# Effects of hirudotherapy on liver functions, lipid profile, and insulin sensitivity in rats with metabolic syndrome

**Authors:** Alican Bilden, Seda Koçak, Halime Tozak Yıldız, Fatih Çakır, Merve Kahraman, Muttalip Çiçek

PMC · DOI: 10.1186/s12906-025-05241-x · BMC Complementary Medicine and Therapies · 2026-01-08

## TL;DR

This study shows that hirudotherapy improves liver function, lipid levels, and insulin sensitivity in rats with metabolic syndrome, suggesting it could be a promising complementary treatment.

## Contribution

The study is the first to demonstrate hirudotherapy's effects on metabolic syndrome in a rat model, highlighting its potential as a biotherapeutic approach.

## Key findings

- Hirudotherapy reduced liver enzymes AST and ALT, indicating hepatoprotective effects.
- It improved glucose tolerance and reduced hyperglycemia in rats with metabolic syndrome.
- Hirudotherapy decreased systolic blood pressure and showed histopathological improvements in liver damage.

## Abstract

Metabolic syndrome (METS) is a multifactorial cardiometabolic disorder characterized by abdominal obesity, insulin resistance, hypertension, dyslipidemia, and hyperglycemia, substantially increasing the risk of type 2 diabetes and cardiovascular diseases. The variable effectiveness of lifestyle and pharmacological interventions has heightened interest in complementary approaches. Hirudotherapy, containing a wide range of bioactive compounds, may offer therapeutic benefits. This study aimed to evaluate the effects of hirudotherapy on metabolic parameters in a rat model of METS.

Twenty-four male Wistar rats were divided into four groups: Control (n = 6), METS (n = 6), METS + 4-week hirudotherapy (n = 6), and METS + 8-week hirudotherapy (n = 6). METS was induced through a modified high-fat and fructose-enriched diet. The effects of hirudotherapy on liver enzymes (AST, ALT), lipid profile (TG, LDL cholesterol, HDL cholesterol), hemodynamic parameters (systolic/diastolic blood pressure, mean arterial pressure, heart rate), glucose metabolism (OGTT, AUC), and liver histopathology were assessed. Pellet and water intake were monitored to evaluate possible influences on appetite regulation.

Hirudotherapy demonstrated hepatoprotective activity, yielding significant reductions in AST and ALT levels (p < 0.05). TG levels increased in METS, while LDL cholesterol showed partial improvement and HDL cholesterol remained unchanged. Systolic blood pressure significantly decreased in the hirudotherapy-treated groups, with no significant differences in diastolic pressure or heart rate. OGTT and AUC analyses revealed improved glucose tolerance and reduced hyperglycemia following hirudotherapy (p < 0.05). Histopathology showed marked improvements in steatosis, sinusoidal dilatation, and hydropic degeneration, although minor hemorrhagic foci persisted. Differences in pellet consumption suggested a potential regulatory effect on appetite and metabolic balance.

Hirudotherapy may exert beneficial effects in METS by improving liver function, modulating lipid metabolism, enhancing insulin sensitivity, and reducing inflammation. Its influence on food intake may further support metabolic homeostasis. These findings support hirudotherapy as a potential biotherapeutic approach and warrant further mechanistic and clinical investigations.

## Linked entities

- **Diseases:** metabolic syndrome (MONDO:0000816), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Diseases:** dyslipidemia (MESH:D050171), abdominal obesity (MESH:D056128), type 2 diabetes (MESH:D003924), insulin resistance (MESH:D007333), inflammation (MESH:D007249), hemorrhagic (MESH:D006470), steatosis (MESH:D005234), hypertension (MESH:D006973), hyperglycemia (MESH:D006943), cardiovascular diseases (MESH:D002318), METS (MESH:D024821)
- **Chemicals:** TG (MESH:D013866), fructose (MESH:D005632), lipid (MESH:D008055), glucose (MESH:D005947), water (MESH:D014867)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12857106/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12857106/full.md

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Source: https://tomesphere.com/paper/PMC12857106