Interaction between ascorbic acid and gallic acid in a model of fructose-mediated protein glycation and oxidation

Background: Dietary plant-based foods contain combinations of various bioactive compounds such as phytochemical compounds and vitamins. The combined effect of these vitamins and phytochemicals remains unknown, especially in the prevention of diabetes and its complications. The present study aimed to investigate the combined effect of ascorbic acid and gallic acid on fructose-induced protein glycation and oxidation. Results: Ascorbic acid (15 \u3bcg/mL) and gallic acid (0.1 \u3bcg/mL) reduced fructose-induced formation of advanced glycation end products (AGEs) in bovine serum albumin (BSA; 10 mg/mL) by 15.06% and 37.83%, respectively. The combination of ascorbic acid and gallic acid demonstrated additive inhibition on the formation of AGEs after 2 weeks of incubation. In addition, synergistic inhibition on the formation of amyloid cross-\u3b2 structure and protein carbonyl content in fructose-glycated BSA was observed. At the same concentration, the combination of ascorbic acid and gallic acid produced a significant additive effect on the 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity. Conclusion: Combining natural compounds such as ascorbic acid and gallic acid seems to be a promising strategy to prevent the formation of AGEs

Investigating the Impact of Dragon Fruit Peel Waste on Starch Digestibility, Pasting, and Thermal Properties of Flours Used in Asia

As a by-product of dragon fruit consumption, dragon fruit peel (DFP) was developed into powder as a natural ingredient. Nevertheless, the effect of DFP on the physicochemical properties of flours used in Asian food processing and cooking remains unknown. In this study, starch digestibility, thermal, pasting, and physicochemical properties of DFP and flours (potato, rice, glutinous rice, and wheat) were characterized. It was found that DFP contained 65.2% dietary fiber together with phenolic compounds, betacyanins, and antioxidant activity. The results demonstrated that DFP (from 125 to 500 mg) reduced starch digestibility of flours, rapidly digestible starch, and slowly digestible starch, along with an increased proportion of undigested starch. A marked increase in phenolic compounds, betacyanins, and antioxidant activity occurred when DFP and flour were incubated for 180 min under simulated gastrointestinal digestion. The results indicate that bioactive compounds in DFP were highly bioaccessible and remained intact after digestion. Moreover, DFP exerted a significantly lower gelatinization enthalpy of flours with increasing peak viscosity and setback with decreasing pasting temperature. FTIR confirmed the decreased ratio at 1047/1022 cm−1, indicating the disruption of short-range orders of starch and DFP. These findings would expand the scope of DFP food applications and provide a knowledge basis for developing DFP flour-based products

Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity

Recently, the mechanisms responsible for anti-glycation activity of cyanidin and its derivatives on the inhibition of methylglyoxal (MG)-induced protein glycation and advanced glycation-end products (AGEs) as well as oxidative DNA damage were reported. In this study, we investigated the protective effect of cyanidin against MG-induced oxidative stress and apoptosis in rat INS-1 pancreatic β-cells. Exposure of cells to cytotoxic levels of MG (500 µM) for 12 h caused a significant reduction in cell viability. However, the pretreatment of cells with cyanidin alone (6.25–100 μM) for 12 h, or cotreatment of cells with cyanidin (3.13–100 μM) and MG, protected against cell cytotoxicity. In the cotreatment condition, cyanidin (33.3 and 100 μM) also decreased MG-induced apoptosis as determined by caspase-3 activity. Furthermore, INS-1 cells treated with MG increased the generation of reactive oxygen species (ROS) during a 6 h exposure. The MG-induced increase in ROS production was inhibited by cyanidin (33.3 and 100 μM) after 3 h stimulation. Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione. In contrast, cyanidin reversed the inhibitory effect of MG on Glo-1 activity and glutathione levels. Interestingly, cyanidin alone was capable of increasing Glo-1 activity and glutathione levels without affecting Glo-1 mRNA expression. These findings suggest that cyanidin exerts a protective effect against MG-induced oxidative stress and apoptosis in pancreatic β-cells by increasing the activity of Glo-1

