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Adipokines, Inflammation, and Metabolic Diseases / Regulation of Appetite and Obesity · Journal article
Laboratory Animal Research · September 4, 2026
Early or partial results. Treat as a signal, not a conclusion.
This transgenic mouse study examined whether adipocyte-specific overexpression of MC2R—the ACTH receptor—could promote weight loss or alter glucocorticoid levels. The intervention produced minimal effects on thermogenesis, lipolysis, body weight, or serum corticosterone under basal, high-fat diet, or stress conditions, suggesting limited therapeutic potential for obesity or GC dysregulation via this target in vivo.
Transgenic mouse model study with controlled experimental conditions. Transgenic mice with adipocyte-specific MC2R overexpression. Intervention: Adipocyte-specific MC2R overexpression via AAV-DIO system. Compared with: Basal, high-fat diet, and stress-induced conditions; response to exogenous ACTH administration.
MC2R overexpression in adipocytes failed to promote weight reduction under basal, high-fat diet, or stress-induced conditions No significant effects on thermogenic and lipolytic markers reported Adipocyte-specific MC2R overexpression did not sequester ACTH or decrease elevated serum corticosterone levels after exogenous ACTH administration
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These negative findings in an animal model suggest that MC2R-targeted approaches may not be a viable therapeutic strategy for obesity or glucocorticoid-related disorders. The work tempers in vitro observations and cautions against translating MC2R agonism in adipocytes to human therapy.
Single-centre mechanistic study in a transgenic mouse model with negative findings; provides useful in vivo evidence against a hypothesis but lacks the design or effect size to guide clinical practice.
As stated by the source record.
These negative findings in an animal model suggest that MC2R-targeted approaches may not be a viable therapeutic strategy for obesity or glucocorticoid-related disorders. The work tempers in vitro observations and cautions against translating MC2R agonism in adipocytes to human therapy.
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BACKGROUND: Obesity is often associated with elevated glucocorticoid (GC) levels mediated by melanocortin 2 receptor (MC2R), the adrenocorticotropic hormone (ACTH) receptor expressed in the adrenal gland. Meanwhile, previous in vitro studies in non-adrenal cells suggest a potential role for MC2R in lipid metabolism in murine primary adipocytes; however, the functional relevance of MC2R in vivo remains poorly understood. Here, we assessed the metabolic effects and therapeutic potential of MC2R in obesity and GC regulation in vivo by generating mice with adipocyte-specific MC2R overexpression using the adeno-associated virus doublef-floxed inverse orientation (AAV-DIO) system. RESULTS: Our findings show that under basal, high-fat diet (HFD), and stress-induced conditions, MC2R overexpression in adipocytes has minimal effects on thermogenic and lipolytic markers and is insufficient to promote weight reduction in mice. Moreover, adipocyte-specific overexpression of MC2R failed to sequester the ACTH and decrease elevated serum corticosterone levels after exogenous ACTH administration. CONCLUSIONS: These findings demonstrate that adipocyte-specific MC2R overexpression does not induce strong metabolic benefits, suggesting that MC2R-directed gene therapy may not be an effective treatment strategy for obesity.
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