The AtlasAmino acidsNonpolar, aliphatic

AlanineAla · A

The amino acid with a single methyl group: the carrier that brings muscle’s nitrogen and carbon to the liver, the substrate of ALT, and, in its mirror form, the target of vancomycin.

Status Reference · not yet an episodeSources 37Reviewed October 2026

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Skeletal formula — every corner and every line end is a carbon, and the hydrogens on carbon are left implied.

Molecule · Ala · 6 heavy atoms

Alanine

C₃H₇NO₂89.09 g/mol

The amino acid with a single methyl group: the carrier that brings muscle’s nitrogen and carbon to the liver, the substrate of ALT, and, in its mirror form, the target of vancomycin.

Built fromthe charted ones open their own entry

C3CarbonH7Hydrogen N Nitrogen O2Oxygen

Codes: Ala · A
Formula: C₃H₇NO₂
Molar mass: 89.09 g/mol
Systematic name: (2S)-2-aminopropanoic acid
Side chain: Methyl: a single carbon; small and nonpolar.
Class: Nonpolar, aliphatic
In the diet: Dispensable
Carbon skeleton: Glucogenic
pKa: α-COOH 2.34 · α-NH₃⁺ 9.69
Isoelectric point: pH 6.01
Hydropathy: +1.8 (Kyte–Doolittle)
Codons: GCU GCC GCA GCG

pKa and isoelectric point: Nelson and Cox, Lehninger Principles of Biochemistry, table of amino acid properties (free amino acid, 25 °C). Hydropathy: Kyte and Doolittle, J Mol Biol 1982. Essentiality: Reeds, J Nutr 2000. Formula and mass computed from the structure.

In brief

What it is

An amino acid with a methyl group for a side chain: small, nonpolar and uncharged. The body makes it from pyruvate by transamination, in one step ¹.

Why it matters

Alanine is the main amino acid muscle releases and the liver takes up to make glucose, the glucose–alanine cycle ^2,3. Its enzyme, alanine aminotransferase, is ALT, the most commonly measured marker of liver injury ⁴. And D-alanine, its mirror image, is the part of the bacterial cell wall that vancomycin grips ⁵.

Where it runs short

In children with ketotic hypoglycemia, the commonest form of low blood sugar in childhood, fasting alanine was low and an alanine infusion restored blood glucose, pointing to a shortage of the substrate rather than a failure of the liver ⁶.

Where it turns

In fatty liver, impaired amino acid disposal raises plasma alanine, and alanine stimulates glucagon, a feedback loop between liver and pancreas called the liver–α-cell axis ^7,8.

A molecule that is a fuel line between organs is also a reading of how well the liver and the mitochondria are working.

The molecule

Alanine is the second-simplest amino acid: glycine with a methyl group. The methyl adds a stereocentre and a little bulk without any reactive group, which makes alanine a neutral, compact building block that proteins fold easily around.

It is the strongest helix former of all the amino acids, by a small margin over leucine and arginine ⁹.

Charge · pHAlanine carries almost no net charge at the pH of blood.

Move across the chart to read the charge at any pH.

Computed from its pKa values (α-carboxyl 2.34, α-amino 9.69) by the Henderson–Hasselbalch equation, for the free amino acid in water at 25 °C. Inside a folded protein the same groups can shift by a unit or more. The faint lines are the other amino acids.

HydropathyAlanine scores +1.8: the 7th most water-avoiding of the twenty.

Kyte–Doolittle hydropathy index: positive values avoid water and tend to be buried inside a folded protein, negative values sit on its surface. Each letter is an amino acid; choose one to open it.

The genetic codeAlanine has 4 codons. The code is redundant, so most single-letter changes at the third position still write alanine.

