Authors
Eric Francelino Andrade, Hellen Paulo Silva, Thays Cristina Dos Santos, Karen Rodrigues Lima, Maíra Gabrielle de Abreu Ribeiro, Pedro Gustavo Machado, Maria Luiza Nonato Salvador, Jaqueline do Carmo Lima, Débora Ribeiro Orlando, Leonara Teixeira Alves, Elizabethe Adriana Esteves, Marco Fabrício Dias-Peixoto, Alan Rodrigues Teixeira Machado, Leonardo Barros Dobbss, Luciano José Pereira
Published in
Climacteric : the journal of the International Menopause Society. Pages 1-9. Jul 15, 2026. Epub Jul 15, 2026.
Abstract
Estrogen deficiency promotes metabolic dysfunction and bone loss. This study thus evaluated the effects of biomass-derived humic acid (HA) on ovariectomy-induced metabolic and bone alterations in mice.
Female C57BL/6 mice (n = 6/group) were assigned to Sham, Sham + HA, ovariectomized (OVX) or OVX + HA groups. Estrogen deprivation was induced by bilateral ovariectomy. After a 14-day recovery period, HA (80 mg/kg/day) was administered orally for 28 days. Body mass, food intake, serum glucose, lipid profile, creatinine, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Tibial calcium and phosphorus content and bone surface topography were assessed by scanning electron microscopy coupled with energy dispersive X-ray spectroscopy, and receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) staining intensity in the femoral head was evaluated by immunohistochemistry. Data were analyzed using two-way analysis of variance with the Bonferroni post hoc test.
OVX animals presented increased body mass gain, fasting glucose, dyslipidemia, creatinine and AST compared with Sham animals (p < 0.05). HA attenuated these alterations (p < 0.05) and reduced body weight gain. OVX-induced reductions in tibial mineral content and increased bone porosity were partially reversed by HA (p < 0.05), with a descriptive shift toward a less pro-resorptive RANKL/OPG staining profile.
Biomass-derived HA mitigates metabolic dysfunction and bone loss from estrogen deficiency, supporting its potential as adjunct therapy.
PMID:
42454408
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.
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