Sulforaphan for glucose control in diabetics

Sulforaphan for glucose control in diabetics
reference
Axelsson AS, Tubbs e, Mecham B, et al. Sulforaphan reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes. Scientific transl. Med . 2017; 9 (394): EAAH4477.
objective
to find new drugs that can help to tackle an important pathological mechanism of type 2 diabetes mellitus-the ability of the liver to produce glucose through gluconeogenesis.
study design
randomized, double blind, placebo -controlled study
participant
The test doctors recruited 103 Scandinavian patients with type 2 diabetes mellitus (T2D), who was diagnosed within 10 years before the start of the course. The participants had either well -controlled or poorly controlled T2D; Badly controlled T2D was defined as a glyced hemoglobin (HBA1C) level over 50 mmol/mol. As a reference: 48 mmol/mol or more correspond to a HBA1C of 6.5 %; 42 to 47 mmol/mol correspond to a HBA1C of 6.0 % to 6.4 % (prediabetes); And an HBA1C of less than 42 mmol/mol stands for normal blood sugar. Seven and ninety patients ended the study; 60 had a well -set and 37 a poorly set T2D. Seventeen of patients with poorly controlled illness were obese. All up to 3 participants (who were well controlled) took metformin.
Participants with poorly controlled disease were divided into 2 groups - not obese and obese (BMI> 30 kg/m2) - since hepatic glucose production is more impaired in obese patients.
study parameters evaluated
The blood levels of sober glucose (a representation of hepatic glucose production) and hemoglobin A1C were determined at the beginning and at the end of the study. After initial blood tests (sober glucose, HBA1C and an oral glucose tolerance test), the participants received 1 dose of broccolism pross extract (BSE) or placebo every day. The BSE contained 150 mmol Sulforaphan (SFN) per dose. At the end of the 12-week period, blood tests were repeated.
primary result measurements
Change of sober glucose and hemoglobin-a1c level compared to the starting value after 12 weeks.
important knowledge
Sulforaphan given as a concentrated BSE improved the sober blood sugar level and lowered the HBA1C levels in obese patients with T2D. The extent of the reduction of the HBA1C was larger for participants with higher HBA1C values at the beginning of the study (–0.2 mmol/mol per 1 mmol/mol higher HBA1C at the beginning; p = 0.004). The connection between the HBA1C output values and the extent of the change was not significant in the placebo group ( p = 0.5). There was also a connection between the BMI and the change in the HBA1C in the BSE treatment group, whereby the extent of the reduction in overweight participants was larger (–0.4 mmol/mol per 1 kg/m2 or higher BMI; p = 0.015). The connection between the BMI and the change in the HBA1C was not significant for obese participants in the placebo group.
These results are remarkable when you consider that more than 400 million people worldwide suffer from diabetes and that an even larger number of predicatis suffers.
There was no security concerns when using SFN and it was well tolerated.
practice implications
In this study, the authors report on the advantages of SFN as a BSE when regulating blood sugar levels in diabetics.
preclinical experiments
the clinical study described here was preceded by extensive research in order to identify a new drug for the treatment of diabetes. The researchers generated a signature of illness based on diabetes-associated Gennetzen in the liver tissue, the location of the overproduction of glucose at T2D, and then compared them with drug signatures from a large database. After searching the extensive database, they found that SFN had most overlaps with the gene signatures relevant to diabetes in connection with hepatic glucose production.
They first tested the effect of SFN on glucose production using a rat hepatom cell line. The incubation of these cells with SFN showed a dose -dependent decrease in blood glucose production. This mechanism can be partially explained by the nuclear translocation of the core factor erythroid 2-related factor 2 (NRF2) and the associated downhill regulation of key enzymes for gluconeogenesis.
Then they tested SFN on various animal models in Vivo. They examined the glucose intolerance in rats that were fed with high -fat and fructose diets. Both diets had a benefit, and in fact the extent of the use was quite similar to the use of metformin. In addition, the rats to which SFN was administered had a reduced hepatic glucose production, which in turn had a similar benefit to metformin. In addition, there was an advantage in glucose tolerance for mice that suffered from diet -related diabetes.
clinical study
After the potential of SFN for the treatment of diabetes supported both in-vitro and in vivo studies, the researchers continued to test his effects on glucose control in people with T2D, the clinical study described in this review. The results showed that SFN in the form of concentrated BSE improved the blood sugar level in the sober state and lowered the HBA1C level in overweight patients with T2D.
These results are remarkable when you consider that more than 400 million people suffer from diabetes worldwide and that an even larger number of prediabetes suffers. 1 A poorly controlled blood sugar also increases the risk of cancer, especially for breast cancer.
The SFN in this study was administered as a dried powder of an aqueous extract from broccola sprouts. The choice of BSE was influenced by other clinical studies, the BSE used as a source for SFN, including studies on cancer,
clinically, we probably would have better results with an entire plant, such as: B. sprouted broccoli seeds, since the chewing process and microbial enzymes in our mouth (myrosinase) contribute to activating SFN. This can be achieved by consuming about 100 g broccola sprouts.
- World Health Organization. Diabetes facts. (Link away). Updated in July 2017. Access on August 29, 2017.
- ahmadieh h, azar st. Type 2-diabetes mellitus, oral diabetes medication, insulin therapy and general breast cancer risk. Isrn endocrinol . 2013; 2013: 181240.
- Boyle P, Boniol M, Koechlin a, et al. Diabetes and breast cancer risk: a meta-analysis. br j krebs . 2012; 107 (9): 1608-1617.
- Royston KJ, Udayakumar N., Lewis K., Tollefsbol to. A new combination of Withafer A and Sulforaphan inhibits the epigenetic machinery, the cellular viability and induces the apoptosis of breast cancer cells. int. J. Mol. Sci . 2017; 18 (5): E1092.
- Jiao Z, Chang J, Li J, Nie D, Cui H, Guo D. Sulforaphane increases the NRF2 expression and protects alveolar epithelial cells from damage caused by cigarette bouquet extract. mol med rep . 2017; 16 (2): 1241-1247.
- Cipolla BG, Mandron E, Lefort JM, et al. Effect of Sulforaphan in men with a biochemical recurrence after radical prostate. Krebs Prev Res (Phila) . 2015; 8 (8): 712-719.