Broccoli sprouts may help prediabetes, but only with the right gut bacteria

By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Feb 11 2025

Scientists found that while broccoli sprout extract can help regulate blood sugar, only people with certain gut bacteria see real benefits—paving the way for personalized nutrition in diabetes prevention.

Study: Effect of broccoli sprout extract and baseline gut microbiota on fasting blood glucose in prediabetes: a randomized, placebo-controlled trial. Image Credit: ami mataraj / Shutterstock

One in three adults worldwide has prediabetes, yet most are unaware of their condition. Without intervention, up to 70% will develop type 2 diabetes. Can a simple dietary extract from broccoli sprouts change this trajectory?

Prediabetes affects millions worldwide, increasing the risk of type 2 diabetes, cardiovascular diseases, and metabolic disorders. Current preventive measures primarily include lifestyle interventions, such as diet and exercise, which have variable effectiveness and limited accessibility.

Pharmacological treatments, such as metformin, are often not prescribed due to side effects and inconsistent metabolic responses.

Recent research highlights the gut microbiota's role in glucose metabolism, suggesting that microbial composition may influence individual responses to dietary interventions.

Sulforaphane, an active compound in broccoli sprout extract, has demonstrated potential in reducing hepatic glucose production. However, its efficacy in prediabetes remains uncertain.

Understanding the combined influence of BSE and gut microbiota on glucose regulation is essential for developing personalized interventions. Moreover, recent findings suggest that the ability to activate sulforaphane may depend on specific bacterial genes present in the gut, such as the BT2160 operon, which plays a crucial role in converting sulforaphane precursors into their active form.

Further research is required to determine the factors influencing the metabolic response to BSE.

About the Study

A randomized, double-blind, placebo-controlled trial was conducted on drug-naive individuals with prediabetes. Participants aged 35-75 years with impaired fasting glucose levels (6.1-6.9 mmol/L) and a body mass index (BMI) between 27-45 kg/m² were enrolled after screening 450 individuals. Exclusion criteria included conditions affecting blood glucose metabolism.

Ultimately, 89 participants were enrolled (44 receiving BSE and 45 receiving placebo), but only 35 participants in the BSE group and 39 in the placebo group were included in the final analysis due to dropouts.

Participants received a dried powder extract of BSE, which was dissolved in water, delivering 150 µmol of sulforaphane daily. They were instructed to maintain their usual diet and physical activity. Compliance was monitored through diary logs and telephone follow-ups. Adverse events and discontinuations were recorded.

Fasting blood glucose, insulin resistance using the homeostasis model assessment-estimated insulin resistance (HOMA-IR), and beta-cell function using the homeostasis model assessment-beta (HOMA-B) were measured at baseline and after treatment.

Gut microbiota composition was analyzed using metagenomic sequencing of stool samples. A key exploratory analysis investigated whether gut bacteria, particularly those containing the BT2160 operon, could influence sulforaphane activation and subsequent glucose response.

A post hoc cluster analysis categorized participants into subgroups based on pathophysiological traits to identify potential responders.

Study Results

The study enrolled 89 participants, with 44 receiving BSE and 45 receiving a placebo. However, only 35 in the BSE group and 39 in the placebo group completed the study and were included in the final analysis. Fifteen participants discontinued, primarily due to gastrointestinal side effects (9 in BSE, 6 in placebo).

BSE resulted in a 0.2 mmol/L reduction in fasting blood glucose compared to placebo (95% confidence interval -0.44 to -0.01, p=0.04), which did not meet the predefined outcome of 0.3 mmol/L.

No significant differences were observed between groups in secondary metabolic markers, including BMI, HOMA-IR, glycated hemoglobin (HbA1c), or lipid profiles.

Exploratory subgroup analysis revealed that individuals with mild obesity, low insulin resistance, and reduced insulin secretion—classified as mild age-related diabetes (MARD)—exhibited a more pronounced glucose-lowering response, with a mean reduction of 0.4 mmol/L (p=0.008). Those with severe insulin-resistant diabetes (SIRD) or mild obesity-related diabetes (MOD) did not experience significant changes in glucose levels.

Gut microbiota composition differed among subgroups. Participants with a greater glycemic response had higher baseline levels of butyrate-producing bacteria, such as Faecalibacterium and Eubacterium, and lower levels of facultative anaerobes linked to metabolic dysfunction.

Moreover, the study identified a critical bacterial gene, BT2160, which is involved in the activation of sulforaphane. Participants with a greater abundance of this gene in their gut microbiota had higher serum sulforaphane concentrations and a stronger reduction in fasting glucose. Those with lower BT2160 expression showed minimal metabolic benefits from BSE.

A machine learning analysis further identified baseline hepatic markers, such as gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP), alongside specific gut microbial species, as predictive factors for treatment outcomes.

Notably, participants who achieved remission (fasting glucose <6.1 mmol/L) had significantly higher BT2160 abundance and lower GGT levels, suggesting that both microbial and liver health markers influence metabolic response.

Conclusions

To summarize, this study has significant implications for diabetes prevention at both individual and global levels. Personalized nutritional interventions based on gut microbiota profiling could improve metabolic outcomes and reduce reliance on pharmacological treatments. For individuals, this means an accessible and natural approach to lowering blood glucose, particularly for those with a favorable gut microbiota composition.

On a community level, the findings highlight the potential to develop targeted nutritional strategies that could alleviate the growing burden of diabetes-related healthcare costs. Globally, integrating microbiome-based interventions into public health initiatives could pave the way for more effective, sustainable diabetes prevention strategies.

However, it is important to note that the study follow-up was only 12 weeks, and long-term effects remain uncertain. Future research should focus on refining stratification methods to enhance precision in prediabetes treatment and assess whether BSE can sustain glycemic improvements over longer periods.