WATER EXTRACT OF CAESALPINIA PULCHERRIMA FLOWERS INCREASES GLUCOSE UPTAKE IN INSULIN RESISTANT ADIPOCYTES IN A DOSEDEPENDENT MANNER

2020 ◽  
Vol 7 (2) ◽  
pp. 172-175
Author(s):  
Angela B.F. Carrington-Dyall ◽  
Ahmad Idrees Shekaib ◽  
Nickelia E. Clarke-Jordan
Keyword(s):  
Glucose Uptake ◽  
Pancreatic Beta Cell ◽  
Water Extract ◽  
Direct Effects ◽  
Glucose Load ◽  
Bicarbonate Buffer ◽  
Vacuum Filtration ◽  
Insulin Resistant ◽  
Flower Extract ◽  
Antidiabetic Effects

Caesalpinia pulcherrima (CP) flower extract has been shown to have antidiabetic effects on pancreatic beta cell regeneration and improved skeletal muscle glucose utilisation. However, little is known about its effect on adipocytes, particularly insulin resistant adipocytes. This study investigated the possibility of improving glucose uptake in adipocytes obtained from chickens which are naturally insulin resistant via direct effects of water extract of Caesalpinia pulcherrima flowers. The extract was prepared by boiling air dried CP flowers in a water based modified Krebs Ringer Bicarbonate buffer for 5mins and sterilizing the filtrate via vacuum filtration. A glucose load of 18mM and 10% ITS was added to the extract. In the absence of adipocytes, the glucose concentration of the CP extract remained unchanged (p=0.5087). Insulin resistance in the chicken adipocytes was confirmed by delayed and limited glucose uptake (maximum 2.9% + 1.62% in 60mins). This was reversed via the addition of the water extract of the CP flowers as concentrations as low as 2.8mg/ml doubled glucose uptake and concentrations as low as 5.6mg/ml increased the rate of glucose uptake to that of insulin sensitive cells. These results suggest that water extract of CP flowers directly modulate glucose uptake into insulin resistant cells at concentrations as low as 2.8mg/ml following a 5mins decoction preparation.

scholarly journals Water Extract of Mungbean (Vigna radiata L.) Inhibits Protein Tyrosine Phosphatase-1B in Insulin-Resistant HepG2 Cells

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1452
Author(s):  
Orathai Saeting ◽  
Kasemsiri Chandarajoti ◽  
Angsuma Phongphisutthinan ◽  
Parichat Hongsprabhas ◽  
Sudathip Sae-tan
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Protein Tyrosine Phosphatase ◽  
Hepg2 Cells ◽  
Tyrosine Phosphatase ◽  
Water Extract ◽  
Protein Tyrosine ◽  
Insulin Resistant ◽  
Expression Of Genes ◽  
Ptp 1B

The present study aimed to investigate the effects of mungbean water extract (MWE) on insulin downstream signaling in insulin-resistant HepG2 cells. Whole seed mungbean was extracted using boiling water, mimicking a traditional cooking method. Vitexin and isovitexin were identified in MWE. The results showed that MWE inhibited protein tyrosine phosphatase (PTP)-1B (IC50 = 10 μg/mL), a negative regulator of insulin signaling. MWE enhanced cellular glucose uptake and altered expression of genes involved in glucose metabolism, including forkhead box O1 (FOXO1), phosphoenolpyruvate carboxykinase (PEPCK), and glycogen synthase kinase (GSK)-3β in the insulin-resistant HepG2 cells. In addition, MWE inhibited both α-amylase (IC50 = 36.65 mg/mL) and α-glucosidase (IC50 = 3.07 mg/mL). MWE also inhibited the formation of advanced glycation end products (AGEs) (IC50 = 2.28 mg/mL). This is the first study to show that mungbean water extract increased cellular glucose uptake and improved insulin sensitivity of insulin-resistant HepG2 cells through PTP-1B inhibition and modulating the expression of genes related to glucose metabolism. This suggests that mungbean water extract has the potential to be a functional ingredient for diabetes.

scholarly journals HYPOGLYCEMIC ACTIVITY OF THE AQUEOUS EXTRACT OF CAESALPINIA PULCHERRIMA FLOWERS IS INDEPENDENT OF INSULIN STIMULATION AND SUPPRESSED IN THE PRESENCE OF METFORMIN

2020 ◽  
Vol 7 (2) ◽  
pp. 152-156
Author(s):  
Angela B.F. Carrington-Dyall ◽  
Ahmad Idrees Shekaib ◽  
Nickelia E. Clarke-Jordan
Keyword(s):  
Cell Culture ◽  
Culture Media ◽  
Water Extract ◽  
Hypoglycemic Activity ◽  
Glucose Disposal ◽  
Metformin Hydrochloride ◽  
Therapeutic Equivalence ◽  
Independent Manner ◽  
Bicarbonate Buffer ◽  
Insulin Resistant

