# Ashwagandha (Withania somnifera) in insulin resistance and metabolic syndrome: A literature review on mechanisms

**Authors:** Emad Azimi, Maryam Rameshrad, Mahboobeh Ghasemzadeh Rahbardar, Hossein Hosseinzadeh

PMC · DOI: 10.22038/ijbms.2025.86747.18741 · Iranian Journal of Basic Medical Sciences · 2026-01-01

## TL;DR

This paper reviews how ashwagandha may help manage metabolic syndrome by improving insulin resistance and reducing inflammation and cholesterol.

## Contribution

The paper compiles and summarizes various research findings on ashwagandha's mechanisms in managing metabolic syndrome.

## Key findings

- Ashwagandha improves insulin sensitivity and pancreatic insulin secretion.
- It reduces oxidative stress and inflammation while lowering cholesterol.
- Ashwagandha modulates gene expression related to lipid metabolism and bile acid secretion.

## Abstract

Metabolic syndrome is characterized by obesity, insulin resistance, dyslipidemia, and hypertension. Withania somnifera, commonly known as ashwagandha or Indian winter cherry, belongs to the Solanaceae family. W. somnifera, particularly its powdered root, is a fundamental component of traditional Indian medicine. W. somnifera (Ashwagandha) exhibits pharmacological activities, including immunomodulatory, anti-stress, and neuroprotective effects in animal models. Also, preclinical and clinical studies demonstrate its anti-inflammatory and antiviral properties. In rodent studies, ashwagandha regulates apoptosis and modulates reactive oxygen species (ROS) levels as well as mitochondrial activity. Additionally, it improves endothelial function in rats, dogs, and human brain endothelial cells. Research conducted in both living organisms and controlled laboratory conditions has demonstrated that W. somnifera alleviates the symptoms of metabolic syndrome. It positively affects diabetes by inhibiting dipeptidyl peptidase-4 (DPP-4), α-glucosidase, and α-amylase, while simultaneously increasing pancreatic insulin secretion and improving insulin sensitivity in organs. It has a vasodilatory and diuretic effect. Ashwagandha reduces the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. It modulates the gene expression of peroxisome proliferator-activated receptor (PPAR)-γ. It regulates the gene expression of sterol regulatory element-binding protein (SREBP)-1c and CYP7A1. It increases the secretion of bile acids that eliminate excess cholesterol. It reduces oxidative stress and inflammation while protecting the body from the harmful effects of elevated cholesterol. This study aims to compile a variety of research findings on the effectiveness of ashwagandha in managing metabolic syndrome.

## Linked entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], Srebf1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 78968], CYP7A1 (cytochrome P450 family 7 subfamily A member 1) [NCBI Gene 1581]
- **Diseases:** metabolic syndrome (MONDO:0000816), diabetes (MONDO:0005015)
- **Species:** Mus musculus (taxon 10090), Canis lupus familiaris (taxon 9615)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 483665], DPP4 (dipeptidyl peptidase 4) [NCBI Gene 478767], CYP7A1 (cytochrome P450 family 7 subfamily A member 1) [NCBI Gene 486962]
- **Diseases:** inflammation (MESH:D007249), dyslipidemia (MESH:D050171), insulin resistance (MESH:D007333), Metabolic syndrome (MESH:D024821), diabetes (MESH:D003920), obesity (MESH:D009765), hypertension (MESH:D006973)
- **Chemicals:** cholesterol (MESH:D002784), bile acids (MESH:D001647), ROS (MESH:D017382)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rodentia (rodent, order) [taxon 9989], Rattus norvegicus (brown rat, species) [taxon 10116], Canis lupus familiaris (dog, subspecies) [taxon 9615], Withania somnifera (ashwagandha, species) [taxon 126910]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12867099/full.md

## References

125 references — full list in the complete paper: https://tomesphere.com/paper/PMC12867099/full.md

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Source: https://tomesphere.com/paper/PMC12867099