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Published on: June 2, 2015
Sulforaphene-Enriched Raphanus sativus L. Seed Extract Promotes Norepinephrine-Induced Thermogenesis and Weight Loss
Gihyun Hur1, Tae Kyung Lee1, Jong Hun Kim2,3
1Department of Agricultural Biotechnology, Seoul National University, Seoul, Republic of Korea.
Sulforaphene-enriched radish seed extract (RSE) combats obesity by reducing fat mass and inflammation in adipose tissue. It enhances thermogenesis and modulates immune cell interactions, particularly macrophages, offering potential as a natural anti-obesity agent.
Area of Science:
- Metabolic Syndrome and Obesity Research
- Adipose Tissue Biology
- Nutraceuticals and Natural Products
Background:
- Obesity-related metabolic syndromes involve complex interactions within adipose tissue (AT) comprising adipocytes and immune cells.
- Understanding these cellular crosstalk is crucial for developing effective therapeutic strategies against metabolic diseases.
- Sulforaphene-enriched radish seed extract (RSE) has demonstrated anti-obesity properties, particularly in adipocytes.
Purpose of the Study:
- To investigate the potential of RSE in preventing metabolic diseases by examining its impact on AT cell interactions.
- To elucidate the molecular mechanisms underlying RSE's anti-obesity effects using transcriptomic analysis.
- To evaluate RSE's efficacy in a high-fat diet (HFD) induced mouse model.
Main Methods:
- Transcriptomic analysis (RNA-sequencing) and gene ontology (GO) enrichment were performed on adipose tissue from mice fed a high-fat diet with or without RSE.
- Cellular composition was analyzed using CIBERSORTx, and thermogenesis was assessed via metabolic cage experiments measuring norepinephrine (NE) levels.
- Key gene expressions and protein levels were validated using qRT-PCR and Western blot assays.
Main Results:
- RSE administration significantly reduced body weight (14.5%) and fat mass (35.8%), increased rectal temperature, and enhanced energy expenditure.
- RSE boosted norepinephrine levels and upregulated thermogenic gene expression via β-adrenergic receptor signaling, while down-regulating immune-related pathways.
- Transcriptomic and histological analyses revealed reduced immune cell infiltration, particularly macrophages (M1, LAMs, SAMs), and decreased inflammation markers.
Conclusions:
- RSE mitigates high-fat diet-induced obesity by enhancing adipose tissue thermogenesis and attenuating immune cell-driven inflammation.
- RSE modulates macrophage-adipocyte interactions, reducing lipid-associated and sympathetic neuron-associated macrophages, thereby decreasing inflammation and regulating NE clearance.
- These findings highlight RSE's potential as a natural anti-inflammatory and thermogenic agent for managing obesity and related metabolic disorders.
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