ArticleJournal of endocrinological investigation2026
Altered serum amylin and preptin levels in women with polycystic ovary syndrome: a comparative analysis based on obesity status.
Article in Journal of endocrinological investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPolycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder frequently associated with insulin resistance. Amylin and preptin, peptides secreted by pancreatic β cells, are major contributors to insulin secretion and glucose homeostasis. This study assessed serum amylin and preptin concentrations in women with PCOS and evaluated their associations with anthropometric, metabolic, and reproductive parameters. MATERIALS AND
methodsThis prospective, case-control study included females of reproductive age with PCOS and age-matched healthy controls. Participants were classified as obese and non-obese. Serum amylin and preptin were measured using ELISA, whereas hormonal and biochemical parameters were assessed using standard automated laboratory assays.
resultsWomen with PCOS exhibited markedly reduced circulating concentrations of amylin and preptin compared with the control group. Amylin levels were consistently lower regardless of obesity status, whereas the reduction in preptin was more pronounced in non-obese individuals. A positive correlation between the two peptides was observed across all groups, with stronger associations in the control subjects. In women with PCOS, both peptides demonstrated only modest correlations with fasting glucose, insulin, HOMA-IR, and QUICKI. Despite these reductions, HOMA-β values were significantly elevated in PCOS, suggesting preserved or compensatory β-cell activity. In addition, women with PCOS showed adverse anthropometric and lipid profiles, along with increased luteinizing hormone, testosterone, and LH/FSH ratio.
conclusionThe combined assessment of amylin and preptin suggests alterations in β-cell-derived peptide secretion in PCOS that are not solely explained by adiposity. Notably, these changes occurred despite significantly elevated HOMA-β values, indicating preserved or compensatory β-cell activity. Together, these findings suggest differential regulation of β-cell peptides in PCOS, although the underlying mechanisms require further investigation.
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