The 64 codons of the standard genetic code. Codons for alanine are marked.
1st ↓ 2nd →	U	C	A	G	3rd
U	UUUPhe	UCUSer	UAUTyr	UGUCys	U
	UUCPhe	UCCSer	UACTyr	UGCCys	C
	UUALeu	UCASer	UAAStop	UGAStop	A
	UUGLeu	UCGSer	UAGStop	UGGTrp	G
C	CUULeu	CCUPro	CAUHis	CGUArg	U
	CUCLeu	CCCPro	CACHis	CGCArg	C
	CUALeu	CCAPro	CAAGln	CGAArg	A
	CUGLeu	CCGPro	CAGGln	CGGArg	G
A	AUUIle	ACUThr	AAUAsn	AGUSer	U
	AUCIle	ACCThr	AACAsn	AGCSer	C
	AUAIle	ACAThr	AAALys	AGAArg	A
	AUGMet	ACGThr	AAGLys	AGGArg	G
G	GUUVal	GCUAla	GAUAsp	GGUGly	U
	GUCVal	GCCAla	GACAsp	GGCGly	C
	GUAVal	GCAAla	GAAGlu	GGAGly	A
	GUGVal	GCGAla	GAGGlu	GGGGly	G

Where it comes from

Alanine is made from pyruvate, the end product of glycolysis, by transamination from glutamate. Two enzymes do it: ALT1, in the cytoplasm of liver cells, and ALT2, in mitochondria and found in muscle ^1,10.

Muscle makes alanine continuously from pyruvate and the amino groups of other amino acids broken down there; at rest, alanine alone accounted for 35 to 40% of the net amino acid exchange between the leg and the splanchnic organs ³.

DispensableMade from pyruvate by the two alanine aminotransferases, ALT1 in the cytoplasm and ALT2 in mitochondria ^1,10.

How much

None; the body makes it from pyruvate ¹⁰.

Where it is in food

All protein. Most dietary alanine is used by the gut and liver before it reaches the circulation ¹¹.

In the bottle · enzymatic or fermentedIndustrial L-alanine has mainly been made enzymatically from L-aspartic acid, itself derived from petroleum; fermentation from sugar in engineered Escherichia coli has been commercialized as an alternative ¹².

What the body does with it

Philip Felig’s studies around 1970 established alanine as the principal amino acid released by human muscle and extracted by the liver for gluconeogenesis, at rest, after a fast and after four to six weeks of starvation ². That is the glucose–alanine cycle: alanine carries both an amino group, for urea, and a carbon skeleton, for glucose, from muscle to liver ¹³.

In exercise the flow increases: across the working leg, alanine was the only amino acid consistently released at every intensity, and splanchnic alanine uptake exceeded that of any other amino acid ³.

Alanine also signals. It stimulates glucagon, and in fatty liver the liver’s impaired amino acid disposal raises alanine and glucagon together, a loop called the liver–α-cell axis ^7,8. Given intravenously, though, arginine stimulated glucagon more than an equal dose of alanine ¹⁴.

The glucose–alanine cycle also runs backwards as a signal, and the liver can stop listening. The glucagon–alanine index — fasting glucagon multiplied by fasting alanine — is a proposed read-out of hepatic glucagon resistance, on the logic that a liver that is ignoring glucagon lets alanine accumulate and glucagon rise together. In 46 Japanese people with type 2 diabetes it was examined against ultrasound steatosis and shear-wave elastography ¹⁵. Forty-six people is a pilot, and the index is at the stage where it is worth naming and not worth acting on.

In three sentences each

The glucose–alanine cycle

Muscle transfers amino groups to pyruvate to make alanine and sends it into the blood; the liver removes the amino group for urea and turns the pyruvate back into glucose. Of 20 amino acids, alanine was the main one released by muscle at rest and in starvation ^2,13.

More in exercise

During exercise, alanine was the only amino acid consistently released by working muscle, in proportion to the work load, and the liver’s uptake of it rose with it ³.

The best helix former

Among the twenty, alanine is the most favorable residue in an α-helix, and glycine, apart from proline, the least, by about 1 kcal/mol ⁹.

How it is made, moved and broken down

Swallowed alanine is mostly used by the gut and liver: in healthy adults the splanchnic bed extracted 69% of an enteral alanine tracer on first pass, and most of that was oxidized ¹¹.

