Participants with prediabetes who had a higher abundance of a specific gut microbiota gene known as BT2160 experienced a greater reduction in fasting blood glucose when treated with broccoli sprout extract, according to a recent study. 

Researchers conducted a randomized, double-blind, placebo-controlled trial to evaluate the effects of broccoli sprout extract (BSE) on fasting blood glucose in participants with prediabetes. The study, published in Nature Microbiology, included 74 drug-naive participants aged 35 to 75 years with impaired fasting glucose (6.1 to 6.9 mmol/L) and a body mass index (BMI) of 27 to 45 kg/m². The participants were randomly assigned to receive either 150 μmol of sulforaphane-containing BSE (n = 35) or placebo (n = 39) once daily for 12 weeks. The primary outcome was a reduction of at least 0.3 mmol/L in fasting blood glucose compared with placebo, while secondary outcomes included changes in BMI, insulin resistance (HOMA-IR), insulin secretion (HOMA-B), glycated hemoglobin (HbA1c), lipid profiles, and fatty liver index.

BSE treatment resulted in a mean fasting glucose reduction of 0.2 mmol/L compared with placebo (95% confidence interval [CI] = −0.44 to −0.01, P = .04), falling short of the prespecified primary outcome threshold of 0.3 mmol/L, which was set based on prior efficacy data in type 2 diabetes. No statistically significant differences were observed in secondary outcomes, including BMI, HOMA-IR, HOMA-B, HbA1c, insulin clearance, lipid levels, or dietary and physical activity changes. Adverse effects, primarily gastrointestinal symptoms, were reported more frequently in the BSE group (n = 9/35) compared with the placebo group (n = 6/39). Notably, five BSE participants and two placebo participants discontinued the study as a result of these effects.

Led by Chinmay Dwibedi, of the Department of Neuroscience and Physiology at the Sahlgrenska Academy at the University of Gothenburg in Sweden, and colleagues, the researchers used exploratory analyses and identified a subgroup of participants with mild obesity, low insulin resistance, and reduced insulin secretion (MARD-like characteristics) who exhibited a 0.4 mmol/L reduction in fasting glucose (95% CI = −0.6 to −0.1, P = .008). No significant response was observed in participants classified with moderate obesity-related diabetes or severe insulin-resistant diabetes.

Exploratory microbiota analysis suggested that responders had a distinct gut microbiota composition, including an increased abundance of butyrate-producing bacteria such as Faecalibacterium prausnitzii and a Bacteroides-encoded transcriptional regulator (BT2160), which may contribute to glucoraphanin conversion to bioactive sulforaphane. These findings require further validation in larger cohorts. Participants with higher baseline BT2160 abundance demonstrated greater sulforaphane serum concentrations (P = .046) and improved glycemic response.

These findings indicated that metabolic response to BSE may be associated with host pathophysiology and gut microbiota composition. Additional research is necessary to determine the role of microbiome-mediated sulforaphane activation in prediabetes.

Full disclosures can be found in the published study.