Varities of Sweet Potato inType 2 Diabetes

Discussion

4.1. Varieties of Ipomoea Batatas (Sweet Potato)

Developed for Type 2 Diabetes

Sweet potatoes are distinguished by their color, width, thickness, shape of the leaves, size, and color of the skin and flesh of the tubers [40].

 Research on the anti-diabetic activity includes white [14,15,16,23,24,28,30,31,32,34], purple [20,22,33,35,37,39], orange [29,38], and Japanese green sweet potatoes [25].

 Understanding of the Ipomoea batatas varieties that are proven to exhibit anti-diabetic activity will facilitate the identification and isolation of specific bioactive components that can serve as starting molecules or models for creating a novel synthetic medicine [41,42].

4.2. Types and Concentrations of Phytochemicals Contained in Ipomoea batatas Which Have Anti-Diabetic Effects

The leaves of white sweet potato have a total polyphenol concentration of 6.4 g/100 g, which is greater than that of the orange varieties as well as Japanese green sweet potatoes [16,25,38]. The plant parts used also have an impact on the variation in polyphenol concentration. 

The total polyphenols in the leaves are more significant

 when compared to the tuber [43]. Green leaves have higher total phenolics than green or purple leaves [44].

 Different maturity stages of sweet potato plants exhibit a significant amount of variation in flavonols and phenolic acids of the sweet potato leaves. The quantity of bioactive compounds rises as the plant ages [45].

 Anthocyanin concentrations are more significant in purple than orange tuber sweet potatoes. The concentration of phenolic acids in purple tubers is ten times greater than that,60]. in orange and white sweet potatoes [46].

4.3. Mechanism of Action Chemical Components in Ipomoea batatas for Anti-Diabetic Effects

4.3.1. Protects the Integrity of Islet Structures and Modulates Pancreatic β Cell Function

β-pancreatic cells are responsible for insulin secretion.

 Therefore, maintaining the islet structure of pancreatic β cells is essential for treating diabetes. 

The results of the pancreatic histopathological analysis showed that the administration of white sweet potato ethanol extract at doses of 80 and 150 mg per kg BW

 of mice for four weeks could improve the islet structure by enlarging the islet area and inhibiting apoptosis of β-pancreatic cells [47,48]. 

In addition, administering purple sweet potato extract

 containing anthocyanins and protein at a dose of 200 mg/kg body weight reduced oxidative stress and pancreatic damage in diabetic mice [20]. 

However, a larger dose of cloned B 0059-3 sweet potato extract obtained from Bandungan, West Java, Indonesia was required to protect β-pancreatic cells [19]. 

The ability to protect and modulate the function of pancreatic β polyphenols contained in ethanol extracts of white and purple sweet potato is more significant than resveratrol and polyphenols contained in Ginger (Zingiber officinale) rhizome [49,50]. 

The administration of polyphenol or protein-bound anthocyanins and free anthocyanins induced the expression of AMP-activated protein kinase (AMPK) in the liver, significantly increased levels of glucose transporter type 2 (GLUT2), glucokinase protein (GK), and insulin receptor α (INSR) [20,51].

4.3.2. Increased Insulin Secretion and Improved Insulin Sensitivity

In vivo studies have demonstrated that the administration of Caiapo, glycoprotein acid, and 3,4,5-tricaffeoylquinic results in an increased insulin sensitivity [15,24,25,52]. The effectiveness of Caiapo as an antidiabetic was proven by conducting clinical trials on 30 patients given Caiapo 4 g/day orally, once a day, in the morning before meals. Caiapo administration led to a significant reduction in HbA1c compared to the placebo group after 2 and 3 months of the administration. In addition, from the study’s results, it was found that the administration of Caiapo caused the average fasting blood glucose level to reach 126 mg/dl, weight loss, and a significant decrease in postprandial glucose levels and cholesterol [14]. The caffeoylquinic derivative significantly increased glucagon-like peptide-1 (GLP-1) secretion [25,53] and glycoprotein acid increased modulation of insulin sensitivity (adiponectin) [28,54]. Similar results were obtained from the administration of polyphenols, such as phenolic acids and flavonoids, from the sweet potato leaf extract, with an improved insulin sensitivity through activation of insulin signaling in the skeletal muscles [23]. Flavonoids, such as methyl decanoate, have the potential to increase insulin sensitivity in skeletal muscles [22,55,56,57]. The increased insulin sensitivity is due to Akt phosphorylation, thereby activating insulin signals in the skeletal muscles of phosphatidylinositol 3-kinase/protein kinase B/glucose transporter 4 (PI3K/AK

T/GLUT-4) and liver (PI3K/AKT/GSK-3β) [23,31,47,58,59,60].

