Trials and Studies on Acanthosis Nigricans - High insulin levels as present in insulin resistance disorders are common indicators of acanthosis nigricans. Obese people have much lower concentrations of IGFBP-2 and insulin-like growth factor 1 binding protein.
Clinical Trials and Research Studies on Acanthosis Nigricans
New York (USA), June 16, 2013
Clinical Trials and Research Studies
High insulin levels as present in insulin resistance disorders are the common indicators of acanthosis nigricans. At these levels, insulin could turn more potent by combining with certain insulin-like growth factor 1 receptors (IGF-1Rs). However, IGF-1 binds with much greater affinity that is hundred or thousand times more.
Insulin promotes acanthosis nigricans through direct activation of the IGF-1 leading to cell proliferation. At high levels, insulin stimulates growth and replication of fibroblasts after entering dermoepidermal region. Fasting insulin concentration is intense in obese people leading to higher incidence of acanthosis nigricans.
However, pathogenetically acanthosis nigricans functions differently. Obese people do not have such high levels of insulin to induce IGF-1Rs. Higher incidence of acanthosis nigricans concentrations in neck and body regions with folds is probably due to friction and perspiration in these areas. Indirectly high insulin levels could promote acanthosis nigricans, as it increases free IGF-1 levels in circulation. IGF binding proteins (IGFBPs) regulate IGF-1 levels. These are free and metabolically active.
Obese people have much lower concentrations of IGFBP-2 and insulin-like growth factor 1 binding protein. Plasma concentrations increase promoting cell growth and differentiation. Theoretically, lower concentrations of IGFBP-1 and IGFBP-2 would boost free IGF-1 levels. Nonetheless, therapy with IGF-1 has lowered insulin resistance syndromes and acanthosis nigricans conditions. As insulin binds better with IGF-1 than with IGF-1 receptor, hence insulin is less effective at lowering IGF-1Rs than IGF-1.
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