Lactiplantibacillus pentosus CECT 8039 attenuates weight gain and adipokine markers in a murine diet-induced obesity model
In HFD-fed mice over 28 days, L. pentosus BB supplementation was associated with 13.2% lower relative body-weight gain and an 85.5% reduction in circulating leptin compared with the HFD control group.
| Population | C57BL/6 mice (in vivo) and STC-1 and Caco-2/THP-1 cell models (in vitro); dynamic multi-compartment colonic fermentation model inoculated with human microbiota |
|---|---|
| Intervention | Lactiplantibacillus pentosus CECT 8039 (L. pentosus BB) administered for 28 days (in vivo) or as treatment in the fermentation model |
| Comparator | HFD control group without probiotic supplementation (in vivo); stabilization condition without probiotic (in vitro) |
| Outcome | Relative body-weight gain; Circulating leptin; Circulating resistin; Circulating adiponectin; Colonic SCFAs (acetate, propionate, butyrate); GLP-1 release (STC-1 cells); Pyy and Cck mRNA expression |
Summary of findings
| Outcome | Effect | 95% CI | Certainty | Clinical relevance | Notes |
|---|---|---|---|---|---|
| Relative body-weight gain | MD -13.2 ± 4.7% vs HFD control; 95% CI not reported | — | Very low | — | 1 studies |
| Circulating leptin | reduction 85.5 ± 20.1% vs HFD control; 95% CI not reported | — | Very low | — | 1 studies |
| Circulating resistin | reduction 25.8 ± 9.4% vs HFD control; 95% CI not reported | — | Very low | — | 1 studies |
| Circulating adiponectin | change not statistically significant; exact values not reported | — | Very low | — | 1 studies |
| Colonic SCFAs (acetate, propionate, butyrate) | fold-change vs stabilization: acetate 2.53x, propionate 7.34x, butyrate 5.08x (ascending colon); 95% CI not reported | — | Very low | — | 1 studies |
| GLP-1 release (STC-1 cells) | statistically significant increase in transverse-colon condition only; exact values and 95% CI not reported | — | Very low | — | 1 studies |
| Pyy and Cck mRNA expression | Cck: significant increase in all 3 compartments; Pyy: significant increase in ascending and descending colon conditions; exact values and 95% CI not reported | — | Very low | — | 1 studies |
Context
Diet-induced obesity is associated with dysfunction of the microbiota–enteroendocrine axis. Microbiota-derived SCFAs modulate satiety hormones including GLP-1, PYY, and CCK. Identifying probiotics that intervene in this axis is relevant for adjunct metabolic management strategies.
What the study showed
In vivo, HFD mice without probiotic gained 34.9 ± 5.5% body weight; the probiotic group showed 13.2 ± 4.7% lower relative gain (95% CI not reported). Circulating leptin decreased 85.5 ± 20.1% and resistin 25.8 ± 9.4% in the probiotic vs. HFD group; adiponectin change did not reach statistical significance. In the fermentation model, acetate, propionate, and butyrate increased 2.53×, 7.34×, and 5.08× in the ascending colon post-probiotic. GLP-1 release reached statistical significance only under the transverse-colon condition; Pyy mRNA increased significantly in ascending and descending compartments; Cck increased in all three.
How it was done
Multi-platform preclinical study: (1) dynamic multi-compartment colonic fermentation model with inoculated human microbiota; (2) STC-1 cells and Caco-2/THP-1 co-culture exposed to fermentation samples; (3) mice fed HFD for 28 days with or without L. pentosus BB supplementation. Murine sample size not specified in the provided text; in vivo duration was 28 days.
Effect magnitude
13.2 ± 4.7% reduction in relative weight gain and 85.5 ± 20.1% reduction in leptin; no 95% CIs reported for any in vivo outcome, precluding precision assessment.
Risk of bias
Absence of 95% CIs and standardized effect sizes for in vivo outcomes. Murine n not specified in the abstract, limiting power assessment. The fermentation model is simulated and does not fully replicate the human intestinal environment. No formal risk-of-bias tool (RoB 2 or ROBINS-I) applies to this preclinical study, but absence of described randomization and blinding limits internal validity. SCFA-mediated causality is not established.
What this study does NOT prove
This study does not prove clinical efficacy in humans with obesity, nor does it establish direct causality between SCFA increases and the observed metabolic outcomes. Results in C57BL/6 HFD mice are not directly extrapolable to the human population.
In clinical practice
Data are exclusively preclinical (murine and cellular); there is no basis for clinical recommendation of L. pentosus BB in patients with obesity. Clinicians should await controlled clinical trials in humans before any therapeutic adoption.
Limitations
Absence of 95% CIs and standardized effect sizes for in vivo outcomes. Murine n not specified in the abstract, limiting power assessment. The fermentation model is simulated and does not fully replicate the human intestinal environment. No formal risk-of-bias tool (RoB 2 or ROBINS-I) applies to this preclinical study, but absence of described randomization and blinding limits internal validity. SCFA-mediated causality is not established.
What is still missing
RCTs in humans with obesity evaluating L. pentosus BB on weight, adipokine, and fecal SCFA outcomes. Dose-response and long-term safety studies are needed.
Technical appendix
Version history
- 1.0 · 2026-10-14 — Auto-generated under Evidence Standard v1.0