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Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes

Annika S Axelsson, Emily Tubbs, Brig Mecham, Shaji Chacko, Hannah A Nenonen, Yunzhao Tang, Jed W Fahey, Jonathan M J Derry, Claes B Wollheim, Nils Wierup, Morey W Haymond, Stephen H Friend, Hindrik Mulder, Anders H Rosengren
Science Translational Medicine 2017 9(394):eaah4477

Bibliography

PubMed
PMID 28615356
Trial registry
View on ClinicalTrials.gov Registered trial — results not yet published in a peer-reviewed journal.
Funding
Supported by the Ragnar Söderberg Foundation, Swedish Foundation for Strategic Research, Lantmännen Research Foundation, Novo Nordisk Foundation, ALF Region Skåne, Hjelt Foundation, Lewis B. and Dorothy Cullman Foundation, and Knut and Alice Wallenberg Foundation via the Wallenberg Centre for Molecular and Translational Medicine.
Competing interests
Annika S. Axelsson and Anders H. Rosengren were inventors on patent applications covering sulforaphane for exaggerated hepatic glucose production; rights were licensed to Lantmännen AB. Lantmännen provided broccoli sprout extract and placebo and its research fund financed part of the study. Lund University sponsored the academic investigation, and the paper states Lantmännen had no influence on procedures, analysis or interpretation. Other authors declared no competing interests.

Study snapshot

DesignRandomized parallel placebo-controlled clinical trial within a translational mechanistic study
ModelAdults with type 2 diabetes
Sample97 participants
InterventionConcentrated broccoli sprout extract delivering 150 µmol sulforaphane daily versus placebo.
Duration12 weeks
EndpointsHbA1c; Fasting blood glucose; Glycemic control; Hepatic glucose-production mechanisms

What the study showed, in plain terms

This translational study used cell, animal and human experiments to identify sulforaphane as a candidate modulator of excessive hepatic glucose production, then tested a concentrated broccoli sprout extract in adults with type 2 diabetes.

Key findings

In the human trial, the strongest glycemic signal was reported in obese participants with dysregulated type 2 diabetes, where the sulforaphane intervention reduced fasting glucose and HbA1c-related measures. The study also linked sulforaphane to NRF2-dependent suppression of gluconeogenic pathways in preclinical models.

What this study can and cannot tell us

The headline clinical benefit was concentrated in a subgroup rather than establishing uniform efficacy across all people with type 2 diabetes. The intervention was a specific high-dose broccoli sprout extract and should not be generalized to ordinary dietary broccoli or all supplements.

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