Anaerobic Glycolysis Puns

I just finished studying the citric acid cycle, and I pretty much have it memorized. Should I do the same for all of these other processes? Specifically, is it essential that I memorize all of the enzymes involved, and the yields from each step?

If there are other cellular process not listed here that are worth studying, please let me know.

Does anaerobic respiration only use glycolysis to then ferment, or are all steps used in aerobic respiration also used by anaerobic respiration? What's the difference?

I know this could be googled, but I've been getting mixed answers that hopefully some of you can clear up.

FA states that arsenic causes anaerobic glycolysis to produce 0 ATP on one page, and then two pages later finally details the MOA, which is inhibition of lipoic acid and the pyruvate dehydrogenase complex. But the pyruvate dehydrogenase complex just links glycolysis and the TCA cycle -- you would still get your net 2 ATP from glycolysis even if you can't enter the TCA cycle, correct? I'm unsure if this was an error of if I'm just not getting something. Thanks so much!

The front of the card asks for the net NADH produced through anaerobic glycolysis, and the original card says (2)

I have two sources (Crush Step 1 figure 2-18 and Rapid Review Biochemistry pg 67) that state that there would be NO NET NADH PRODUCTION WITH ANAEROBIC GLYCOLYSIS.

I know Zanki isn't vetted, and I know that it's got mistakes to be fixed, but I was wondering if anyone else noticed this errata?

I have suffered with neurological symptoms mimicking B12 deficiency since 18. It was precipitated by a vegan diet and courses of proton pump inhibitors (Stomach acid reducing medications)

My doctors said I fit the bill for it but my B12 numbers were always high and did not fit the bill, My MRIs are also clean, and I have low inflammation markers and I’m not showing antibodies.

Despite a myriad of other issues like childhood ADHD, and severe anxiety in adulthood.

This confused me until I did a DNA test and found that I carry the MHTFR gene, I also have the PNO gene that reduces pyroxidine conversion to Pyroxidal-phosphate conversion in the liver.

P-5-P is directly involved in the synthesis of GABA, Serotonin and Dopamine. It also helps the body clear AGEs (Advanced glycation end products) that come from eating processed food, red meats and fried foods.

P-5-P also supports haemoglobin and restores oxygenation in cells. Cancer is one Avenue being researched with P-5-P because cancer cells are cells that shift to a state where they don’t use oxygen but fermentation and anaerobic glycolysis.

P-5-P levels are reduced in cancer, diabetes, Alzheimer’s, depression, Anxiety fibromyalgia, diabetes etc…

I’ve started taking 100mg of P-5-P along with 100mg magnesium and 40mg of riboflavin (Riboflavin restores MHTFR metabolism)

I’m worried about B6 toxicity ; I’ve seen one study (Cell study) which showed B6 toxicity is caused by the inactive form pyroxidine, inhibiting the active form pyroxidal-5-phosphate. B6 paradox, Supplementation with high pyroxidine inhibits B6 function.

Pyroxidine increases BAX and capase 8 two neurotoxic cell death signallers but not P-5-P.

There are studies of B6 deficiency epilepsy where 100mg/per kg cured the seizures but not pyroxidine (Most common form)

Should I be worried about just 100mg?

A site called BiosynergyPro, does dry blood testing. And he states he can see all whats going in in the body. If ones tissues are to acidic etc. And see if cells not are permeable enough, to take in nutrition etc!

Is there any science to back all this up?

He states this as an example:

"As blood sugar increases, oxygen delivery to your body decreases.

As oxygen delivery to your body decreases, energy production can drop up to 18 x due a very inefficient form of energy production called anaerobic glycolysis (intracellular fermenting of sugars).

Fermenting of sugars produce high levels of lactic acid as a byproduct.

This lactic acid starts to accumulate outside of the cells and in the tissues.

Acid tissues = even lower levels of oxygen at the tissue level.

Oxygen is the enemy of cancer, viruses and energy.

Start monitoring your blood sugar levels. You may be horrified at what you discover.

** MSM (organic sulfur) will pull lactic acid out of the body as quick as it's produced."

Seems really amazing if this is true tho 👍

I got a passage question asking "Which of the following is LEAST likely to occur in a muscle fiber that is metabolizing anaerobically?". Two of the wrong answers are:

a) "Depletion of stores of glycogen": Does glycogen get depleted in anaerobic respiration? I've never heard of this happening.

b) "Acidification of the cytoplasm": Is this because ATP gets hydrolyzed, but the H+ doesn't get pumped into ETC, so cytoplasm becomes acidic?

