Mainly I'm confused about how much ATP is made per NADH, FADH2, and Acetyl-CoA, since I'm seeing different values online.

I'm going based on 2.5 per NADH, 1.5 per FADH2, and 10 per Acetyl-CoA.

However, I've seen 3 ATP/NADH, 2 ATP/FADH2, and 12 per Acetyl-CoA tossed around online!

Here's the rules I'm using... can someone please correct me if I'm wrong, or if I'm missing some rules for some special fatty acids?

I will use "C" to denote number of carbons in the fatty acid (FA):

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Even # of Carbons in FA:

• Acetyl-CoA = C / 2
  • Acetyl-CoA goes into Krebs & ETC --> Produces 3 NADH, 1 FADH2, and 1 ATP per Acetyl-CoA.
  • 10 ATP per Acetyl-CoA because [(3 NADH * 2.5) + (1 FADH2 * 2.5) + 1] = 10 ATP
• NADH = (C / 2) - 1
  • 2.5 ATP per NADH
• FADH2 = (C / 2) - 1 - (# of unsaturated pi bonds)
  • 1.5 ATP per FADH2
• -2 ATP investment

Example of Even # C: 16 C Palmitic acid

• 8 Acetyl-CoA * 10 = 80 ATP
• 7 NADH * 2.5 = 17.5 ATP
• 7 FADH * 1.5 = 10.5 ATP
• Investment = -2 ATP

Net ATP = 80 + 17.5 + 10.5 - 2 = 78 + 28 = 106 ATP

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Odd # of Carbons in FA:

• Acetyl-CoA = (C - 3) / 2
• Succinyl-CoA = 1; made from 3 Carbons
  • Succinyl-CoA goes into Krebs --> Produces 1 NADH + 1 FADH2
  • 4 ATP per Succinyl-CoA because 2.5 + 1.5 = 4 ATP
• NADH = (C / 2) - 1
  • 2.5 ATP per NADH
• FADH2 = (C / 2) - 1 - (# of unsaturated pi bonds)
  • 1.5 ATP per FADH2
• -2 ATP investment

Example of Odd # C: 15 C fatty acid with 2 double bonds

• 1 Succinyl-CoA = 4 ATP
• Acetyl-CoA = (15-3)/2 = 6 * 10/ATP = 60 ATP
• NADH = (15-3)/2 - 1 = 5 * 2.5/ATP = 12.5 ATP
• FADH = (15-3)/2 - 1 - (2 pi bonds) = 3 * 1.5/ATP = 4.5 ATP
• Investment = -2 ATP

Net ATP = 4 + 60 + 12.5 + 4.5 - 2 = 64 + 17 - 2 = 79 ATP

title, testing tmrw so any quick answer will help, thank u!

how much in detail would one recommend to study these? i have krebs, glycolysis, gluconeogenisis, glycogeneolysis/glycogenesis and pentose phosphate pathway memorized (intermediates and everything) but i was wondering how high yield these other 2 pathways are in terms of memorizing intermediates and enzymes... i understand the basic steps, i just haven't force memorized them yet.

edit: and ketogenesis? thank you!

How picky is the MCAT when using the terms fatty acids and ketone bodies? For example, during starvation, fatty acid degradation is maximized and tha brain uses mainly ketone bodies as an energy source due to glucose scarcity. In the MCAT, is the claim 'brain uses fatty acid as an energy source during starvation' conceptually equivalent to saying the brain uses ketone bodies as a source fuel during glucose depletion?

How would you calculate the total ATP for beta oxidation of one molecule which has double bonds? For example 20:2(🔺10,15) or 22:2(🔺10,15), etc?

I understand how to do it for a single bonds. Are there any short cuts for the double bonded ones?