Cyanidin Attenuates Methylglyoxal-Induced Oxidative Stress and Apoptosis in INS-1 Pancreatic β-Cells by Increasing Glyoxalase-1 Activity

Recently, the mechanisms responsible for anti-glycation activity of cyanidin and its derivatives on the inhibition of methylglyoxal (MG)-induced protein glycation and advanced glycation-end products (AGEs) as well as oxidative DNA damage were reported. In this study, we investigated the protective effect of cyanidin against MG-induced oxidative stress and apoptosis in rat INS-1 pancreatic β-cells. Exposure of cells to cytotoxic levels of MG (500 µM) for 12 h caused a significant reduction in cell viability. However, the pretreatment of cells with cyanidin alone (6.25-100 μM) for 12 h, or cotreatment of cells with cyanidin (3.13-100 μM) and MG, protected against cell cytotoxicity. In the cotreatment condition, cyanidin (33.3 and 100 μM) also decreased MG-induced apoptosis as determined by caspase-3 activity. Furthermore, INS-1 cells treated with MG increased the generation of reactive oxygen species (ROS) during a 6 h exposure. The MG-induced increase in ROS production was inhibited by cyanidin (33.3 and 100 μM) after 3 h stimulation. Furthermore, MG diminished the activity of glyoxalase 1 (Glo-1) and its gene expression as well as the level of total glutathione. In contrast, cyanidin reversed the inhibitory effect of MG on Glo-1 activity and glutathione levels. Interestingly, cyanidin alone was capable of increasing Glo-1 activity and glutathione levels without affecting Glo-1 mRNA expression. These findings suggest that cyanidin exerts a protective effect against MG-induced oxidative stress and apoptosis in pancreatic β-cells by increasing the activity of Glo-1

Acute effect of Clitoria ternatea flower beverage on glycemic response and antioxidant capacity in healthy subjects: a randomized crossover trial

Abstract Background Clitoria ternatea L., a natural food-colorant containing anthocyanin, demonstrated antioxidant and antihyperglycemic activity. The aim of this study was to determine the effects of Clitoria ternatea flower extract (CTE) on postprandial plasma glycemia response and antioxidant status in healthy men. Methods In a randomized, crossover study, 15 healthy men (ages 22.53 ± 0.30 years; with body mass index of 21.57 ± 0.54 kg/m2) consumed five beverages: (1) 50 g sucrose in 400 mL water; (2) 1 g CTE in 400 mL of water; (3) 2 g CTE in 400 mL of water; (4) 50 g sucrose and 1 g CTE in 400 mL of water; and (5) 50 g sucrose and 2 g CTE in 400 mL of water. Incremental postprandial plasma glucose, insulin, uric acid, antioxidant capacities and lipid peroxidation were measured during 3 h of administration. Results After 30 min ingestion, the postprandial plasma glucose and insulin levels were suppressed when consuming sucrose plus 1 g and 2 g CTE. In addition, consumption of CTE alone did not alter plasma glucose and insulin concentration in the fasting state. The significant increase in plasma antioxidant capacity (ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC), trolox equivalent antioxidant capacity (TEAC), and protein thiol) and the decrease in malondialdehyde (MDA) level were observed in the subjects who received 1 g and 2 g CTE. Furthermore, consumption of CTE protected sucrose-induced reduction in ORAC and TEAC and increase in plasma MDA. Conclusions These findings suggest that an acute ingestion of CTE increases plasma antioxidant capacity without hypoglycemia in the fasting state. It also improves postprandial glucose, insulin and antioxidant status when consumed with sucrose. Trial registration Thai Clinical Trials Registry: TCTR20170609003 . Registered 09 September 2017. ‘retrospectively registered’

The effect of Aloe vera juice and acemannan on postprandial lipemic, antioxidant, and inflammatory response in high-fat meal fed overweight/obese men: A randomized crossover-controlled study