https://doi.org/10.1152/ajpheart.00100.2021

Abstract

Various skeletal muscle abnormalities are known to occur in heart failure (HF), and are closely associated with exercise intolerance. Particularly, abnormal energy metabolism caused by mitochondrial dysfunction in skeletal muscle is a cause of decreased endurance exercise capacity. However, to date, no specific drug treatment has been established for the skeletal muscle abnormalities and exercise intolerance occurring in HF patients. Sodium-glucose transporter 2 (SGLT2) inhibitors promote glucose excretion by suppressing glucose reabsorption in the renal tubules, which has a hypoglycemic effect independent of insulin secretion. Recently, large clinical trials have demonstrated that treatment with SGLT2 inhibitors suppresses cardiovascular events in patients who have HF with systolic dysfunction. Mechanisms of the therapeutic effects of SGLT2 inhibitors for HF have been suggested to be diuretic, suppression of neurohumoral factor activation, renal protection, and improvement of myocardial metabolism, but has not been clarified to date. SGLT2 inhibitors are known to increase blood ketone bodies. This suggests that they may improve the abnormal skeletal muscle metabolism in HF, i.e., improve fatty acid metabolism, suppress glycolysis, and utilize ketone bodies in mitochondrial energy production. Ultimately, they may improve aerobic metabolism in skeletal muscle, and suppress anaerobic metabolism and improve aerobic exercise capacity at the level of the anaerobic threshold. The potential actions of such SGLT2 inhibitors explain their effectiveness in HF, and may be candidates for new drug treatments aimed at improving exercise intolerance. In this review, we outlined the effects of SGLT2 inhibitors on skeletal muscle metabolism, with a particular focus on ketone metabolism.

I've noticed a distinct lack of science-related sets, so I've decided to make some. Here's a biology set. Someone who has taken a 101 level bio course should know most of these words.

abiogenesis,action potential,active site,active transport,adenosine,adrenaline,aerobe,agar,agonist,allele,allergen,alpha helix,amino acid,anabolism,anaerobe,animal,antagonist,antibody,antigen,aorta,apex predator,apoptosis,aqueous humor,archaea,artery,atrium,autotroph,axon,bacillus,bacteria,bacteriophage,beta sheet,bile,bilirubin,binary fission,bioaccumulation,biofilm,biology,biomagnification,biome,Calvin cycle,capillary,carbohydrate,cardiovascular system,catalase,cell,cellular respiration,cellulose,cell wall,central dogma,central nervous system,centriole,cerebrum,chitin,chlorophyll,chloroplast,chromosome,cilia,circadian rhythm,coccus,codon,colony forming unit,community,competition,competitive exclusion principle,cortisol,cotyledon,crepuscular,CRISPR,crossing over,crystal violet,cuticle,cyanobacteria,cytoplasm,definitive host,denaturation,deoxyribonucleic acid,dermis,differentiation,diffusion,digestion,digestive system,diploid,disk diffusion test,diurnal,dopamine,ecosystem,embryo,endangered,endemic,endocrine system,endoplasmic reticulum,endospore,endosymbiotic theory,endotherm,ectotherm,enzyme,epidemic,epidermis,erythrocyte,eukaryote,eusociality,eutrophication,evolution,excretion,exoskeleton,extinct,extremophile,fermentation,flagellum,food chain,food web,fossil,fruiting body,fungus,gamete,gametophyte,gel electrophoresis,gene,genetic drift,genotype,germinate,glycolysis,golgi apparatus,gonad,gradualism,Gram stain,habitat,haploid,hemoglobin,heterotroph,hibernation,histamine,histone,homeostasis,hormone,host,Hox gene,hypertonic,hypotonic,immune system,immunoglobulin,incubate,innoculation,insulin,intercalation,invasive species,isotonic,keratin,keystone species,kinesin,Krebs cycle,last common ancenstor,leucocyte,lichen,ligament,lignin,lipid,lysosome,macromolecule,macrophage,meiosis,membrane,migration,mitochondria,mitosis,molt,monocot,mRNA,mutation,mutualism,mycelium,natural selection,neuron,neurotransmitter,niche,nocturnal,nucleolus,nucleus,optic nerve,organ,organelle,osmosis,ovum,pandemic,parasite,parasympathetic nervous system,pathogen,peptidoglycan,peripheral nervous system,petri dish,phagocytosis,phenotype,phloem,phospholipid,photosynthesis,photosystem,phototropism,pioneer species,pistil,plankton,plant,plasma,plasmid,platelet,pollen,polymerase chain reaction,polypeptide,polyploi

I take sodium pyruvate for my mitochondrial disease. It helps because my body heavily relies on anaerobic glycolysis and having some extra pyruvate bolsters that effect. It's possible that it is only beneficial when consuming a normal high complex carb diet. It's also possible that it's beneficial in ketosis too.

That being said, would pyruvate be gluconeogenic substrate in a ketotic state? Or will it be converted to acetyl-coenzyme A? The acetyl-CoA would not enter the Krebs cycle and convert to oxaloacetate, though, right? Because oxaloacetate is downregulated in ketosis. The acetyl-CoA is metabolized into ketone bodies, right?

So what determines whether the pyruvate will be used in gluconeogenesis or in generation of ketone bodies? I want to know what happens in "normal" people and what people might think would happen in mitochondrial complex I deficiency.

If the pyruvate is perhaps used for both, maybe minimizing gluconeogenesis with metformin will bolster the acetyl-CoA:ketone activity. Unfortunately, I'm largely immune to the AMPK activating effects of metformin, because its mechanism of action for doing so is through inhibition of complex I. Not much there to inhibit in my case.

Any insight will be appreciated, thanks.