Open Access

Review

Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas

by 📷Isabella D. Cooper 1,*📷,📷Kenneth H. Brookler 2 and📷Catherine A. P. Crofts 3📷1Translational Physiology Research Group, School of Life Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK2Research Collaborator, Aerospace Medicine and Vestibular Research Laboratory, Mayo Clinic, Scottsdale, AZ 85259, USA3School of Public Health and Interdisciplinary Studies, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland 0627, New Zealand*Author to whom correspondence should be addressed.Academic Editor: Susan J. BurkeBiomedicines 2021, 9(9), 1165; https://doi.org/10.3390/biomedicines9091165

Received: 22 July 2021 / Revised: 27 August 2021 / Accepted: 2 September 2021 /

Published: 6 September 2021

(This article belongs to the Special Issue Emerging Paradigms in Insulin Resistance)
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Abstract

Patients with type 2 diabetes mellitus (T2DM) and/or cardiovascular disease (CVD), conditions of hyperinsulinaemia, have lower levels of osteocalcin and bone remodelling, and increased rates of fragility fractures. Unlike osteoporosis with lower bone mineral density (BMD), T2DM bone fragility “hyperinsulinaemia-osteofragilitas” phenotype presents with normal to increased BMD. Hyperinsulinaemia and insulin resistance positively associate with increased BMD and fragility fractures. Hyperinsulinaemia enforces glucose fuelling, which decreases NAD+-dependent antioxidant activity. This increases reactive oxygen species and mitochondrial fission, and decreases oxidative phosphorylation high-energy production capacity, required for osteoblasto/cytogenesis. Osteocytes directly mineralise and resorb bone, and inhibit mineralisation of their lacunocanalicular space via pyrophosphate. Hyperinsulinaemia decreases vitamin D availability via adipocyte sequestra

Hey guys,

How much should we know about the beta oxidation and fatty acid synthesis pathways?

So far for FA synthesis, all I know is:

1. citrate shuttled out of mitochondria
2. converted to acetyl-coA --> malonyl-coA --> palmitate (rate limiting enzyme: acetyl-coA carboxylase)

And for FA oxidation, I know:

FA is cleaved into acetyl coA but that's it

Could someone clarify the details I should know?

Posting these to help anyone as much as they helped me! Please let me know if you think I am missing any important details or need to fix anything!!

Thanks in advance and happy studying!!!

https://preview.redd.it/ccplkefs1fc71.png?width=816&format=png&auto=webp&s=1f435e757b264f94ecd3acc60ea1609f0211eecd

https://preview.redd.it/2nbeuw8s1fc71.png?width=796&format=png&auto=webp&s=afe0884a0b11ca5c16b49937622ea50ad48f1f12

https://preview.redd.it/jfj9ur3s1fc71.png?width=818&format=png&auto=webp&s=63fa3dcbe61e94d650c0b00c812fdcf1f3483062

https://preview.redd.it/wnz7blzr1fc71.png?width=786&format=png&auto=webp&s=cd190317af8a80419edac35a9c8df3d7e4546149

What is the regulatory reaction of Beta oxidation? I tried searching it online but couldn't find anything. Any help would be greatly appreciated and thank you in advance.

I am currently going through beta-oxidation and all I really grasped out of it was this based on what my Princeton review book told me but I really feel like I am missing stuff. Is there anything else that I need to know?? I am lost and confused

https://preview.redd.it/wcfsjn4g0ta71.png?width=1056&format=png&auto=webp&s=e694e0e81caef36370e47a2ebc15a7776e46a3c4

Is it just me or is beta oxidation way more important than Kaplan gives it credit for? I feel like I’ve seen it as a passage on all of my NS FL’s so far. Granted it’s commonly used as a simple test of if you know what oxidation looks like, but still I feel like the beta oxidation presses and fatty chain synthesis are way more important then the credit they’re given.

What do you guys think?

SciTechDaily: Hidden Structure Found in Essential Metabolic Machinery – “I Didn’t Think It Was Real”. https://scitechdaily.com/hidden-structure-found-in-essential-metabolic-machinery-i-didnt-think-it-was-real/

Discovery “requires us to rethink everything we thought we knew about peroxisomes.”

In his first year of graduate school, Rice University biochemist Zachary Wright discovered something hidden inside a common piece of cellular machinery that’s essential for all higher order life from yeast to humans.