Carbon skeleton · glucogenicTransamination returns it to pyruvate, the starting point of gluconeogenesis ². Given by mouth, most is oxidized: 86% of an enteral alanine tracer was recovered as CO₂ ¹¹.

The glucose–alanine cycleMuscle to liver and back ^2,13.

Pyruvate + glutamate (muscle)
Alanine aminotransferase 2GPT2 · vitamin B6
Alanine + 2-oxoglutarate
Alanine aminotransferase 1GPT · vitamin B6
Pyruvate + glutamate
GluconeogenesisPC, PCK1, G6PC · ATP, GTP
Glucose, back to muscle

D-alanine in bacteriaThe target of vancomycin and D-cycloserine ^5,16.

L-Alanine
Alanine racemasealr · vitamin B6
D-Alanine
D-Ala-D-Ala ligaseddl · ATP
D-Ala-D-Ala

Where it matters most

Muscle: Main exporter of alanine, more so during exercise ^2,3.
Liver: Main consumer, for gluconeogenesis and urea; ALT1 is cytosolic in hepatocytes ^2,10.
Brain: Mitochondrial ALT2 is needed for brain growth; its loss causes microcephaly and intellectual disability ¹.
Pancreatic α-cells: Alanine stimulates glucagon, linking liver and α-cell ⁷.

When it goes wrong

Too little

Ketotic hypoglycemia of childhood

In affected children fasting plasma alanine was lower than in controls and fell further before they became hypoglycemic on a low-carbohydrate diet; an alanine infusion restored blood glucose, consistent with a shortage of gluconeogenic substrate ⁶.

How it is foundFasting glucose, ketones and alanine ⁶.

Inherited

GPT2 deficiency

GPT2 · autosomal recessive

Intellectual and developmental disability with postnatal microcephaly, and in about 80% a progressive spastic paraplegia; mice without the enzyme have small brains, low alanine and defects in replenishing the Krebs cycle ¹.

How it is foundExome sequencing; low plasma alanine ¹.

Biomarker

Raised ALT without liver disease

One hour of weightlifting raised AST, ALT, LDH, CK and myoglobin significantly for a week in healthy men, enough to be mistaken for drug-induced liver injury ¹⁷.

How it is foundCK alongside ALT; repeat after rest ¹⁷.

Drug

Alanine for hypoglycemia in type 1 diabetes

Because alanine releases glucagon, 40 g by mouth was tested for hypoglycemia in type 1 diabetes. It raised glucose slowly and steadily rather than quickly ¹⁸; as a bedtime dose with a little glucose it tended to keep glucose higher in the second half of the night, not significantly, while terbutaline did ¹⁹.

How it is measured

Alanine is measured in the plasma amino acid panel ²⁰, but the measurement that matters clinically is ALT. Its “normal” range is contested: upper limits drawn from healthy, lean people are much lower than laboratory ranges ⁴, and in US survey data even ALT values within conventional limits tracked rising rates of fatty liver and fibrosis ²¹. Exercise, muscle injury and macroenzymes can all raise it without liver disease ^10,17.

The number itself is not standardized. There is no universal agreement on the upper limit of normal for ALT, and reference values vary roughly two-fold between institutions — from 30 to 60 U/l — because laboratories built their ranges on different reference populations using different analysers and assays ²². A result reported as normal in one hospital can be reported as raised in another, from the same blood.

That matters most where a threshold decides treatment. Two linked systematic reviews commissioned to inform the 2024 WHO guidelines on chronic hepatitis B examined how well antiviral therapy works according to baseline HBV DNA and ALT, precisely because the 2015 guidance withheld treatment from people with persistently normal ALT and low viral load ²³. An unstandardized cut-off is a clinical decision wearing a laboratory's clothes.