For years I thought that anaerobic glycolysis was when there was insufficient oxygen and pyruvate was converted to lactate, and aerobic glycolysis was when there was sufficient oxygen in the presence of mitochondria, and pyruvate went into the mitochondria, then went through TCA cycle and oxphos. These definitions were based mostly on textbooks (many textbooks) and what professors told me. HOWEVER, I'm coming across several sources that say that aerobic glycolysis is when there is sufficient oxygen in the presence of mitochondria, and pyruvate gets converted to lactate anyway (the attached image is one such example of this latter definition, from an MIT paper from 2011; I'll post a link to the article in the comments). Also, fwiw, searching aerobic glycolysis in Wikipedia redirects to aerobic fermentation, which lists the latter definition. Any information to help clarify this for me would be very much appreciated.

https://preview.redd.it/cpnwta9zbwk71.png?width=828&format=png&auto=webp&s=c17ab57c40f08bc0de3f2995a41d64990371775b

Do your worst!

For context I'm a Refuse Driver (Garbage man) & today I was on food waste. After I'd tipped I was checking the wagon for any defects when I spotted a lone pea balanced on the lifts.

I said "hey look, an escaPEA"

No one near me but it didn't half make me laugh for a good hour or so!

Edit: I can't believe how much this has blown up. Thank you everyone I've had a blast reading through the replies 😂

Most places say it’s classified as a particle, how come?

Pilot on me!!

Dad jokes are supposed to be jokes you can tell a kid and they will understand it and find it funny.

This sub is mostly just NSFW puns now.

If it needs a NSFW tag it's not a dad joke. There should just be a NSFW puns subreddit for that.

Edit* I'm not replying any longer and turning off notifications but to all those that say "no one cares", there sure are a lot of you arguing about it. Maybe I'm wrong but you people don't need to be rude about it. If you really don't care, don't comment.

What did 0 say to 8 ?

" Nice Belt "

So What did 3 say to 8 ?

" Hey, you two stop making out "

They’re on standbi

I won't be doing that today!

You take away their little brooms

This morning, my 4 year old daughter.

Daughter: I'm hungry

Me: nerves building, smile widening

Me: Hi hungry, I'm dad.

She had no idea what was going on but I finally did it.

Thank you all for listening.

There hasn't been a post all year!

I understand that the passage is king but we should understand the concept behind relevant foundational concepts too so my question is: how come complex I activity increases in a hypoxic state? And how could O2 consumption possibly increase when there is decreased O2 (indicated by hypoxic state)? I see that the graphs support this but tbh I didn't think much about the data and graphs honestly because I just figured that in a hypoxic state, aerobic respiration would decrease and vice versa and figured I could save time by using the fundamental concepts which is really helpful at times but it didn't work out here.

I was kind of using the approach that NDU was going to be associated with aerobic respiration and phosphoglucose isomerase (glycolysis enzyme) associated with anaerobic respiration. Can someone explain where I went wrong?

https://preview.redd.it/97901xirahb71.png?width=2452&format=png&auto=webp&s=1c8042b470b339a4fb6647c3eed953e1f7c507df

https://preview.redd.it/65f631jrahb71.png?width=2442&format=png&auto=webp&s=464aa2ffc36fbd4a8d2e3bf9529b81f9918bec97

It’s pronounced “Noel.”

After all his first name is No-vac

For full text go to http://www.aginganddisease.org/CN/abstract/abstract148117.shtml and click on [PDF].

Abstract：

> Coenzyme I (nicotinamide adenine dinucleotide, NAD+/NADH) and coenzyme II (nicotinamide adenine dinucleotide phosphate, NADP+/NADPH) are involved in various biological processes in mammalian cells. NAD+ is synthesised through the de novo and salvage pathways, whereas coenzyme II cannot be synthesised de novo. NAD+ is a precursor of coenzyme II. Although NAD+ is synthesised in sufficient amounts under normal conditions, shortage in its supply due to over consumption and its decreased synthesis has been observed with increasing age and under certain disease conditions. Several studies have proved that in a wide range of tissues, such as liver, skin, muscle, pancreas, and fat, the level of NAD+ decreases with age. However, in the brain tissue, the level of NADH gradually increases and that of NAD+ decreases in aged people. The ratio of NAD+/NADH indicates the cellular redox state. A decrease in this ratio affects the cellular anaerobic glycolysis and oxidative phosphorylation functions, which reduces the ability of cells to produce ATP. Therefore, increasing the exogenous NAD+ supply under certain disease conditions or in elderly people may be beneficial. Precursors of NAD+ have been extensively explored and have been reported to effectively increase NAD+ levels and possess a broad range of functions. In this review article, we discuss the pharmacokinetics and pharmacodynamics of NAD+ precursors.

What, then, is Chinese rap?

Edit:

Notable mentions from the comments:

• Spanish/Swedish/Swiss/Serbian hits

• French/Finnish art

• Country/Canadian rap

• Chinese/Country/Canadian rock

• Turkish/Tunisian/Taiwanese rap

There hasn't been a single post this year!

(Happy 2022 from New Zealand)

If it isn’t, what does?