Insulin and skin describes the interconnected physiological relationship where the pancreatic hormone insulin, primarily known for regulating glucose metabolism, also exerts significant trophic and pathological effects on the integumentary system. High levels of circulating insulin, a state known as hyperinsulinemia, can directly stimulate the proliferation of keratinocytes and fibroblasts, leading to various dermatological manifestations. This connection is clinically relevant as skin changes can often serve as early, visible indicators of underlying metabolic dysfunction and insulin resistance. Recognizing these signs is crucial for proactive intervention in hormonal health.
Origin
This is a descriptive clinical phrase combining ‘insulin,’ the hormone named from the Latin insula for ‘island’ (referring to the Islets of Langerhans), with ‘skin,’ the largest organ. The relationship between systemic metabolic disease and dermatological pathology has been a subject of study in endocrinology and dermatology for decades. It is a key area in the clinical assessment of metabolic syndrome.
Mechanism
The mechanism centers on the fact that skin cells possess insulin and insulin-like growth factor 1 (IGF-1) receptors. In hyperinsulinemia, the excess insulin spills over to bind with IGF-1 receptors, which have a lower affinity but are structurally similar. This binding stimulates cellular growth pathways, leading to conditions like acanthosis nigricans, characterized by thickened, darkened skin folds. Furthermore, insulin resistance drives systemic inflammation, which can exacerbate inflammatory skin conditions such as acne and psoriasis, underscoring the hormone’s profound influence on dermal health.
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