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Background <p>Secretin, a gastrointestinal hormone, has piqued researchers’ interest due to its metabolic activities beyond digestion. It stimulates cAMP-mediated pathways and secretin receptors in the pancreas, brain, adipose tissue, and gastrointestinal system. This hormone improves insulin sensitivity, β-cell activity, lipolysis, intestinal lipid absorption, and activates brown adipose tissue (BAT) to increase calorie expenditure and satiety. Secretin also interacts with gut hormones such as GLP-1, PYY, and ghrelin, highlighting its position in the gut-brain axis. Secretin affects insulin resistance, adipokine modulation, ovarian steroidogenesis, and inflammatory markers in PCOS, implying that it has therapeutic promise for metabolic and reproductive disorders.</p> Methodology <p>Using the databases PubMed, Google Scholar, Medline, and Embase, a&#xa0;systematic&#xa0;literature review was conducted.&#xa0;The data was collected by employing these databases, providing secretin’s Physiological and pathological role in metabolic disorders.&#xa0;The articles were examined using Rayyan, an online tool, to ensure an efficient and thorough review process. This review is registered in PROSPERO.</p> Results <p>Quantitative data analysis demonstrated that secretin significantly increases glucose uptake in BAT, with a substantial inverse association between BAT and caudate glucose metabolism (r = −0.54, p = 0.037), indicating a brain-BAT metabolic axis. SCTR animals fed a high-fat diet showed significantly reduced weight gain (44.7 ± 1.4&#xa0;g vs 49.6 ± 0.9&#xa0;g; p &lt; 0.05) and improved glycemic profiles compared to wild-type mice. PKA-HSL pathway activation contributed to substantial spikes in adipocyte lipolysis in vitro (p &lt; 0.0001). These findings highlight secretin’s role in thermogenesis, lipid mobilization, and systemic energy management, which supports its therapeutic potential in metabolic diseases.</p> Graphical Abstract <p></p>

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Harnessing Secretin: A Systematic Review of its Emerging Role in Metabolic and Reproductive Health

  • 期刊论文

  • 发表日期：

    2025年10月30日

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  • Nakul Mahawar,
  • Gautam Saxena,
  • Aditya Srivastava,
  • Bhawna Chhabra,
  • Havagiray Chitme

摘要

Background

Secretin, a gastrointestinal hormone, has piqued researchers’ interest due to its metabolic activities beyond digestion. It stimulates cAMP-mediated pathways and secretin receptors in the pancreas, brain, adipose tissue, and gastrointestinal system. This hormone improves insulin sensitivity, β-cell activity, lipolysis, intestinal lipid absorption, and activates brown adipose tissue (BAT) to increase calorie expenditure and satiety. Secretin also interacts with gut hormones such as GLP-1, PYY, and ghrelin, highlighting its position in the gut-brain axis. Secretin affects insulin resistance, adipokine modulation, ovarian steroidogenesis, and inflammatory markers in PCOS, implying that it has therapeutic promise for metabolic and reproductive disorders.

Methodology

Using the databases PubMed, Google Scholar, Medline, and Embase, a systematic literature review was conducted. The data was collected by employing these databases, providing secretin’s Physiological and pathological role in metabolic disorders. The articles were examined using Rayyan, an online tool, to ensure an efficient and thorough review process. This review is registered in PROSPERO.

Results

Quantitative data analysis demonstrated that secretin significantly increases glucose uptake in BAT, with a substantial inverse association between BAT and caudate glucose metabolism (r = −0.54, p = 0.037), indicating a brain-BAT metabolic axis. SCTR animals fed a high-fat diet showed significantly reduced weight gain (44.7 ± 1.4 g vs 49.6 ± 0.9 g; p < 0.05) and improved glycemic profiles compared to wild-type mice. PKA-HSL pathway activation contributed to substantial spikes in adipocyte lipolysis in vitro (p < 0.0001). These findings highlight secretin’s role in thermogenesis, lipid mobilization, and systemic energy management, which supports its therapeutic potential in metabolic diseases.

Graphical Abstract