Insulin Resistance & the Skin
The skin is one of the most visible and accessible organs in the body — and it is also one of the most sensitive mirrors of internal metabolic health. Insulin resistance and the skin are connected through multiple, well-characterised biological pathways, and several cutaneous manifestations can appear years — sometimes a decade — before a formal diagnosis of prediabetes or type 2 diabetes. Recognising these skin signs is not merely cosmetic: it is a genuine clinical opportunity for early metabolic intervention.
This post covers the key skin manifestations of insulin resistance, the underlying mechanisms linking metabolic dysfunction to skin disease, how insulin resistance affects barrier function and wound healing, and the connections to inflammatory skin conditions including acne, psoriasis, and seborrheic dermatitis.
How does insulin resistance affect the skin? Insulin resistance drives skin changes through several mechanisms: hyperinsulinaemia directly activates IGF-1 receptors on keratinocytes and dermal fibroblasts, causing abnormal cell proliferation (acanthosis nigricans, skin tags); elevated androgens secondary to insulin excess drive acne, hirsutism, and androgenetic alopecia; chronic low-grade systemic inflammation worsens psoriasis, atopic dermatitis, and rosacea; and impaired insulin signalling in the skin disrupts the barrier function, glycerol transport, and aquaporin expression — compromising skin hydration and wound healing.1,2,3
Insulin Resistance: A Brief Primer
Insulin resistance is a metabolic state in which target cells fail to respond adequately to normal concentrations of circulating insulin. To compensate, the pancreas produces progressively more insulin — resulting in hyperinsulinaemia — until, eventually, beta-cell capacity is exhausted and blood glucose rises. This compensatory hyperinsulinaemia phase can persist for years or decades before progressing to prediabetes or type 2 diabetes, and it is during this pre-diabetic window that the skin changes described in this post typically emerge.1,2
The current global scale of this problem is significant: approximately 382 million individuals live with diabetes, 40–50% of the global population may be at "high risk" (prediabetes), and 70–80% of people with obesity have insulin resistance. Virtually every patient with type 2 diabetes has some degree of insulin resistance.2 The conventional diagnostic tools — fasting glucose, HbA1c, HOMA-IR — are useful but imprecise and require laboratory testing. The skin manifestations of insulin resistance offer something the lab cannot: a real-time, visible, zero-cost diagnostic signal that is present years before formal disease.
Skin Signs of Insulin Resistance: A Clinical Recognition Guide
González-Saldivar et al. (2016) published the most comprehensive clinical review of skin manifestations of insulin resistance to date — an open-access paper in Dermatology and Therapy that examined the full spectrum from biochemical mechanisms to clinical diagnosis.2 Tripathy et al. (2026, J Clin Med) extended this picture to include the bidirectional relationships between metabolic syndrome and inflammatory skin disease.1 The key cutaneous markers are:
Acanthosis Nigricans (AN)
Velvety, hyperpigmented thickening of skin in flexural areas — posterior neck, axillae, groin. Present in 85–95% of children with type 2 diabetes. The most reliable cutaneous marker of insulin resistance.2,3
Skin Tags (Acrochordons)
Benign pedunculated growths typically on the neck, axillae, and groin. Consistently associated with hyperinsulinaemia and metabolic syndrome. Multiple acrochordons warrant metabolic investigation.2,3
Acne Vulgaris
Insulin stimulates ovarian and adrenal androgen production, increasing sebum output and C. acnes proliferation. High-glycaemic diets demonstrably worsen acne through IGF-1 and androgen pathways.2,4
Androgenetic Alopecia
Excess insulin amplifies 5α-reductase activity and androgen conversion in hair follicles — particularly in women with PCOS where insulin resistance and hyperandrogenism overlap significantly.2
Hirsutism
Excess facial and body hair in women driven by hyperinsulinaemia stimulating ovarian theca cell androgen production. A hallmark of HAIR-AN syndrome (hyperandrogenism, insulin resistance, AN).2
Psoriasis
Bidirectional: metabolic syndrome worsens psoriasis severity, and psoriasis promotes insulin resistance. Shared pathways include TNF-α, IL-17, IL-6, and adipokine dysregulation.1,5
Hidradenitis Suppurativa
Strongly associated with metabolic syndrome and insulin resistance. Obesity-related mechanical occlusion combined with metabolic inflammation drives this follicular occlusive condition.1,2
Dry Skin / Impaired Barrier
Insulin signalling regulates glycerol transport and aquaporin-3 (AQP3) expression in keratinocytes. Insulin resistance impairs both — reducing skin hydration and transepidermal water loss defence.6
Acanthosis Nigricans: The Skin's Metabolic Warning Sign
Acanthosis nigricans deserves particular attention because it is both the most specific cutaneous marker of insulin resistance and the most clinically actionable — its presence should directly prompt metabolic investigation.
