RESUMEN
Diabetes is a chronic disease caused by an imbalance of insulin release to the bloodstream in response to excessive glucose influx, which causes hyperglycemia. White saffron (Curcuma mangga Val.), an Indonesian aromatic spice, contains essential phytochemicals and has a number of potential health benefits. Here, we examined the effects of oral administration of white saffron powder (WSP): 1.5 and 4.5 g (WSP 1.5 and WSP 4.5) in streptozotocin (STZ)-induced diabetic rats. WSP was administered orally on a daily basis for one month and its antidiabetic, anti-inflammatory, and antioxidative effects were investigated by measuring the concentrations of blood glucose, insulin, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin 8 (IL-8), malondialdehyde (MDA), and superoxide dismutase (SOD) activity. In response to high WSP intervention (WSP 4.5), treated rats showed increased insulin level and SOD activity and reduced blood glucose, IL-6, IL-8, TNF-α, and MDA levels, which were closely related to the positive control (PC) group. In addition, Hematoxylin and Eosin (H&E) staining of the pancreatic tissues showed that WSP 4.5-treated rats had significant improvement in ß-cell regeneration, which taken together reflected the antidiabetic potential of Curcuma mangga Val.
RESUMEN
BACKGROUND: There would be over 600 million people living with diabetes by 2040 as predicted by the World Health Organization. Diabetes is characterized by raised blood sugar and insulin resistance. Insulin regulates the influx of glucose into the cell by upregulating the glucose transporter type 4 (GLUT4) expression on the plasma membrane. Besides, PPAR-γ also controls the metabolism of glucose in adipose tissues. Curcuma mangga Val., denoted as C. mangga, is a native Indonesian medicinal plant that has many beneficial effects, including an antidiabetic potential. PURPOSE: In this research, we aimed to disclose the hypoglycemic activity of ethanol extract of C. mangga (EECM) in 3T3-L1 fibroblasts-derived adipocyte cells in regulating glucose uptake as confirmed by the GLUT4 and PPAR-γ gene expression. METHODS: The uptake of glucose was determined using radioactive glucose, while the gene expression of GLUT4, PPAR-γ, and ß-actin was quantified using mRNA segregation and real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR). RESULTS: We discovered that EECM interventions (200 and 50 µg/mL) increased glucose uptake in lipid-laden 3T3-L1 cells by 14.75 and 8.86 fold compared to the control non-insulin, respectively (p < 0.05). At the same doses, they also increased GLUT4 mRNA expression by 8.41 and 11.18 fold compared to the control non-insulin, respectively (p < 0.05). In contrast, EECM interventions (200 and 50 µg/mL) showed lower levels of PPAR-γ mRNA expression compared to the control metformin, indicating the anti-adipogenic potentials of EECM. CONCLUSION: EECM showed hypoglycemic activity in lipid-laden 3T3-L1 cells by improving glucose ingestion into the cells, which was mediated by increased GLUT4 expression and downregulated PPAR-γ expression.