And in the commonest liver disease of all, the enzyme is the thing that did NOT predict what happened. In a multicentre cohort of patients with metabolic dysfunction-associated steatotic liver disease and liver stiffness of at least 8 kPa, one-year changes in liver stiffness predicted liver-related events over the following years — and one-year changes in ALT and in the controlled attenuation parameter did not ²⁴. Watching the transaminase fall is not the same as watching the disease retreat.

A LOW ALT has its own meaning, which is usually missed because the reference range is one-sided in practice. In 653 adults aged 55 and over, serum ALT activity and its isoenzymes were lower in those with sarcopenia, and the enzyme is after all a muscle enzyme as well as a liver one ²⁵.

ALT (alanine aminotransferase)Measured to assess liver injury; with AST it defines a hepatocellular pattern ²⁶.A raised ALT predicts liver-related death ²⁶. Upper limits drawn from truly healthy people, 30 U/L for men and 19 U/L for women, picked up hepatitis C viremia better than the conventional 40 and 30 ⁴.The old ranges were set in populations that included people with undiagnosed liver disease ⁴. In US adults, steatotic liver disease rose from 17% at ALT 10 U/L or less to 52% at 31 to 40, all “normal” ²¹. Weightlifting raised ALT and AST for at least a week in healthy men ¹⁷, and the standard assay cannot tell liver ALT from muscle ALT ¹⁰.
Plasma alaninePart of the amino acid panel ²⁰.Low in ketotic hypoglycemia; low in GPT2 deficiency ^1,6.

Food, supplements and the evidence

Establishedreplicated in people, for a named outcome

Glucose, not alanine, is the right first treatment for hypoglycemia; alanine’s effect is slow ¹⁸.

Uncertainsmall, short, mixed, surrogate or preclinical

β-Alanine, an isomer, for high-intensity exercise lasting one to four minutes ²⁷.
β-Alanine for strength and power, where the question has moved from whether to how much. A 2025 systematic review of nine studies in 197 trained participants argues that dosing strategy rather than duration is what separates the trials that work from the ones that do not, at 4 to 6.4 g a day split through the day ²⁸. That is a hypothesis about why the literature disagrees with itself, not yet a demonstration that it is right.

Sold asthe claim on the label, against the evidence

“β-Alanine for sprints, and β-alanine with creatine for everything.” On repeated sprint ability — short, maximal, repeated efforts, which is exactly what the buffering story predicts it should help — a multilevel meta-analysis of 17 randomized trials found no effect on mean performance, peak performance or fatigue decrement, unmoved by dose, duration, exercise mode or training status ²⁹. On the stack, a network meta-analysis of 52 trials in trained adults compared creatine alone, β-alanine alone and both together ³⁰. Buying two things does not make either of them work better than the trials say it does.
Note that none of this is about alanine. β-Alanine is an isomer with its amino group on the far carbon, it is not proteinogenic, and the body makes it from aspartate with an enzyme that has nothing to do with the glucose–alanine cycle ³¹. A label saying “alanine” and a label saying “beta-alanine” are two different molecules sold for two unrelated reasons, and the shelf rarely says so.

What is strange about it

D-alanine, alanine’s mirror image, is how bacteria finish their cell walls: two D-alanines at the end of each precursor are joined in the cross-linking step. Vancomycin works by gripping that D-Ala-D-Ala end, and resistant bacteria swap the last D-alanine for D-lactate or D-serine ^5,32. The tuberculosis drug D-cycloserine kills by blocking the enzyme that joins the two D-alanines ¹⁶.

β-Alanine, sold to athletes, is not alanine at all but an isomer with the amino group one carbon further along; it is the building block of carnosine, not of protein, and in excess, in hyper-β-alaninemia, it is toxic ^27,33.

BMAA, a non-protein amino acid built on alanine and made by cyanobacteria, is suspected of contributing to the ALS–parkinsonism–dementia complex of Guam, and living near water bodies with cyanobacterial blooms has been linked to ALS risk in case–control studies ^34,35.