This comprehensive review established that skin manifestations of insulin resistance — particularly acanthosis nigricans and acrochordons — offer a reliable, real-time, and non-invasive way to detect insulin resistance in clinical practice. The gold standard for diagnosing insulin resistance (the euglycaemic insulin clamp) is complex, invasive, costly, and clinically unfeasible. Laboratory indices like HOMA-IR are indirect and imprecise. Acanthosis nigricans, however, is visible, immediate, and has been validated as a clinical marker for insulin resistance in multiple epidemiological studies across diverse populations including Iranian, UAE, and Japanese cohorts.2
The mechanism is well-characterised. Elevated circulating insulin — at high concentrations — activates insulin-like growth factor-1 (IGF-1) receptors on epidermal keratinocytes and dermal fibroblasts, driving abnormal cell proliferation. This produces the characteristic epidermal hyperkeratosis and papillomatosis histologically, and the velvety, darkened, thickened plaques clinically.3 Free IGF-1 levels are also elevated in metabolic syndrome, compounding the effect.
Critically, AN is reversible with meaningful weight reduction — by reducing both insulin resistance and compensatory hyperinsulinaemia. Metformin, which improves insulin sensitivity, is also associated with improvement in AN lesions. This reversibility confirms AN as a dynamic metabolic marker rather than a fixed structural change.3
Insulin Resistance and Acne: The IGF-1 and Androgen Connection
The relationship between insulin resistance and acne is one of the most clinically underappreciated connections in dermatology. The mechanism operates through at least three overlapping pathways:
- IGF-1 pathway: Insulin and IGF-1 stimulate sebaceous gland activity, increase sebum lipid synthesis, and promote keratinocyte proliferation in the follicular infundibulum — creating the comedonal environment that precedes inflammatory acne.2,4
- Androgen amplification: Hyperinsulinaemia stimulates ovarian and adrenal androgen production and reduces sex hormone-binding globulin (SHBG) — increasing free androgen levels available to pilosebaceous units.2
- Reduced IGFBP-3: Insulin reduces levels of insulin-like growth factor binding protein-3, a compound with anti-proliferative and pro-apoptotic effects in sebocytes — removing a natural brake on sebaceous hyperactivity.4
The epidemiological evidence is consistent: populations with lower glycaemic load diets demonstrate lower rates of acne. High-glycaemic diets — refined carbohydrates, sugar, dairy in susceptible individuals — reliably worsen acne through these pathways. In my practice, dietary and metabolic investigation is a standard part of acne assessment, particularly in patients with persistent or treatment-refractory disease. A skin condition treated with antibiotics and topicals while high-glycaemic eating continues is being treated from one end while fed from the other.
How Insulin Resistance Disrupts Skin Barrier Function
Beyond the visible markers of hyperinsulinaemia, a critically important but less visible consequence of insulin resistance is its effect on basic skin barrier function.
In high-fat diet (HFD) mice with established insulin resistance, the skin showed: impaired barrier function (significantly increased transepidermal water loss), diminished glycerol transport (reduced aquaporin-3 expression — the protein responsible for glycerol and water movement through keratinocytes), reduced expression of key barrier genes (filaggrin, loricrin), and downregulated lipid synthesis. Crucially, inhibiting insulin signalling directly in keratinocyte cell cultures reproduced these changes — confirming that insulin resistance in the skin cells themselves (not just systemic metabolic effects) directly impairs barrier function. The skin of insulin-resistant mice was also thinner, with reduced dermal collagen.6
This has broad clinical implications. Patients with insulin resistance — particularly those with central obesity or prediabetes — may present with chronically dry, sensitive, barrier-compromised skin that is not responding to topical moisturisers because the underlying metabolic disruption is continuously undermining barrier repair. Addressing the metabolic root cause improves barrier function in a way that no topical can fully compensate for.