This study investigated the impact of Aloe barbadensis Miller (Aloe vera) juice with acemannan on postprandial metabolic markers, antioxidant status, inflammatory responses, and appetite in overweight/obese men following high-fat (HF) meal consumption. In a randomized crossover trial with 16 participants, four meal conditions were tested: (1) HF meal, (2) HF meal with A. vera juice (350 mL), (3) HF meal with A. vera juice plus 0.5 g acemannan, and (4) HF meal with A. vera juice plus 1 g acemannan. Enriching A. vera juice with 1 g acemannan significantly reduced postprandial serum triglycerides, and free fatty acids after the HF meal (p < 0.05). Supplementing the HF meal with A. vera juice and acemannan suppressed postprandial glucose, enhanced postprandial antioxidant capacity and reduced tumor necrosis factor-α levels at 6 h (p < 0.05). Notably, the high-concentration acemannan positively influenced appetite by increasing fullness and decreasing hunger ratings. These findings suggest that acemannan enhances A. vera juice benefits in mitigating postprandial dysmetabolism

Anthocyanin-Enriched Riceberry Rice Extract Inhibits Cell Proliferation and Adipogenesis in 3T3-L1 Preadipocytes by Downregulating Adipogenic Transcription Factors and Their Targeting Genes

Riceberry rice (Oryza sativa L.) is a new pigmented variety of rice from Thailand. Despite its high anthocyanin content, its effect on adipogenesis and adipocyte function remains unexplored. We investigated whether Riceberry rice extract (RBE) impacted cell proliferation by examining viability and cell cycle, using preadipocyte 3T3-L1 cells. To test RBE&rsquo;s effect on adipocyte formation, cells were cultured in adipogenic medium supplemented with extract and adipocyte number and triglyceride levels were quantified. Furthermore, Akt1 phosphorylation along with RT-qPCR and intracellular calcium imaging were performed to obtain an insight into its mechanism of action. The effect of RBE on adipocyte function was investigated using glucose uptake and lipolysis assays. Treatment of cells with RBE decreased preadipocyte number without cytotoxicity despite inducing cell cycle arrest (p &lt; 0.05). During adipogenic differentiation, RBE supplementation reduced adipocyte number and triglyceride accumulation by downregulating transcription factors (e.g., PPAR&gamma;, C/EBP&alpha;, and C/EBP&beta;) and their target genes (p &lt; 0.05). The Akt1 phosphorylation was decreased by RBE but insignificance, however, the extract failed to increase intracellular calcium signals. Finally, the treatment of adipocytes with RBE reduced glucose uptake by downregulating Glut4 mRNA expression and enhanced isoproterenol-induced lipolysis (p &lt; 0.05). These findings suggest that RBE could potentially be used in the treatment of obesity by inhibiting adipocyte formation and proliferation

Anthocyanin-Enriched Riceberry Rice Extract Inhibits Cell Proliferation and Adipogenesis in 3T3-L1 Preadipocytes by Downregulating Adipogenic Transcription Factors and Their Targeting Genes

Riceberry rice ( L.) is a new pigmented variety of rice from Thailand. Despite its high anthocyanin content, its effect on adipogenesis and adipocyte function remains unexplored. We investigated whether Riceberry rice extract (RBE) impacted cell proliferation by examining viability and cell cycle, using preadipocyte 3T3-L1 cells. To test RBE\u27s effect on adipocyte formation, cells were cultured in adipogenic medium supplemented with extract and adipocyte number and triglyceride levels were quantified. Furthermore, Akt1 phosphorylation along with RT-qPCR and intracellular calcium imaging were performed to obtain an insight into its mechanism of action. The effect of RBE on adipocyte function was investigated using glucose uptake and lipolysis assays. Treatment of cells with RBE decreased preadipocyte number without cytotoxicity despite inducing cell cycle arrest ( \u3c 0.05). During adipogenic differentiation, RBE supplementation reduced adipocyte number and triglyceride accumulation by downregulating transcription factors (e.g., PPARγ, C/EBPα, and C/EBPβ) and their target genes ( \u3c 0.05). The Akt1 phosphorylation was decreased by RBE but insignificance, however, the extract failed to increase intracellular calcium signals. Finally, the treatment of adipocytes with RBE reduced glucose uptake by downregulating Glut4 mRNA expression and enhanced isoproterenol-induced lipolysis ( \u3c 0.05). These findings suggest that RBE could potentially be used in the treatment of obesity by inhibiting adipocyte formation and proliferation