Ketotic hypoglycemia, the commonest cause of low blood sugar in a previously healthy small child, has quietly stopped being a diagnosis. Ketosis and hypoglycemia on prolonged fasting are now understood as NORMAL physiology in young children, and the term covers both the low end of that normal distribution and a growing list of rare disorders of fasting adaptation that molecular genetics has pulled out of it ³⁶. The name survives; what it means has changed underneath it.

β-Alanine's own biology has been examined by removing it. GADL1 is the enzyme that decarboxylates aspartate to β-alanine in brain and muscle, and deleting it in mice lowers carnosine and anserine across tissues — and, on metabolomic, transcriptomic and proteomic analysis of three brain regions, perturbs energy and lipid metabolism widely and in a sex-specific way ³¹. The supplement aisle treats β-alanine as a buffering precursor; the mouse that cannot make it has a different problem entirely.

There is one place β-alanine's famous side effect may be the point. Aquagenic pruritus — itching triggered by contact with water — has almost no effective treatment, and case reports and a patient survey describe relief with prophylactic oral β-alanine. A 2026 viewpoint proposes the mechanism, through MrgprD-expressing sensory neurons and mast-cell regulation, and is careful to call itself a proposal ³⁷. The paraesthesia that athletes tolerate as a nuisance acts on the same system.

Where it connects

In the Atlas

GlyGlycineNonpolar, aliphatic SerSerinePolar, uncharged AspAspartateNegatively charged GluGlutamateNegatively charged HisHistidinePositively charged

Topics on the map

On the map

A star in The rest of the amino acids, one of 6. Muscle ships nitrogen to the liver as alanine, and the liver makes glucose from it. ALT, the liver test, is its enzyme; 'normal' ALT is set too high.

Find it on the map

Sources

37 sources, numbered as they are cited. Every one was checked against PubMed or its publisher before it was cited here; the note under each says what it shows and what it does not.