It also connects insulin resistance to the worsening of multiple inflammatory skin conditions. A compromised barrier increases skin reactivity to triggers, reduces the threshold for Staphylococcus aureus colonisation in eczema, and amplifies the inflammatory response in conditions like rosacea and seborrheic dermatitis.
Insulin Resistance and Wound Healing
Impaired wound healing is one of the most clinically significant — and most dangerous — consequences of insulin resistance in the skin. The skin relies on insulin signalling for essentially every phase of the wound healing cascade: inflammation resolution, keratinocyte migration and proliferation, angiogenesis, and collagen remodelling.
In insulin-resistant diabetic rats, wounds showed significantly delayed healing compared to non-resistant controls. The addition of topical insulin to wound dressings substantially accelerated cutaneous wound healing — increasing re-epithelialisation, angiogenesis, and the expression of VEGF (vascular endothelial growth factor) and TGF-β1. Topical insulin bypassed systemic insulin resistance by delivering insulin directly to insulin-signalling deficient skin cells — restoring the proliferative and reparative functions that were impaired by the metabolic state. This research supports the principle that insulin-resistant skin is fundamentally deficient in a critical growth and repair signal.7
Clinically, this means that patients with insulin resistance — well before they develop overt diabetic complications — may already be experiencing impaired healing of even minor skin injuries, increased susceptibility to post-inflammatory scarring, and slower resolution of inflammatory skin lesions. It is another reason to treat insulin resistance as a skin health issue, not only a metabolic one.
Insulin Resistance, Metabolic Syndrome, and Inflammatory Skin Disease
The most recent and comprehensive synthesis of this field comes from Tripathy et al. (2026, Journal of Clinical Medicine, PMC12787260) — an open-access review examining the bidirectional relationship between metabolic syndrome and inflammatory skin disease.1
This review identified that psoriasis, acne vulgaris, hidradenitis suppurativa, androgenetic alopecia, acanthosis nigricans, and atopic dermatitis are all bidirectionally associated with metabolic syndrome and insulin resistance. The shared underlying mechanisms include: altered insulin and IGF signalling in skin cells, chronic inflammation through TNF-α, IL-6, IL-17, and adipokine dysregulation (particularly elevated leptin and reduced adiponectin), and oxidative stress from chronic hyperglycaemia. The bidirectionality is clinically important — not only does insulin resistance worsen skin disease, but severe inflammatory skin disease itself promotes insulin resistance through the same cytokine and inflammatory pathways.1
Psoriasis and Insulin Resistance
Psoriasis patients have significantly elevated rates of metabolic syndrome, insulin resistance, and type 2 diabetes compared to the general population — and this is not simply a consequence of shared lifestyle risk factors. The cytokines central to psoriasis pathogenesis (TNF-α, IL-17, IL-6) directly interfere with insulin signalling in hepatic and peripheral tissues, promoting insulin resistance. Simultaneously, insulin resistance amplifies the same inflammatory cytokine milieu that drives psoriatic inflammation — creating a genuine feed-forward loop.1,5
Hidradenitis Suppurativa
Hidradenitis suppurativa (HS) has one of the strongest associations with metabolic syndrome of any inflammatory skin condition. In the rosacea section of my practice, I consistently see patients with HS who have never had a metabolic assessment. The combination of follicular occlusion, mechanical friction from obesity, and the chronic systemic inflammation of hyperinsulinaemia creates a uniquely hostile environment for the apocrine-rich skin of the axillae, groin, and inframammary folds.1,2
Seborrheic Dermatitis, Rosacea, and the Metabolic Connection
While the associations between insulin resistance and psoriasis or acne are well-established, the connections to seborrheic dermatitis and rosacea are less formally characterised but clinically consistent and mechanistically plausible.
