ABSTRACT
Background:A good number of medicinal and dietary plants are used for diabetes treatment in Burkina Faso. Aim of the Study:The present study aimed to investigate the antidiabetic activity of Guiera senegalensisgalls extracts and its potential mechanisms in streptozotocin-induced diabetic rats. Methodology:The methanol extract was administered by gavage to healthy Wistar rats for the determination of toxicity, to normal and diabetic Wistar rats forthe determination of glucose reduction level, lipid profile, insulin level and glycaemic parameters in serum. The histology and immunohistochemistry of thepancreas were also determined.Results:The acute toxicity results showed that the medium lethal dose (LD50) of the methanol galls extract of Guiera senegalensisis greater than 2000 mg/kg body weight in rats. Guiera senegalensismethanolic extract (250 mg/kg) and the tolbutamide (100 mg/kg) recorded a significantly (p < 0.05)lower level of triglyceride compared to the diabetic group. The methanol extract (250 and 500 mg/kg pc) significantly (p < 0.05)decreased the blood glucose level and increased the serum insulin level in diabetic rats. Interestingly, improved ß-cell function and antioxidant status were also observed in G. senegalensis-treated diabetic rats when compared to tolbutamide-treated diabetic rats.Conclusion:These data showed direct evidence that G. senegalensishas antidiabetic activity by decreasing blood glucose level, improving insulin secretion and β-cell functions and modulating antioxidant status
ABSTRACT
Several studies indicated that pancreatic ß-cell death occurs in both type 1 and type 2 diabetes. This experimental study was designed to determine the effect of gestational diabetes on the ß-cells in 16-week-old rat offspring. By this aim, adult Wistar rats aged 10-12 weeks were randomly allocated in control and diabetic groups. The diabetic group received 40 mg/kg/body weight of streptozotocin (STZ) on day zero of gestation. After delivery, diabetic offspring of GDM mothers and controls at the age of 16 weeks were sacrificed and pancreases harvested and fixed. The number of ß-cells and were counted by Gomori's method staining. Also, apoptosis in pancreas tissue of diabetic and control offspring was detected by TUNEL assay. Results showed a significant reduction in ß-cell number in offspring of GDM (p<0.05). TUNEL assay showed that the number of apoptotic cells increased in GDM compared to controls (P<0.05). This study revealed that gestational diabetes induces pancreatic beta-cells apoptosis in 16-week-old rat offspring.
Varios estudios indican que la muerte de las células ß del páncreas se produce tanto en la diabetes Tipo 1 como en la Tipo 2. Este estudio experimental fue diseñado para determinar el efecto de la diabetes gestacional en las células ß del páncreas en crías de ratas de 16 semanas. Para ello, ratas Wistar adultas de entre 10-12 semanas fueron asignadas al azar en dos grupos: control y diabetes. El grupo diabetes recibió 40 mg / kg / peso corporal de estreptozotocina (STZ) en el día cero de la gestación. Después del parto, a las 16 semanas, las crías de las madres diabéticas y controles de madres con diabetes gestacional (MDG), fueron sacrificadas para la extracción del páncreas, el cual posteriormente fue fijado. Se contó el número de células ß del páncreas mediante tinción con el método de Gomori. Además, se detectó apoptosis en el tejido del páncreas de la descendencia diabética y el grupo control mediante un ensayo TUNEL. Los resultados mostraron una reducción significativa en el número de células b en la descendencia de MDG (p <0,05). El ensayo TUNEL mostró que el número de células apoptóticas aumentó en MDG en comparación con los controles (P <0,05). Este estudio reveló que la diabetes gestacional induce apoptosis de células ß en el páncreas de crías de ratas de 16 semanas.
Subject(s)
Animals , Rats , Apoptosis , Diabetes, Gestational/pathology , Islets of Langerhans/pathology , Blood Glucose/analysis , In Situ Nick-End Labeling , Pancreas/pathology , Rats, WistarABSTRACT
The present study compares two computer models of the first part of glucose catabolism in different organisms in search of evolutionarily conserved characteristics of the glycolysis cycle and proposes the main parameters that define the stable steady-state or oscillatory behavior of the glycolytic system. It is suggested that in both human pancreatic b-cells and Saccharomyces cerevisiae there are oscillations that, despite differences in wave form and period of oscillation, share the same robustness strategy: the oscillation is not controlled by only one but by at least two parameters that will have more or less control over the pathway flux depending on the initial state of the system as well as on extra-cellular conditions. This observation leads to two important interpretations: the first is that in both S. cerevisiae and human b-cells, despite differences in enzyme kinetics and mechanism of feedback control, evolution seems to have kept an oscillatory behavior coupled to the glucose concentration outside the cytoplasm, and the second is that the development of drugs to regulate metabolic dysfunctions in more complex systems may require further study, not only determining which enzyme is controlling the flux of the system but also under which conditions and how its control is maintained by the enzyme or transferred to other enzymes in the pathway as the drug starts acting.