What Wright saw in 2015 — subcompartments inside organelles called peroxisomes — is described in a study published today in Nature Communications.

“This is, without a doubt, the most unexpected thing our lab has ever discovered,” said study co-author Bonnie Bartel, Wright’s Ph.D. advisor and a member of the National Academy of Sciences. “This requires us to rethink everything we thought we knew about peroxisomes.”

Peroxisomes are compartments where cells turn fatty molecules into energy and useful materials, like the myelin sheaths that protect nerve cells. In humans, peroxisome dysfunction has been linked to severe metabolic disorders, and peroxisomes may have wider significance for neurodegeneration, obesity, cancer and age-related disorders.

Much is still unknown about peroxisomes, but their basic structure — a granular matrix surrounded by a sacklike membrane — wasn’t in question in 2015. Bartel said that’s one reason Wright’s discovery was surprising.

Zachary Wright Zachary Wright is a postdoctoral research associate in Rice University’s Department of BioSciences. Credit: Photo by Jeff Fitlow/Rice University

“We’re geneticists, so we’re used to unexpected things. But usually they don’t come in Technicolor,” she said, referring to another surprising thing about Wright’s find: beautiful color images that show both the walls of the peroxisome subcompartments and their interiors. The images were possible because of bright fluorescent reporters, glowing protein tags that Wright employed for the experiments. Biochemists modify the genes of model organisms — Bartel’s lab uses Arabidopsis plants — to tag them with fluorescent proteins in a controlled way that can reveal clues about the function and dysfunction of specific genes, including some that cause diseases in people, animals and plants.

Wright, now a postdoctoral research associate in Bartel’s lab, was testing a new reporter in 2015 when he spotted the peroxisome subcompartments.

“I never

TL;DR Why is oxygen needed in those reactions?

Hi. I understand to both concepts, but there is still one thing what I cant figure out. In both cases, you need oxygen. My question is, why? In all steps of beta oxidation, you need only water, CoA, NAD, FAD and a of course a lot of enzymes. As for the aerobic glycolysis, I cant see any reason, why reaction needs oxygen, when it is only decarboxylation and then binding rest to the CoA. Thanks for your help.

Beta Oxidation

Beta (males follow) Only Hoes Only Thots

Oxidation Hydration Oxidation Thiolysis

I should be studying.

Sooo many specific questions about these in the SB. I memorized the rate limiting enzymes and the important intermediates but the SB asks even more specific. Does the real MCAT ask this too? Pls let me know what is the most important because I dont have time to memorize every single thing

Hello, if anyone can explain the processes of both Beta Oxidation of Fatty Acid Synthesis, I’d really appreciate it!! I’m having trouble understanding them and Kaplan’s explanation didn’t help me too much 😔 thank you in advance!

I understand that, for example, an 18-C carbon fatty acid would require 8 rounds.

What if we had a 17-C fatty acid?

If someone has an easy way to explain the deal with odd-C fatty acid oxidation it would be appreciated:)

I'm reading through the section on ketone bodies in the Kaplan biochem book. It says that the acetyl-CoA from fatty acid degradation cannot be used for gluconeogenesis and I'm very confused about why that is. Isn't pyruvate carboxylase literally activated by acetyl-CoA?

The book goes on to say that only odd-numbered fatty acids can act as a source of carbon for gluconeogenesis. Why?

I was told in my lecture today that "fats burn in the flame of carbohydrates" and I dont really understand why, Im familiar with the steps in both processes and dont see why one needs the other

I'm reading TBR's closing paragraph on beta-oxidation and it states the following:

https://preview.redd.it/f3srcdviisy41.png?width=940&format=png&auto=webp&s=a0c3e09de36161e938178022c7b35fb1ffee2f32

I don't understand why a basal level of carbohydrate degradation is required for beta-oxidation to continue. Carbohydrate degradation produces acetyl-CoA, NADH, FADH2, GTP - none of which are required for beta-oxidation to occur. In fact, shouldn't the presence of acetyl-CoA, NADH, and/or FADH2 inhibit beta-oxidation? And considering the other main substrate of beta-oxidation, it's the conversion of glycerol to pyruvate - pyruvate shunts into Krebs to form more acetyl-CoA.

