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Re-thinking peripheral dysfunctions in obesity: The emerging role of sulphaceutics and sulphanutraceutics
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DOI：10.1111/bph.70557.png)
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Abstract
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Obesity is a chronic, relapsing, multisystem disease in which cardiometabolic risk arises from excess adiposity and progressive dysfunction of peripheral organs, ultimately disrupting endocrine and metabolic crosstalk among tissues. Within this network, sulphur-based biology, centred on hydrogen sulphide and related reactive sulphur species, has emerged as a key regulator of metabolic homeostasis, vascular tone, inflammatory response and mitochondrial function. Here, we review the chemical and mechanistic landscape of sulphaceutics (pharmacological sulphur-releasing agents) and sulphanutraceutics (diet-derived organosulphur compounds), focusing on their capacity to reprogramme peripheral dysfunctions in obesity. Evidence from experimental models, also supported by emerging human data, indicates that sulphur-based interventions can enhance skeletal muscle insulin signalling and performance, restore endothelial reactivity and reduce vascular inflammation, thereby modulating adipose expansion and inflammatory tone. These actions reflect the engagement of upstream redox-sensitive regulatory nodes rather than non-specific antioxidant effects, consistent with a system pharmacology mode of action.
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