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A cross talk study on sitagliptin mediated reclamation on TGF β signalling, DPP 4, miR-29a and miR-24 expression in

Dipti Nanda1, Anuradha Carani Venkatraman1, Kalpana Kalaivanan1

  • 1Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, India.

Tissue & Cell
|April 11, 2024
PubMed

Insights

Sitagliptin (STG) shows potential benefits for Polycystic Ovary Syndrome (PCOS) by improving lipid profiles, reducing inflammation, and mitigating fibrosis in rats. These effects are linked to regulating miR-29a expression, highlighting a novel therapeutic avenue for PCOS management.

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Pharmacology

Background:

  • Polycystic Ovary Syndrome (PCOS) is a complex endocrine and metabolic disorder affecting women of reproductive age.
  • Current PCOS treatments are limited, necessitating research into novel therapeutic strategies.
  • Dietary factors, such as high-fat, high-fructose diets, significantly exacerbate PCOS pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic potential of sitagliptin (STG) in a rat model of PCOS.
  • To evaluate the effects of STG on metabolic, inflammatory, and fibrotic markers in PCOS-induced rats.
  • To explore the role of microRNAs (miRNAs) in the mechanism of STG action in PCOS.

Main Methods:

  • PCOS was induced in rats using testosterone propionate (TP) administration.
  • Rats were fed either a control diet (CD) or a high-fat, high-fructose diet (HFFD).
  • Sitagliptin (STG) was administered intraperitoneally during the final 15 days of the experiment.
  • Ovarian tissue was analyzed for lipid accumulation, fibrosis, inflammatory markers, and protein/miRNA expression (NF-κB-p65, TGF-β1, miR-24, miR-29a).

Main Results:

  • STG treatment significantly improved lipid profiles, decreasing cholesterol, TG, LDL-C, and VLDL-C, while increasing HDL-C.
  • STG reduced inflammatory markers (IL-6, TNF-α) and decreased the expression of NF-κB-p65, TGF-β1, and downstream signaling proteins.
  • STG increased the expression of miR-24 and miR-29a, suggesting a role in mitigating PCOS-related dyslipidemia and fibrosis.
  • HFFD exacerbated PCOS symptoms more severely than the control diet, emphasizing the role of diet.

Conclusions:

  • Sitagliptin demonstrates significant therapeutic potential against PCOS-induced dyslipidemia, inflammation, and ovarian fibrosis in rats.
  • The beneficial effects of STG appear to be mediated, at least in part, by the regulation of miR-29a expression via DPP-4.
  • Dietary interventions play a crucial role in PCOS development and progression, underscoring the importance of lifestyle modifications alongside pharmacological treatments.
Keywords:
ApoptosisDyslipidaemiaFibrosisPCOSSitagliptinmiR-24 and miR-29a

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