1
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GPT2 deficiency; mouse model.
2
Felig P, Pozefsky T, Marliss E, et al. Alanine: key role in gluconeogenesis.Science · 1970 · 167(3920):1003–1004doi:10.1126/science.167.3920.1003 · PMID 5411169
The principal amino acid released by muscle.
3
Felig P, Wahren J. Amino acid metabolism in exercising man.J Clin Invest · 1971 · 50(12):2703–2714doi:10.1172/JCI106771 · PMID 5129318
Alanine 35–40% of net amino acid exchange.
4
Prati D, Taioli E, Zanella A, et al. Updated definitions of healthy ranges for serum alanine aminotransferase levels.Ann Intern Med · 2002 · 137(1):1–10doi:10.7326/0003-4819-137-1-200207020-00006 · PMID 12093239
6,835 blood donors; 30 U/L men, 19 U/L women.
5
Stogios PJ, Savchenko A. Molecular mechanisms of vancomycin resistance.Protein Sci · 2020 · 29(3):654–669doi:10.1002/pro.3819 · PMID 31899563
D-Ala-D-Ala and its replacement.
6
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Eight children and seven controls.
7
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Review; alanine as a glucagonotropic amino acid.
8
Wewer Albrechtsen NJ, Færch K, Jensen TM, et al. Evidence of a liver-alpha cell axis in humans: hepatic insulin resistance attenuates relationship between fasting plasma glucagon and glucagonotropic amino acids.Diabetologia · 2018 · 61(3):671–680doi:10.1007/s00125-017-4535-5 · PMID 29305624
1,408 people.
9
Pace CN, Scholtz JM. A helix propensity scale based on experimental studies of peptides and proteins.Biophys J · 1998 · 75(1):422–427doi:10.1016/s0006-3495(98)77529-0 · PMID 9649402
Alanine 0, glycine 1 kcal/mol.
10
Glinghammar B, Rafter I, Lindström AK, et al. Detection of the mitochondrial and catalytically active alanine aminotransferase in human tissues and plasma.Int J Mol Med · 2009 · 23(5):621–631doi:10.3892/ijmm_00000173 · PMID 19360321
ALT1 and ALT2; the assay does not separate them.
11
Battezzati A, Haisch M, Brillon DJ, et al. Splanchnic utilization of enteral alanine in humans.Metabolism · 1999 · 48(7):915–921doi:10.1016/s0026-0495(99)90229-9 · PMID 10421236
Twelve adults; 69% first-pass extraction.
12
Liu P, Xu H, Zhang X. Metabolic engineering of microorganisms for L-alanine production.J Ind Microbiol Biotechnol · 2022 · 49(2):kuab057doi:10.1093/jimb/kuab057 · PMID 34410417
Enzymatic and fermentation routes.
13
Felig P. The glucose-alanine cycle.Metabolism · 1973 · 22(2):179–207doi:10.1016/0026-0495(73)90269-2 · PMID 4567003
The cycle described.
14
Suppli MP, Høgedal A, Bagger JI, et al. Intravenous arginine stimulates glucagon secretion more than equimolar alanine, leucine, glutamine, and proline.J Endocr Soc · 2025 · 9(10):bvaf139doi:10.1210/jendso/bvaf139 · PMID 40980546
Twelve men.
15
Hattori T, Hamaguchi M, Hashimoto Y, et al. Associations of fasting glucagon and the glucagon–alanine index with hepatic steatosis and liver stiffness in Japanese individuals with type 2 diabetes.Diabetes Obes Metab · 2026 · 28(8):7393–7402doi:10.1111/dom.70854 · PMID 42244477
46 people. The index is interesting; the sample is a pilot, and the paper says so.
16
Halouska S, Fenton RJ, Zinniel DK, et al. Metabolomics analysis identifies D-alanine-D-alanine ligase as the primary lethal target of D-cycloserine in mycobacteria.J Proteome Res · 2014 · 13(2):1065–1076doi:10.1021/pr4010579 · PMID 24303782
Ddl as the lethal target.
17
Pettersson J, Hindorf U, Persson P, et al. Muscular exercise can cause highly pathological liver function tests in healthy men.Br J Clin Pharmacol · 2008 · 65(2):253–259doi:10.1111/j.1365-2125.2007.03001.x · PMID 17764474
Fifteen men after one hour of weightlifting.
18
Wiethop BV, Cryer PE. Alanine and terbutaline in treatment of hypoglycemia in IDDM.Diabetes Care · 1993 · 16(8):1131–1136doi:10.2337/diacare.16.8.1131 · PMID 8375243
Oral alanine raised glucose slowly.
19
Saleh TY, Cryer PE. Alanine and terbutaline in the prevention of nocturnal hypoglycemia in IDDM.Diabetes Care · 1997 · 20(8):1231–1236doi:10.2337/diacare.20.8.1231 · PMID 9250445
Fifteen patients.
20
Sharer JD, De Biase I, Matern D, et al. Laboratory analysis of amino acids, 2018 revision: a technical standard of the American College of Medical Genetics and Genomics (ACMG).Genet Med · 2018 · 20(12):1499–1507doi:10.1038/s41436-018-0328-6 · PMID 30459394
Methods.
21
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NHANES; 5,245 adults with elastography.
22
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The same blood, the same enzyme, and a reference range that can differ two-fold between two hospitals.
