Antidiabetic Effects of Radish
Recently, the incidence of diabetes has become a major health threat worldwide. Diabetes is one of the leading causes of mortality in humans [91].
In order to prevent the disease, several countries have adapted various therapeutic approaches and scientists are continuously striving to discover potential antidiabetic agents [92].
However, the need to circumvent the uncontrolled homeostasis of glucose metabolism has led to the search of plant-based antidiabetic compounds [92,93,94].
The usage of radish extracts in the treatments of digestive or stomach-related ailments since the ancient times has given a clue for the occurrence of phytochemicals with antidiabetic properties in radishes.
The water soluble extract of radish displayed hypoglycemic properties due to the presence of insulin-like polyphenols or glucose-inhibiting compounds [95,96].
Likewise, several studies have recorded the antidiabetic effects of radish in the in vitro and in vivo environment [15,97,98].
The antidiabetic nature of radish extracts can be due to the following mechanisms: (a) regulation of glucose related hormones, (b) prevention of diabetes-induce oxidative stress and (c) balancing the glucose uptake and absorption [92]
. The radish extracts enhanced the synthesis of
adiponectin, a central regulatory protein involved in the regulation of lipid and glucose metabolism secreted by adipose tissue [99,100].
Adiponectin increases insulin sensitivity and enhances the bodyweight reduction [101].
It synchronizes various metabolic processes and aids in the maintenance of glucose uptake and lipid oxidation processes [101,102].
Moreover, adiponectin regulates several genes involved in inflammation, cellular proliferation, cell death, endosomal trafficking and chromatin remodeling [103].
An increase in the production of adiponectin triggers the adiponectin receptors (ADIPOR1 and 2) and peroxisome proliferator-activated receptor gamma (PPARγ) [101]
. The ADIPOR1 stimulates the genes involved in inflammation and regulation of oxidative stress whereas ADIPOR2 activates adaptor protein, phosphotyrosine interaction, pH domain and leucine zipper containing 1 (APPL1), which in turn increases the expression of genes that are vital for gluconeogenesis and glucose uptake [104,105].
On the other hand, PPARγ maintains the beta oxidation in lipid metabolism. The adiponectin interaction with its receptors results in the phosphorylation of acetyl-CoA carboxylase 2 (ACC2), which increases the oxidation of fatty acids and enhances the insulin sensitivity [101,106,107]. In addition, the increase in the ROS levels have been alleviated by adiponectin mediated regulation of transcription of genes involved in antioxidant machinery, such as superoxide dismutase (SOD) [108]. Overall, the stimulatory effects of radish extract on adiponectin could be an important tactic to combat the diabetes. A detailed illustration of the possible mechanisms involved in the adiponectin mediated prevention of diabetes by radish extract has been shown in
Figure 2.
Similarly, the extracts of Japanese radish sprouts displayed antidiabetic activity in streptozotocin-induced diabetic rats [97].
In addition, the administration of radishes decreased the starch-stimulated glycemic load,
which provided evidence for the prevention of diabetes [109].
Moreover, the occurrence of polyphenols, such as catechin in radishes, improved the insulin secretion [110].
Apart from the regulation of glucose metabolism, the antioxidant activity of radish prevented the oxidative stress induced by diabetes.
For instance, radishes enhanced the synthesis of superoxide dismutase (SOD) like proteins and endogenous glutathione and catalase enzymes to scavenge the free radicals and prevented the peroxidation of lipids under diabetic conditions [111,112].
Similarly, radish extracts with pelargonidin (anthocyanin derivative) aid in the antioxidant activity by decreasing the generation of free radicals and formation of a thiobarbituric acid reactive moiety [113].
Another important antioxidant compound, sulforaphane (isothiocyanate), induces the phase II antioxidant enzymes and maintains the redox balance upon oxidative stress [114]. In addition, the nutritional and secondary metabolites content of radishes can be varied by using a different method of processing for consumption [115]
. Overall, the radish extracts consist of high antidiabetic values although the exact mechanism associated with antidiabetic properties has to be determined in the future, which can be utilized in the antidiabetic drug designing pipelines.
Recently, the incidence of diabetes has become a major health threat worldwide. Diabetes is one of the leading causes of mortality in humans [91]. In order to prevent the disease, several countries have adapted various therapeutic approaches and scientists are continuously striving to discover potential antidiabetic agents [92]. However, the need to circumvent the uncontrolled homeostasis of glucose metabolism has led to the search of plant-based antidiabetic compounds [92,93,94]. The usage of radish extracts in the treatments of digestive or stomach-related ailments since the ancient times has given a clue for the occurrence of phytochemicals with antidiabetic properties in radishes. The water soluble extract of radish displayed hypoglycemic properties due to the presence of insulin-like polyphenols or glucose-inhibiting compounds [95,96]. Likewise, several studies have recorded the antidiabetic effects of radish in the in vitro and in vivo environment [15,97,98]. The antidiabetic nature of radish extracts can be due to the following mechanisms: (a) regulation of glucose related hormones, (b) preventd (c) balancing the glucose uptake and absorption [92]. The radish extracts enhanced the synthesis of adiponectin, a central regulatory protein involved in the regulation of lipid and glucos reduction [101]. It s [101,102]. Moreover, adiponectin regulates several genes involved in inflammation, cellular proliferation, cell death, endosomal trafficking and chromatin remodeling [103]. An increase in the production of adiponectin triggers the adiponectin receptors (ADIPOR1 and 2) and peroxisome proliferator-activated receptor gamma (PPARγ) [101]. The ADIPOR1 stimulates the genes involved in inflammation and regulation of oxidative stress whereas ADIPOR2 activates adaptor protein, phosphotyrosine interaction, pH domain and leucine zipper containing 1 (APPL1), which in turn increases the expression of genes that are vital for gluconeogenesis and glucose uptake [104,105]. On the other hand, PPARγ maintains the beta oxidation in lipid metabolism. The adiponectin interaction with its receptors results in the phosphorylation of acetyl-CoA carboxylase 2 (ACC2), which increases the oxidation of
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