As I discussed in my post on seborrheic dermatitis causes, high-glycaemic diets and insulin spikes are among the most commonly reported dietary flare triggers. The mechanism is direct: elevated insulin promotes sebum overproduction (feeding Malassezia), increases systemic inflammation, and disrupts skin barrier function — all of which enable Malassezia overgrowth. Similarly, in rosacea, the cross-sectional data (Ozbagcivan et al., 2020) found insulin resistance in a significantly higher proportion of rosacea patients than controls, alongside dyslipidaemia and elevated inflammatory markers.
In my practice, a metabolic assessment — including fasting insulin, HOMA-IR, and not just fasting glucose — is now a standard part of my workup for any patient with chronic inflammatory skin disease. The skin signs of insulin resistance are not an endpoint. They are a starting point for a conversation about metabolic health that most dermatology consultations never initiate.
What Does Insulin Resistance Skin Look Like?
The most visible and specific skin sign of insulin resistance is acanthosis nigricans — velvety, darkened, thickened patches appearing in the back of the neck, armpits, and groin — combined with multiple skin tags in the same areas. Together, these findings have a high predictive value for the presence of hyperinsulinaemia.2,3 Other signs that should prompt metabolic consideration include: persistent adult acne that worsens with sugar/carbohydrate intake, new-onset androgenetic alopecia or hirsutism in women (particularly with menstrual irregularity suggesting PCOS), slow-healing minor wounds, and chronically dry or barrier-compromised skin unresponsive to topical treatment.
Can Improving Insulin Resistance Improve Skin Conditions?
Yes — and this is one of the most compelling aspects of the insulin resistance–skin relationship from a clinical perspective. Acanthosis nigricans can fully regress with weight reduction and improvement in insulin sensitivity.3 Acne consistently improves with low-glycaemic dietary interventions that reduce insulin and IGF-1 levels.4 Psoriasis severity is independently associated with insulin resistance — and metabolic interventions including weight loss and metformin have been shown to reduce PASI scores in overweight psoriatic patients.1,5 Addressing insulin resistance is not merely an adjunct to skin treatment; in many patients, it is the central intervention.2
Frequently Asked Questions: Insulin Resistance and the Skin
What skin conditions are caused by insulin resistance?
The most consistently associated skin conditions are acanthosis nigricans (the most specific marker), skin tags (acrochordons), acne vulgaris, androgenetic alopecia, hirsutism, and hidradenitis suppurativa. Insulin resistance is also bidirectionally associated with psoriasis, atopic dermatitis, and seborrheic dermatitis through shared inflammatory and barrier-disruption pathways.1,2
Can you see insulin resistance in the skin before getting a blood test?
Yes — acanthosis nigricans and skin tags in combination are visible, real-time cutaneous markers of insulin resistance that frequently precede abnormal fasting glucose or HbA1c by years. González-Saldivar et al. specifically make the case that these skin signs are more reliable early indicators than many standard laboratory indices.2 If you notice dark, velvety thickening in the neck, axillae, or groin — particularly with multiple skin tags — metabolic investigation is warranted even if your blood glucose is currently normal.
Does diet affect insulin resistance skin signs?
Significantly. High-glycaemic diets — refined carbohydrates, sugar, high-glycaemic-index foods — raise insulin and IGF-1 levels, driving the pathways responsible for acne, sebum overproduction, and seborrheic dermatitis flares. Reducing dietary glycaemic load is one of the most evidence-supported interventions for acne, and is mechanistically relevant to nearly all insulin-resistance-driven skin manifestations.2,4 Acanthosis nigricans can completely regress with dietary change and weight reduction that meaningfully improves insulin sensitivity.3
Is rosacea related to insulin resistance?
The association is clinically consistent, though less formally characterised than for psoriasis or acne. Cross-sectional data shows significantly higher rates of insulin resistance, dyslipidaemia, and metabolic syndrome in rosacea patients than in controls. The shared mechanisms include systemic inflammation, barrier dysfunction, and neurovascular reactivity — all of which are amplified by hyperinsulinaemia and chronic glycaemic fluctuation. I cover this in more detail in my post on rosacea and the gut–skin axis.
What tests should I ask for if I think I have insulin resistance?