23
Im YR, Chen SE, Jagdish R, et al. Efficacy of antiviral therapy in adults with chronic hepatitis B according to baseline hepatitis B virus DNA and alanine aminotransferase concentrations: a systematic review and meta-analysis.Lancet Gastroenterol Hepatol · 2026 · 11(5):397–416doi:10.1016/S2468-1253(25)00301-2 · PMID 41839198
Commissioned to inform the 2024 WHO guidelines. An ALT threshold decides who is offered treatment for a disease that kills slowly.
24
Pennisi G, Infantino G, Di Maria G, et al. One-year changes in liver stiffness measurement, but not in alanine aminotransferase and controlled attenuation parameter, predict long-term liver outcomes in patients with metabolic dysfunction-associated steatotic liver disease.Clin Gastroenterol Hepatol · 2026 · 24(9):2474–2485doi:10.1016/j.cgh.2026.01.020 · PMID 41621770
The title is the result, and the result is about the enzyme everyone watches.
25
Zeng J, Li N, Ge J, et al. Serum ALT activity and its isoenzymes as potential biomarkers for diagnosis of sarcopenia in older adults: a retrospective, cross-sectional study.BMC Geriatr · 2025 · 25(1):53doi:10.1186/s12877-025-05697-z · PMID 39844065
A low ALT in an older person may be saying something about muscle, not about liver.
26
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27
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Effects in one-to-four-minute efforts.
28
Ong SW, Chen WL, Chien KY, et al. Dosing strategies for β-alanine supplementation in strength and power performance: a systematic review.J Int Soc Sports Nutr · 2025 · 22(1):2566368doi:10.1080/15502783.2025.2566368 · PMID 40995761
Nine studies, 197 trained participants, asking whether the dose is the thing rather than the duration.
29
Liang W, Kong D, Wang Y, et al. No ergogenic effect of β-alanine on repeated sprint ability: a systematic review and multilevel meta-analysis of randomized controlled trials.Front Nutr · 2026 · 13:1818755doi:10.3389/fnut.2026.1818755 · PMID 41971372
Seventeen trials, three outcomes, no effect, and no moderation by dose or duration.
30
Bai X, Xu T. Effects of combined versus single supplementation of creatine and beta-alanine on aerobic and anaerobic performance: a systematic review and network meta-analysis.J Int Soc Sports Nutr · 2026 · 23(1):2695133doi:10.1080/15502783.2026.2695133 · PMID 42384726
52 trials, and the comparison the two supplements are usually sold as needing each other for.
31
Homaei SC, Mahootchi E, Srivastava A, et al. Blocking β-alanine synthesis triggers widespread perturbations of energy and lipid metabolism in the brain.Mol Metab · 2026 · 109:102383doi:10.1016/j.molmet.2026.102383 · PMID 42177944
The enzyme that makes β-alanine in the body, deleted, with the brain measured afterwards.
32
Zeng D, Debabov D, Hartsell TL, et al. Approved glycopeptide antibacterial drugs: mechanism of action and resistance.Cold Spring Harb Perspect Med · 2016 · 6(12):a026989doi:10.1101/cshperspect.a026989 · PMID 27663982
Vancomycin binds D-Ala-D-Ala.
33
Shetewy A, Shimada-Takaura K, Warner D, et al. Mitochondrial defects associated with β-alanine toxicity: relevance to hyper-beta-alaninemia.Mol Cell Biochem · 2016 · 416(1–2):11–22doi:10.1007/s11010-016-2688-z · PMID 27023909
Cell studies.
34
Zhang Y, Whalen JK. Production of the neurotoxin beta-N-methylamino-L-alanine may be triggered by agricultural nutrients: an emerging public health issue.Water Res · 2020 · 170:115335doi:10.1016/j.watres.2019.115335 · PMID 31812811
Review; epidemiological association.
35
Bradley WG, Miller RX, Levine TD, et al. Studies of environmental risk factors in amyotrophic lateral sclerosis (ALS) and a phase I clinical trial of L-serine.Neurotox Res · 2018 · 33(1):192–198doi:10.1007/s12640-017-9741-x · PMID 28527102
Case–control and phase I data.
36
Wolfsdorf JI, Derks TGJ, Drachmann D, et al. Idiopathic pathological ketotic hypoglycemia: finding the needle in a haystack.Horm Res Paediatr · 2024 · 98(3):246–257doi:10.1159/000538483 · PMID 38513624
What used to be a diagnosis is now, mostly, a description of normal childhood physiology — with rare real disorders hidden inside it.
37
Piserchio N, Baratta B, Brooks B, et al. Beta-alanine and aquagenic pruritus: proposed neuroimmune mechanism.JMIR Dermatol · 2026 · 9:e90737doi:10.2196/90737 · PMID 41880222
Case reports and a patient survey, and a viewpoint that says clearly it is proposing a mechanism rather than reporting a trial.

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