Clitoria ternatea Flower Extract Attenuates Postprandial Lipemia and Increases Plasma Antioxidant Status Responses to a High-Fat Meal Challenge in Overweight and Obese Participants

High-fat (HF) meal-induced postprandial lipemia, oxidative stress and low-grade inflammation is exacerbated in overweight and obese individuals. This postprandial dysmetabolism contributes to an increased risk of cardiovascular disease and metabolic disorders. Clitoria ternatea flower extract (CTE) possesses antioxidant potential and carbohydrate and fat digestive enzyme inhibitory activity in vitro. However, no evidence supporting a favorable role of CTE in the modulation of postprandial lipemia, antioxidant status and inflammation in humans presently exists. In the present study, we determine the effect of CTE on changes in postprandial glycemic and lipemic response, antioxidant status and pro-inflammatory markers in overweight and obese men after consumption of an HF meal. Following a randomized design, sixteen participants (age, 23.5 ± 0.6 years, and BMI, 25.7 ± 0.7 kg/m2) were assigned to three groups that consumed the HF meal, or HF meal supplemented by 1 g and 2 g of CTE. Blood samples were collected at fasting state and then at 30, 60, 90, 120, 180, 240, 300 and 360 min after the meal consumption. No significant differences were observed in the incremental area under the curve (iAUC) for postprandial glucose among the three groups. Furthermore, 2 g of CTE decreased the iAUC for serum triglyceride and attenuated postprandial serum free fatty acids at 360 min after consuming the HF meal. In addition, 2 g of CTE significantly improved the iAUC for plasma antioxidant status, as characterized by increased postprandial plasma FRAP and thiol levels. Postprandial plasma glutathione peroxidase activity was significantly higher at 180 min after the consumption of HF meal with 2 g of CTE. No significant differences in the level of pro-inflammatory cytokines (interleukin-6, interleukin-1β and tumor necrosis factor-α) were observed at 360 min among the three groups. These findings suggest that CTE can be used as a natural ingredient for reducing postprandial lipemia and improving the antioxidant status in overweight and obese men after consuming HF meals

Cyanidin-3-rutinoside stimulated insulin secretion through activation of L-type voltage-dependent Ca channels and the PLC-IP pathway in pancreatic β-cells

Cyanidin-3-rutinoside (C3R) is an anthocyanin with anti-diabetic properties found in red-purple fruits. However, the molecular mechanisms of C3R on Ca-dependent insulin secretion remains unknown. This study aimed to identify C3R\u27s mechanisms of action in pancreatic β-cells. Rat INS-1 cells were used to elucidate the effects of C3R on insulin secretion, intracellular Ca signaling, and gene expression. The results showed that C3R at 60, 100, and 300 µM concentrations significantly increased insulin secretion via intracellular Ca signaling. The exposure of cells with C3R concentrations up to 100 μM did not affect cell viability. Pretreatment of cells with nimodipine (voltage-dependent Ca channel (VDCC) blocker), U73122 (PLC inhibitor), and 2-APB (IP receptor blocker) inhibited the intracellular Ca signals by C3R. Interestingly, C3R increased intracellular Ca signals and insulin secretion after depletion of endoplasmic reticulum Ca stores by thapsigargin. However, insulin secretion was abolished under extracellular Ca-free conditions. Moreover, C3R upregulated mRNA expression for Glut2 and Kir genes. These findings indicate that C3R stimulated insulin secretion by promoting Ca influx via VDCCs and activating the PLC-IP pathway. C3R also upregulates the expression of genes necessary for glucose-induced insulin secretion. This is the first study describing the molecular mechanisms by which C3R stimulates Ca-dependent insulin secretion from pancreatic β-cells. These findings contribute to our understanding on how anthocyanins improve hyperglycemia in diabetic patients