Earlier, they state that acetyl-CoA from beta-oxidation enters the Krebs Cycle to eventually condense with OAA to form citrate - which loses 2 C via the a-KG and ICD complexes, and this is why we can't form carbohydrates from FAs. Conversely, they state, we can convert carbohydrates to acetyl-CoA and synthesize FA. But acetyl-CoA isn't needed for beta-oxidation??

Somehow, I'm just not able to wrap my head around it. Any help is appreciated. Thanks!

So I know beta-oxidation occurs in matrix and rate-limiting enzyme for beta-oxidation is carnitine acyltransferase ; fatty acid synthesis occurs in the cytosol and rate-limiting enzyme is acetyl-coa carboxylase which makes malonyl coa, is there anything else that is really high yield regarding these 2 pathyways that I should be aware of for the real deal?

For example in systemic primary carnitine deficiency, or in medium chain dehydrogenase deficiency. I don't fully understand the physiologic connection between them and hypoglycemia, am I missing something?

I just finished memorizing glycolysis, TCA, ETC/chemiosmosis, PPP.. And I cannot remember anything for FA synthesis and B-oxidation..

So I was wondering which steps do we need to remember in B-oxidation and F.A. Synthesis?

I know it's in the cytosol and mitochondria but which organs?

I was watching the KA video and was slightly overwhelmed with a details. Must we know the pathways as well as the enzymes, or just be familiar with the overall purpose of the process and the conditions under which they are favored?

Thank you for reading this. My question is based on human fatty acid metabolism (but mostly on the catabolism or 'burning' part). When the body is 'burning fat' i've heard that this is through beta-oxidation. When nutrition researchers discuss ketogenic diets (or starvation), they focus on ketone metabolism, pretty much ignoring beta oxidation. Curiously, when popular websites discuss fat burning in terms of nutrition, they equate ketosis to fat burning. But this leaves me confused.

.

if I understand correctly (maybe not):

• ketones are the product of acetyl-coa 'excess' in the liver that is shuttled to cells in the body and is then converted back to acetyl-coa and burned in the Krebs cycle.
• triglycerides in the cell break down to fatty acids which are in turn cleaved (via beta-oxidation) into units of acetyl-coa which is burned in the Krebs cycle.

this seems to suggest that ketone and fatty acid oxidation are different processes that (as far as i can see here) can run parallel to each other; barring any regulatory pathways like the one that 'favors' glycolysis to lipolysis.

so what am I missing here?

• does the body burn fatty acids and ketones in different pathways?

• are these pathways relatively disconnected (can one or both catabolize fatty acids in their own way, limited only by energy needs) or are they competitive as i understand glucose and fat to be?

• what would 'fat burning' (from a nutritionist's perspective) look like for those two pathways?

• and finally, do you have any good sources for more on this type of fatty acid and ketone metabolism I can focus on?

thank you so much!

(I apologize if I posted this in the wrong forum or if this question was asked before or if it's terribly ignorant. I tried to use my google fu to find it but found tons of stuff that didn't clarify the issue and most disucssions of beta oxidation ignored ketones and those that discussed ketones ignored beta oxidation for the most part. this is why i thought I'd ask. thanks again) edit: thank you for your responses!

Can someone explain how a 16 carbon palmitate molecule produces 8 acetyl CoA in 7 cycles when only 1 acetyl CoA is produced per cycle? Does the last cycle produce 2 acetyl CoA?

I am currently going through beta-oxidation and all I really grasped out of it was this based on what my Princeton review book told me but I really feel like I am missing stuff. Is there anything else that I need to know?? I am lost and confused

https://preview.redd.it/9ez1ve2crga71.png?width=1078&format=png&auto=webp&s=219fe63ba8aa1ad8482168f7f40aa213441aee0a