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Sugar from plant photosynthesis is a basic requirement for life activities. Sugar transporters are the proteins that mediate sugar allocation among or within source/sink organs. The transporters of the major facilitator superfamily (MFS) targeting carbohydrates represent the largest family of sugar transporters in many plants. Strawberry (Fragaria × ananassa Duchesne) is an important crop appreciated worldwide for its unique fruit flavor. The involvement of MFS sugar transporters (STs) in cultivated strawberry fruit sugar accumulation is largely unknown. In this work, we characterized the genetic variation associated with fruit soluble sugars in a collection including 154 varieties. Then, a total of 67 ST genes were identified in the v4.0 genome integrated with the v4.0.a2 protein database of F. vesca, the dominant subgenome provider for modern cultivated strawberry. Phylogenetic analysis updated the nomenclature of strawberry ST homoeologs. Both the chromosomal distribution and structural characteristics of the ST family were improved. Semi-RT-PCR analysis in nine tissues from cv. Benihoppe screened 34 highly expressed ST genes in fruits. In three varieties with dramatically differing fruit sugar levels, qPCR integrated with correlation analysis between ST transcript abundance and sugar content identified 13 sugar-correlated genes. The correlations were re-evaluated across 19 varieties, including major commercial cultivars grown in China. Finally, a model of the contribution of the sugar transporter system to subcellular sugar allocation in strawberry fruits was proposed. Our work highlights the involvement of STs in controlling strawberry fruit soluble sugars and provides candidates for the future functional study of STs in strawberry development and responses and a new approach for strawberry genetic engineering and molecular breeding.

Sulforaphane (SFN) which is abundant in broccoli florets, seeds, and sprouts has been reported to have beneficial effects on attenuating metabolic diseases, such as antiobesity, antidiabetes, and antioxidative activities. However, the effects of SFN on the regulation of type II diabetes through easing nonalcoholic fatty liver (NAFLD) and repairing pancreas tissue are rarely reported. In this study, we found that the administration with different dosages of SFN was able to increase serum insulin level, enhance HOMA‐β index, decrease fasting blood glucose and serum total cholesterol, triglyceride, low‐density lipoprotein (LDL‐C), fibroblast growth factor21 (FGF21) levels, ease NAFLD level, and repair the pancreas tissue. In addition, SFN was able to increase liver antioxidant capacities. In particular, high (10 mg/kg) dosage of SFN exerted a significant beneficial effect for decreasing serum lipopolysaccharide levels. Furthermore, the administration of SFN could also decrease the relative abundance of Allobaculum at the genus level. Low dosage (2 mg/kg) of SFN could increase the relative abundance of Bacteroidetes and decrease the relative abundance of Firmicutes at the phylum level. Overall, our results showed that SFN exerted its antidiabetic effect through easing NAFLD and repairing pancreas tissue in association with modulation of gut microbiota. The ease of NAFLD by SFN was accompanied by enhancing liver antioxidant abilities and improving FGF21 resistance.

The most common complications of obesity are metabolic disorders such as nonalcoholic fatty liver disease (NAFLD), hyperglycemia, and low-grade inflammation. Sulforaphane (SFN) is a hydrolysate of glucosinolate (GLS) that is found in large quantities in cruciferous vegetables. The objective of this research was to evaluate the mechanism by which SFN relieves obesity complications in obese mice. C57BL/6J mice were fed a high-fat diet to induce obesity and treated daily with 10 mg/(kg body weight (bw)) SFN for 8 weeks, while a positive control group was treated daily with 300 mg/(kg bw) metformin. Our results indicated that SFN attenuated NAFLD, inflammation, oxidative stress, adipose tissue hypertrophy, and insulin resistance, as well as regulated glucose and lipid metabolism. SFN regulated glucose and lipid metabolism by deactivating c-Jun N-terminal kinase (JNK) and blocking the inhibitory effect of the insulin signaling pathway. SFN also regulated glucose metabolism by alleviating fibroblast growth factor 21 (FGF21) resistance. Our research provides an empirical basis for clinical treatment with SFN in obesity.