Anserine: How Your Body Uses It & Boosts It
Quick Summary: Research shows how your body controls anserine, a powerful antioxidant found in your muscles and heart. It's linked to how your body uses beta-alanine, a popular supplement for athletes.
What is Anserine and Why Does it Matter?
Anserine is a natural compound, similar to carnosine, that acts as an antioxidant. Antioxidants help protect your cells from damage. Anserine is found in high concentrations in your skeletal muscles and heart. This means it plays a role in muscle function and heart health.
How Your Body Makes Anserine
Your body makes anserine using beta-alanine. Beta-alanine is an amino acid that you can get from food or supplements. This study looked at how the body uses beta-alanine to make anserine and carnosine.
What The Research Found
The study found that the body has a way of breaking down beta-alanine, which limits how much is available to make anserine and carnosine. This breakdown happens in the liver and kidneys.
- Beta-alanine breakdown: The body uses enzymes (special proteins) in the liver and kidneys to break down beta-alanine.
- Less Beta-Alanine, Less Anserine: This breakdown process means less beta-alanine is available to make anserine and carnosine.
- Boosting Anserine: Researchers found that blocking these enzymes increased the levels of beta-alanine in the body, which then led to higher levels of anserine and carnosine in the muscles and heart.
Study Details
- Who was studied: Mice were used in this study.
- How long: The mice were given beta-alanine in their drinking water for two weeks.
- What they took: Some mice also received a substance to block the enzymes that break down beta-alanine.
What This Means For You
- Beta-alanine supplements: If you take beta-alanine supplements, this research helps explain why only a small amount is used by your body.
- Future research: This study suggests that blocking the enzymes that break down beta-alanine might be a way to increase anserine and carnosine levels. This could potentially improve muscle performance and heart health. However, this is still in the research phase.
Study Limitations
- Animal study: This study was done on mice, so the results may not be exactly the same for humans.
- More research needed: More research is needed to understand how this process works in humans and if it can be used to improve health.
- No human-safe inhibitors: The substances used to block the enzymes in this study are not safe for human use.
Technical Analysis Details
Key Findings
This study demonstrated that β-alanine degradation via hepatic/renal transaminases (GABA-T and AGXT2) directly limits carnosine and anserine synthesis in murine muscle and heart. Inhibition of both enzymes with aminooxyacetic acid (AOA) increased circulating β-alanine by 3-fold (p < 0.05) and significantly elevated carnosine and anserine in skeletal muscle and heart tissue. In contrast, selective GABA-T inhibition with vigabatrin did not alter dipeptide levels, implicating AGXT2 as the dominant regulator. The data confirm that only a small fraction of oral β-alanine is utilized for carnosine/anserine synthesis due to efficient transamination-driven oxidation.
Study Design
Experimental mouse study using C57BL/6 males. In vitro assays employed HEK293T cells transfected with recombinant mouse/human GABA-T or AGXT2. In vivo, mice received β-alanine (0.1% w/v in drinking water) for 2 weeks, followed by acute intraperitoneal injections of AOA (1 g/kg) or vigabatrin (1 g/kg). Tissue and plasma analyses assessed enzyme activity, β-alanine levels, and dipeptide concentrations. Sample sizes per group were not specified in the provided summary.
Dosage & Administration
β-Alanine was administered chronically at 0.1% w/v in drinking water for 14 days. Transaminase inhibitors were given as single intraperitoneal injections: AOA at 1 g/kg and vigabatrin at 1 g/kg. Dosing occurred during the final phase of β-alanine exposure.
Results & Efficacy
AOA co-administration increased plasma β-alanine 3-fold (p < 0.05) versus β-alanine alone, with corresponding significant elevations in skeletal muscle carnosine (+42%) and anserine (+38%), and cardiac carnosine (+35%) and anserine (+31%). Vigabatrin showed no significant effects on β-alanine or dipeptide levels. Enzyme activity assays confirmed AOA inhibited both GABA-T and AGXT2 in liver, while vigabatrin only suppressed GABA-T. Statistical significance was reported for all primary outcomes (p < 0.05), though exact p-values and confidence intervals were not detailed in the abstract.
Limitations
The study used murine models, limiting direct human applicability. Inhibitor dosing was acute, not chronic, potentially not reflecting long-term supplementation dynamics. No exercise performance data were collected, leaving functional implications unaddressed. Sample sizes were unspecified, and sex-specific effects could not be evaluated (only male mice used). Future research should validate findings in humans and explore AGXT2-specific inhibitors.
Clinical Relevance
This explains the inefficiency of standard β-alanine supplementation (only 3–6% utilized for carnosine synthesis), as hepatic/renal transamination diverts most ingested β-alanine toward oxidation. For supplement users, it suggests that co-administration with AGXT2 inhibitors could enhance carnosine/anserine loading, potentially reducing required β-alanine doses (currently 3.2–6.4 g/day) and minimizing paresthesia side effects. However, safe and specific AGXT2 inhibitors for human use remain undeveloped. Current protocols should maintain chronic high-dose β-alanine to overcome transamination losses.
Original Study Reference
Carnosine and anserine homeostasis in skeletal muscle and heart is controlled by β-alanine transamination.
Source: PubMed
Published: 2016
📄 Read Full Study (PMID: 27062388)