Unveiling the Nutritional Veil of Sulforaphane: With a Major Focus on Glucose Homeostasis Modulation

Abstract

Abnormal glucose homeostasis is associated with metabolic syndromes including cardiovascular diseases, hypertension, type 2 diabetes mellitus, and obesity, highlighting the significance of maintaining a balanced glucose level for optimal biological function. This highlights the importance of maintaining normal glucose levels for proper biological functioning. Sulforaphane (SFN), the primary bioactive compound in broccoli from the Cruciferae or Brassicaceae family, has been shown to enhance glucose homeostasis effectively while exhibiting low cytotoxicity. This paper assesses the impact of SFN on glucose homeostasis in vitro, in vivo, and human trials, as well as the molecular mechanisms that drive its regulatory effects. New strategies have been proposed to enhance the bioavailability and targeted delivery of SFN in order to overcome inherent instability. The manuscript also covers the safety evaluations of SFN that have been documented for its production and utilization. Hence, a deeper understanding of the favorable influence and mechanism of SFN on glucose homeostasis, coupled with the fact that SFN is abundant in the human daily diet, may ultimately offer theoretical evidence to support its potential use in the food and pharmaceutical industries.

Keywords: bioavailability; glucose homeostasis; human trials; in vitro/in vivo; safety; sulforaphane.

Figure 1

Schematic representation of signaling pathways regulated by SFN against inflammation and oxidation. SFN activates Nrf2, promotes Nrf2 translocation into the nucleus, and subsequently promotes antioxidant gene expression. In addition, SFN inhibits the expression of NF-κB, reduces the expression of inflammatory genes, and reduces inflammation in the whole organism.

Figure 2

The main sources of sulforaphane include broccoli, cabbage, cauliflower, kale, bok choy, Brussels sprouts, and kohlrabi.

Figure 3

Coordination of various organs is required in the regulation of glucose homeostasis. The liver increases blood glucose levels by converting non-glucose compounds in glucose into the blood circulation through gluconeogenesis and can also achieve the conversion of glucose and glycogen according to the blood glucose level. The pancreas lowers blood glucose levels by secreting insulin that promotes glucose uptake into the adipose tissue, as well as inhibiting hepatic glucose production. In addition, in the liver, sulforaphane modulates glucose homeostasis via increasing glucose uptake, liver fatty acid oxidation, glycogen levels, insulin signaling, and inhibiting glucose production and insulin resistance. Similarly, sulforaphane also increases glucose uptake, mitochondrial biogenesis, and glucose aerobic oxidation in adipose tissues.

Figure 4

Impaired glucose homeostasis is closely related to the occurrence of metabolic syndromes including type 2 diabetes, non-alcoholic fatty liver disease, cancer, obesity, diabetic nephropathy, cardiovascular disease, diabetic retinopathy, gestational diabetes, diabetic foot ulcer, and atherosclerosis.