# Effect of Cordyceps militaris Extract on Visceral Adipose Tissue Changes After Ovariectomy in Rodents

**Authors:** Kazuya Kusama, Chisaki Fujii, Kanoko Yoshida, Mikihiro Yoshie, Yoshiyuki Adachi, Hiroaki Miyaoka, Kazuhiro Tamura

PMC · DOI: 10.1155/ije/6699051 · 2026-01-29

## TL;DR

Cordyceps militaris extract may help reduce obesity and related risks in postmenopausal women by targeting fat and hormone changes in mice.

## Contribution

This study demonstrates that Cordyceps militaris extract can mitigate estrogen deficiency-induced obesity in ovariectomized mice.

## Key findings

- CM reduced body weight gain in ovariectomized mice without affecting food intake.
- CM suppressed adipogenic markers and oxidative stress in visceral fat.
- CM increased uterine weight and antioxidant levels in treated rats.

## Abstract

The increasing global prevalence of obesity, exacerbated by factors such as high‐fat diets and reduced physical activity, poses a substantial risk for lifestyle‐related diseases, particularly in postmenopausal women. Premenopausal women initially have a lower incidence of cardiovascular disease than men, but this risk increases after menopause, highlighting menopause as a critical risk factor. Our previous study showed that the extract of Cordyceps militaris (CM) modulates androgen metabolism partially by inhibiting the gene expression of catabolizing enzyme 5α‐reductase. In this study, we investigated the effect of CM on estrogen deficiency‐induced obesity in ovariectomized (OVX) mice fed a 0.1% CM diet (estimated human equivalent dose: 7.5 g/day) for 52 days. OVX mice had increased body weight, which subsequently decreased with CM, without altering daily food intake. Regarding visceral fat, CM suppressed OVX‐induced adipogenic markers (Pparg, Cebpa, Cebpb, Fabp4, and Adipoq) and protein levels of C/EBPβ, PPARγ, and p‐AKT. CM effectively reversed the OVX‐induced reduction in the levels of adipose Cyp17a1 and Hsd17b1, key enzymes involved in steroid hormone biosynthesis, increased the cellular senescence markers p21 and p53, and decreased Lmnb1 expression. CM reduced the expression of oxidative stress markers HO‐1, NRF2, and 4‐HNE. Moreover, CM increased uterine weight and serum superoxide dismutase in 17β‐estradiol‐treated OVX rats. These findings suggested that CM, particularly its component cordycepin, holds promise as a natural agent for mitigating weight gain, particularly in the context of postmenopausal obesity.

## Linked entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050], CEBPB (CCAAT enhancer binding protein beta) [NCBI Gene 1051], FABP4 (fatty acid binding protein 4) [NCBI Gene 2167], ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370], CYP17A1 (cytochrome P450 family 17 subfamily A member 1) [NCBI Gene 1586], HSD17B1 (hydroxysteroid 17-beta dehydrogenase 1) [NCBI Gene 3292], CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026], TP53 (tumor protein p53) [NCBI Gene 7157], LMNB1 (lamin B1) [NCBI Gene 4001], HMOX1 (heme oxygenase 1) [NCBI Gene 3162], GABPA (GA binding protein transcription factor subunit alpha) [NCBI Gene 2551]
- **Proteins:** CEBPB (CCAAT enhancer binding protein beta), PPARG (peroxisome proliferator activated receptor gamma), Akt (Akt kinase)
- **Chemicals:** cordycepin (PubChem CID 6303), 17β-estradiol (PubChem CID 154274)
- **Diseases:** obesity (MONDO:0011122), cardiovascular disease (MONDO:0004995)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** estrogen (MESH:D056828), weight gain (MESH:D015430), cardiovascular disease (MESH:D002318), obesity (MESH:D009765)
- **Chemicals:** cordycepin (MESH:C058120), steroid hormone (MESH:D013256), 4-HNE (-), 17beta-estradiol (MESH:D004958)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116], Mus musculus (house mouse, species) [taxon 10090]

## Figures

12 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12853315/full.md

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Source: https://tomesphere.com/paper/PMC12853315