast growth and ester production.

It's a great article and there's lots of other useful information too. Check it out: http://www.jstage.jst.go.jp/article/jbb/96/2/96_110/_article/-char/en

Pisty_Pete said:

Thanks for all of the input! I found an article that explains the situation quite well. According to the authors, the substrates for acetate ester production, Acetyl CoA and fusel alcohol, are not the limiting factors rather it is the regulation of a pair of genes, alcohol acetyl trasnferases I and II (ATF1 and ATF2). Expression of these genes is repressed (and ester production decreased) by oxygen and unsaturated fatty acids while glucose and nitrogen addition and lowering of fermentor top pressure all serve to increase both yeast growth and ester production.

It's a great article and there's lots of other useful information too. Check it out: http://www.jstage.jst.go.jp/article/jbb/96/2/96_110/_article/-char/en

Click to expand...

Great find, that's exactly what I was looking for.

Agreed, good find Pete. Can't wait to read it.

Pisty_Pete said:

Thanks for all of the input! I found an article that explains the situation quite well. According to the authors, the substrates for acetate ester production, Acetyl CoA and fusel alcohol, are not the limiting factors rather it is the regulation of a pair of genes, alcohol acetyl trasnferases I and II (ATF1 and ATF2). Expression of these genes is repressed (and ester production decreased) by oxygen and unsaturated fatty acids while glucose and nitrogen addition and lowering of fermentor top pressure all serve to increase both yeast growth and ester production.

It's a great article and there's lots of other useful information too. Check it out: http://www.jstage.jst.go.jp/article/jbb/96/2/96_110/_article/-char/en

Click to expand...

Thanks!!! This is exactly what I was looking for today! Some Sunday reading as my beer ferments!:cross:

Cheers everyone! thanks for all the input.