Standard fasting glucose and HbA1c are often normal in early insulin resistance — the compensatory hyperinsulinaemia maintains blood glucose until late in the metabolic progression. More informative tests include: fasting insulin, HOMA-IR (calculated from fasting glucose and fasting insulin), and a full lipid panel (elevated triglycerides and low HDL are common early metabolic syndrome markers). A functional approach uses non-fasting clinical markers — including the skin signs described in this post — alongside these laboratory indices rather than relying on any single test.
A Clinical Perspective: Skin as a Metabolic Readout
In clinical practice, the integration of metabolic assessment into skin consultations remains rare. Patients with acne, seborrheic dermatitis, psoriasis, or rosacea are far more likely to leave a consultation with a prescription than with an insulin measurement. This is a missed opportunity — particularly since the metabolic interventions available (dietary glycaemic reduction, physical activity, targeted supplementation, and where appropriate metformin) are low-risk, broadly beneficial, and address the root cause rather than the surface manifestation.
My approach for any patient with a chronic inflammatory skin condition now includes assessment of metabolic markers — not just skin-focused examination. The skin is telling us something about what is happening systemically. Our job is to listen to it.
Book a functional skin consultation to assess whether insulin resistance, metabolic syndrome, or hormonal imbalance may be contributing to your skin condition — and build a plan that addresses the cause, not just the surface.
Further Reading & Trusted Sources
- González-Saldivar et al. (2016) — Skin Manifestations of Insulin Resistance: From a Biochemical Stance to a Clinical Diagnosis — open access, Dermatology and Therapy.
- Tripathy et al. (2026) — Insulin Resistance, Metabolic Syndrome, and Inflammatory Skin Disease — open access, Journal of Clinical Medicine.
- Aoki & Murase (2019) — Obesity-Associated Insulin Resistance Adversely Affects Skin Function — open access, PLOS ONE.
- Yu et al. (2017) — Topical Insulin Accelerates Cutaneous Wound Healing in Insulin-Resistant Diabetic Rats — open access, Am J Transl Res.
References
- Tripathy K, Dulai AS, Min M, Sivamani RK. Insulin resistance, metabolic syndrome, and inflammatory skin disease. J Clin Med. 2026;15(1):330. doi:10.3390/jcm15010330. PMC12787260.
- González-Saldivar G, Rodríguez-Gutiérrez R, Ocampo-Candiani J, González-González JG, Gómez-Flores M. Skin manifestations of insulin resistance: from a biochemical stance to a clinical diagnosis and management. Dermatol Ther (Heidelb). 2017;7(1):37–51. doi:10.1007/s13555-016-0160-3.
- Barbato MT, Criado PR, Silva AK, Averbeck E, Guerine MB, Sá NB. Association of acanthosis nigricans and skin tags with insulin resistance. An Bras Dermatol. 2012;87(1):97–104. doi:10.1590/s0365-05962012000100012.
- Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. 2009;18(10):833–841.
- Karadag AS, You Y, Danarti R, Al-Khuzaei S, Chen W. Acanthosis nigricans and the metabolic syndrome. Clin Dermatol. 2017;35(1):99–105.
- Aoki M, Murase T. Obesity-associated insulin resistance adversely affects skin function. PLOS ONE. 2019;14(10):e0223528. doi:10.1371/journal.pone.0223528.
- Yu T, Gao M, Yang P, et al. Topical insulin accelerates cutaneous wound healing in insulin-resistant diabetic rats. Am J Transl Res. 2017;9(10):4682–4693. PMC5666074.
- Sierro TJ, Ortega-Springall MF, Smith RL, Vázquez-Herrera NE, Tosti A, Tiwary AK. Association of multiple skin tags with metabolic syndrome and diabetes type 2: a retrospective study. An Bras Dermatol. 2020;95(2):150–155.
- Ucak H, Demir B, Cicek D, et al. Insulin resistance and acne vulgaris — correlation with HOMA-IR. J Eur Acad Dermatol Venereol. 2015;29:851–856.
- Lima AL, et al. Cutaneous manifestations of diabetes mellitus: a systematic review. An Bras Dermatol. 2017;92(1):8–20.
