Dr. Axe Wire · Study decoded · gut
Liver Enzyme Nearly 70% Higher in Children With Obesity
A biomarker study links childhood obesity to higher liver stress enzymes and widespread changes in gut bacteria and blood chemistry.

- What they found: Kynurenine and 3-nitrotyrosine, tied to inflammation and oxidative stress, rose.
- Who was studied: 57 Mexican children grouped by weight: 15 normal weight, 8 overweight, 34 with obesity.
Children with obesity showed a liver stress marker nearly 70% higher than normal-weight peers, plus widespread gut bacteria and blood chemistry shifts, according to an Integrated multi-omics analysis reveals distinct metabolic signatures and gut microbiome alterations across the pediatric obesity spectrum published November 1, 2026 in Gut Microbes.
Researchers studied 57 Mexican children by BMI: 15 normal weight, 8 overweight, 34 with obesity. The team ran liver enzyme panels, untargeted stool and blood chemical profiling, gut bacteria gene sequencing, and antibiotic-resistance testing, with demographics comparable across groups. Gamma-glutamyl transferase, or GGT, a liver stress marker, measured 25.5 U/L in children with obesity versus 15.0 U/L in normal-weight children, a gap of nearly 70%. Profiling found 1,088 altered stool compounds and 1,041 altered blood compounds comparing children with obesity to normal-weight children, touching amino acid processing, energy metabolism and nucleotide pathways. Kynurenine and 3-nitrotyrosine, tied to inflammation and oxidative stress, rose; bile acids and purine-related compounds fell. Sequencing found 78, 95 and 28 differing gut bacteria types across overweight-vs-normal, obese-vs-overweight, and obese-vs-normal comparisons, with the bacterial mix growing more scattered in obesity.
Specific gut bacteria tracked closely with specific gut chemicals, including one bacterial family linked to a short-chain fatty acid gut microbes make from fiber, and another genus linked to a bile acid byproduct. The authors said these pairings map to pathways connecting short-chain fatty acids, bile acids and amino acid byproducts to obesity biology. Short-chain fatty acids generally help maintain the gut lining and regulate inflammation; this study did not test whether restoring them changes outcomes in children.
Liver Stress Enzyme Nearly 70% Higher in Children With Obesity
This cross-sectional snapshot compares groups at one timepoint, showing a link, not proof that obesity causes these biomarker or bacterial patterns. Each group was small, especially the 8 overweight children, so larger studies with more children in each group are a logical next step.
Dr. Axe’s Take
A liver enzyme nearly 70% higher in kids with obesity, paired with gut bacteria that lose their short-chain-fatty-acid producers, tells me the gut and liver are under stress together in childhood obesity, not separately. I'd watch fiber intake closely in kids carrying extra weight: vegetables, beans, berries and whole grains feed the bacteria that make protective fatty acids, while cutting refined carbs and added sugar eases pressure on the liver. I'd also ask a pediatrician about tracking liver enzymes as part of routine bloodwork for kids above a healthy weight. Pair that with daily movement and regular meal timing.
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Study summary
- Who
- 57 Mexican children: 15 normal weight, 8 overweight, 34 with obesity; demographics comparable across groups
- Design
- Observational, cross-sectional biomarker study with liver enzyme testing, stool and blood chemical profiling, gut bacteria gene sequencing and antibiotic-resistance testing
- Dose
- Not applicable; no intervention given, biomarkers measured at one timepoint
- Primary result
- Liver stress enzyme GGT: 25.5 U/L in children with obesity vs 15.0 U/L in normal-weight children, about 70% higher
- Secondary
- 1,088 altered stool compounds and 1,041 altered blood compounds (obese vs normal weight); 78, 95 and 28 gut bacteria types differed across the three group comparisons
- Funding / conflicts
- Funder listed in the journal record: Fundación Gonzalo Río Arronte. Conflicts not reported in the abstract.
- Date
- Nov 1, 2026



