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Viral infections are recognized as contributing factors in the pathogenesis of metabolic diseases. Viruses causing chronic infection are particularly important due to their capacity to induce sustained inflammation. Especially individuals with obesity - who exhibit preexisting metabolic abnormalities, low-grade inflammation, and altered antiviral responses - are at increased risk of viral infection-induced metabolic complications. Despite these associations, the specific metabolic consequences of chronic viral infections in obesity remain insufficiently characterized.

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Adiponectin preserves follicles through ADIPOR1/ADIPOR2-driven fatty acid metabolism

Dae Hyun Lee, Jae Young Shin, Hyeri Park, Jin Seok, ... Gi Jin Kim

Adiponectin preserves follicles through ADIPOR1/ADIPOR2-driven fatty acid metabolism

Background

Adiponectin is a key regulator of glucose and lipid metabolism that improves insulin sensitivity and promotes mitochondrial fatty acid oxidation via ADIPOR1 and ADIPOR2. Ovarian lipid accumulation contributes to metabolic reproductive disorders such as polycystic ovary syndrome (PCOS), yet current hormone-based therapies have limited efficacy and potential adverse effects. We evaluated whether placenta-derived mesenchymal stem cells (PDMSCs) mitigate ovarian lipotoxicity by restoring adiponectin signaling.

Methods

A thioacetamide (TAA) induced rat model of metabolic dysfunction with ovarian lipotoxicity was treated by intravenous transplantation of PDMSCs (2 × 106) cells. Hepatic and ovarian phenotypes were assessed four weeks after transplantation. In parallel, PDMSCs were cocultured with TAA-treated granulosa and primary theca cells, with or without siRNA-mediated knockdown of ADIPOR1 and/or ADIPOR2.

Results

PDMSCs transplantation improved systemic insulin resistance and dyslipidemia and partially restored hepatic and ovarian architecture. PDMSCs treatment increased circulating and ovarian ADIPONECTIN levels and upregulated Adipor1/2 in ovarian tissue, accompanied by activation of the ADIPOR1/2/Fatty acid driven axis and enhanced mitochondrial fatty acid oxidation. These changes were associated with reduced ovarian lipid accumulation and improved endocrine homeostasis, including normalization of anti-Müllerian hormone (AMH), estradiol, and androgen levels, preservation of the primordial follicle pool, and induction of BMP15 expression. In vitro ADIPOR1/2 silencing abrogated these protective effects, supporting a requirement for adiponectin receptor signaling.

Conclusions

PDMSCs ameliorate systemic and ovarian metabolic dysfunction in a TAA-induced model, consistent with adiponectin, ADIPOR1/2 dependent mitochondrial metabolic reprogramming. PDMSCs restore both metabolic and reproductive competence in the context of hepatic-ovarian metabolic crosstalk. These findings support PDMSC-based therapy as a mechanistically informed, multi-target strategy for the treatment of PCOS and metabolic-associated ovarian dysfunction.

Articles in Press

Adiponectin preserves follicles through ADIPOR1/ADIPOR2-driven fatty acid metabolism

Dae Hyun Lee, Jae Young Shin, Hyeri Park, Jin Seok, ... Gi Jin Kim

Adiponectin preserves follicles through ADIPOR1/ADIPOR2-driven fatty acid metabolism

Background

Adiponectin is a key regulator of glucose and lipid metabolism that improves insulin sensitivity and promotes mitochondrial fatty acid oxidation via ADIPOR1 and ADIPOR2. Ovarian lipid accumulation contributes to metabolic reproductive disorders such as polycystic ovary syndrome (PCOS), yet current hormone-based therapies have limited efficacy and potential adverse effects. We evaluated whether placenta-derived mesenchymal stem cells (PDMSCs) mitigate ovarian lipotoxicity by restoring adiponectin signaling.

Methods

A thioacetamide (TAA) induced rat model of metabolic dysfunction with ovarian lipotoxicity was treated by intravenous transplantation of PDMSCs (2 × 106) cells. Hepatic and ovarian phenotypes were assessed four weeks after transplantation. In parallel, PDMSCs were cocultured with TAA-treated granulosa and primary theca cells, with or without siRNA-mediated knockdown of ADIPOR1 and/or ADIPOR2.

Results

PDMSCs transplantation improved systemic insulin resistance and dyslipidemia and partially restored hepatic and ovarian architecture. PDMSCs treatment increased circulating and ovarian ADIPONECTIN levels and upregulated Adipor1/2 in ovarian tissue, accompanied by activation of the ADIPOR1/2/Fatty acid driven axis and enhanced mitochondrial fatty acid oxidation. These changes were associated with reduced ovarian lipid accumulation and improved endocrine homeostasis, including normalization of anti-Müllerian hormone (AMH), estradiol, and androgen levels, preservation of the primordial follicle pool, and induction of BMP15 expression. In vitro ADIPOR1/2 silencing abrogated these protective effects, supporting a requirement for adiponectin receptor signaling.

Conclusions

PDMSCs ameliorate systemic and ovarian metabolic dysfunction in a TAA-induced model, consistent with adiponectin, ADIPOR1/2 dependent mitochondrial metabolic reprogramming. PDMSCs restore both metabolic and reproductive competence in the context of hepatic-ovarian metabolic crosstalk. These findings support PDMSC-based therapy as a mechanistically informed, multi-target strategy for the treatment of PCOS and metabolic-associated ovarian dysfunction.

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