4.3.3. Regulation of Carbohydrate Metabolism

Ethyl caffeate has the ability of α-glucosidase inhibition with an IC50 value 6.77 times lower than acarbose. Flavonoids, such as kaempferol, quercetin, hyperoside, isoquercitrin, and rutin, also showed a stronger inhibition of α-glucosidase compared to acarbose [16]. Phenethyl cinnamates, 3,4,5-tricaffeoylquinic acid, quercetin-3-O-glucosidase, and 7-hydroxy-5-methoxy coumarin also showed excellent α-glucosidase inhibitory activity, where the IC50 values were much lower than that of the positive control acarbose. The increasing number of caffeoyl groups bound to quinic acid and methoxylation in flavonol compounds led to increased inhibition of α-glucosidase [29,61]. The inhibitory ability of α-glucosidase by phenolic acids and flavonoids is possible through binding enzyme surface amino acid residues, thereby altering the conformation of α-glucosidase, distorting the active site, and decreasing enzyme activity [53]. Ethyl caffeate, quercetin, hesperetin, luteolin, rutin, catechins, and cyanidin-3-glucoside also have an α-amylase inhibitory action [16,62]. Anthocyanins and protein-bound anthocyanins were able to control the expression of genes essential in glycolysis, such as phosphofructokinase (PFK) and pyruvate kinase (PK), and suppress the expression of gluconeogenic genes glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) [20].

4.3.4. Suppression of Glucose Production in 

the Liver

Glycoproteins may play a role in suppressing gluconeogenesis [31,63,64]. My The administration

 of acetylated anthocyanins cyanidin, 3-caffeoyl-p-hydroxybenzolsophoroside-5-glucoside, peonidin, and 3-caffeoyl sophoroside-5-glucoside have been shown to decrease glucose production in HepG2 cells. However, only cyanidin reduced the fasting blood glucose levels to 186–205 mg/dL after 1 and 2 h of in vivo administration [39].

4.3.5. Inhibition of Glucose Transport in the Intestine and Increased Uptake of Tissue Glucose

The administration of hexane and a water fraction of purple sweet potato leaf methanol extract increased the glucose uptake in 3T3-L1 adipocyte tissue and rat hepatocytes. Flavonoids, such as quercetin, have a more remarkable glucose uptake ability than other components such as 3-O-β-D-sophoroside, benzyl β-D-glucoside, and 4-hydroxy-3-methoxy benzaldehyde. The ability of some of these active compounds in glucose uptake in adipocyte tissue is most likely through the activation of GLUT4 and regulation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway [22,65]. However, the administration of 5% white sweet potato powdered leaves increased the expression of p-IR, p-AKT, and M-GLUT4, but had no significant effect on the PI3K/AKT pathway [23].

4.3.6. Repair of Insulin Signals and Glycogen Synthesis

There was an increase in mRNA insulin receptor (IR) expression, insulin receptor substrate 2 (IRS-2), PI3K, and AKT genes, and a decrease in glycogen synthase kinase-3β (GSK-3β) expression with white sweet potato extract administration [16]. This proved that these extracts promote liver glycogen synthesis by activating the insulin-mediated PI3K/AKT/GSK-3β signaling pathway [47,66]. Moreover, the administration of ethyl acetate fraction from white sweet potato ethanol extract and flavonoids contained in the water fraction of the extract was able to activate GLUT4 and regulate the phosphatidylinositol 3-kinase (PI3K)/AKT pathway [36].

4.3.7. Inhibition of Inflammatory Pathways

The commercial administration of anthocyanins from purple sweet potato decreased the expression of cyclooxygenase-2, tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. Anthocyanins can inhibit the phosphorylation induction/activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) [67]. The administration of 5 g/kg BW/day Caiapo significantly decreased p38 MAPKs and TNF-α production in diabetic rats. These findings imply that the inhibition of oxidative stress and the creation of pro-inflammatory cytokines, followed by an increase in the pancreatic cell mass, are what cause the hypoglycemic effects of Ipomoea batatas [27].

Ref

Foods. 2023 Jul 24;12(14):2810. doi: 10.3390/foods12142810

Mechanism of Anti-Diabetic Activity from Sweet Potato (Ipomoea batatas): A Systematic Review

Cokorda Istri Sri Arisanti 1,2, I Made Agus Gelgel Wirasuta 2, Ida Musfiroh 1, Emmy Hainida Khairul Ikram 3,4,5, Muchtaridi Muchtaridi 1,5,*