Considering the high prevalence of insulin resistance, antidiabetic strategies that enhance insulin action or act independent of insulin are desirable. Caesalpinia pulcherrima (CP) flowers are known to have antidiabetic properties, but more work is required with respect to this action in insulin resistant adipocytes, particularly, its dependence on insulin and its therapeutic equivalence and/or interactions with other antidiabetic drugs. The purpose of this study was therefore to investigate the insulindependency of the water extract of CP flowers (CP extract) hypoglycemic effects, compare its antidiabetic action in diabetic and non-diabetic glucose loads, and explore its therapeutic equivalence and interactions with metformin. CP extract was prepared by boiling the air-dried flowers in cell culture media prepared in Krebs Ringer Bicarbonate buffer for 5mins. Metformin solution was prepared from a Metformin hydrochloride extended-release tablet to obtain low and therapeutic levels of metformin (0.8-2.4mg/L and). Insulin resistant (IR) adipocytes were exposed to CP extract in cell culture containing either 8mM or 18mM glucose and one of three insulin concentrations. CPextract allowed an efficient glucose disposal in the IR adipocytes in an insulin independent manner (p<0.0001). The percentage of glucose uptake did not significantly differ by models of diabetic and non-diabetic conditions (p=0.4727) although the significantly higher glucose concentration taken up by the IR adipocytes in the presence of IR adipocytes suggest an enhancement of antidiabetic action in hyperglycemic conditions. Expectedly metformin had a higher potency than the CP extract with its therapeutic dose of 1.8-2.4mg/L corresponding to 280mg/l of CP extract (p=0.9996). Additionally, metformin and CP extract appear to compete for similar sites which suppressed the hypoglycemic activity of CPextract.

scholarly journals Nonhepatic response to portal glucose delivery in conscious dogs

2000 ◽  
Vol 279 (6) ◽  
pp. E1271-E1277 ◽  
Author(s):  
Mary Courtney Moore ◽  
Po-Shiuan Hsieh ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Glucose Uptake ◽  
Glucose Infusion ◽  
Glucose Load ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
The Difference ◽  
Arterial Plasma ◽  
Arterial Blood Glucose ◽  
Blood Glucose Concentrations ◽  
Hepatic Glucose Uptake

The glycemic and hormonal responses and net hepatic and nonhepatic glucose uptakes were quantified in conscious 42-h-fasted dogs during a 180-min infusion of glucose at 10 mg · kg−1 · min−1 via a peripheral (Pe10, n = 5) or the portal (Po10, n = 6) vein. Arterial plasma insulin concentrations were not different during the glucose infusion in Pe10 and Po10 (37 ± 6 and 43 ± 12 μU/ml, respectively), and glucagon concentrations declined similarly throughout the two studies. Arterial blood glucose concentrations during glucose infusion were not different between groups (125 ± 13 and 120 ± 6 mg/dl in Pe10 and Po10, respectively). Portal glucose delivery made the hepatic glucose load significantly greater (36 ± 3 vs. 46 ± 5 mg · kg−1 · min−1 in Pe10 vs. Po10, respectively, P < 0.05). Net hepatic glucose uptake (NHGU; 1.1 ± 0.4 vs. 3.1 ± 0.4 mg · kg−1 · min−1) and fractional extraction (0.03 ± 0.01 vs. 0.07 ± 0.01) were smaller ( P < 0.05) in Pe10 than in Po10. Nonhepatic (primarily muscle) glucose uptake was correspondingly increased in Pe10 compared with Po10 (8.9 ± 0.4 vs. 6.9 ± 0.4 mg · kg−1 · min−1, P < 0.05). Approximately one-half of the difference in NHGU between groups could be accounted for by the difference in hepatic glucose load, with the remainder attributable to the effect of the portal signal itself. Even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to alter partitioning of a glucose load among the tissues, stimulating NHGU and reducing peripheral glucose uptake.

Hemodynamic actions of insulin

1994 ◽  
Vol 267 (2) ◽  
pp. E187-E202 ◽  
Author(s):  
A. D. Baron
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Pressor Response ◽  
Physiological Role ◽  
Oxide System ◽  
Maximal Response ◽  
Insulin Resistant ◽  
The Right

There is accumulating evidence that insulin has a physiological role to vasodilate skeletal muscle vasculature in humans. This effect occurs in a dose-dependent fashion within a half-maximal response of approximately 40 microU/ml. This vasodilating action is impaired in states of insulin resistance such as obesity, non-insulin-dependent diabetes, and elevated blood pressure. The precise physiological role of insulin-mediated vasodilation is not known. Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin's overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. In addition, insulin-mediated vasodilation may play a role in the regulation of vascular tone. Data are provided to indicate that the pressor response to systemic norepinephrine infusions is increased in obese insulin-resistant subjects. Moreover, the normal effect of insulin to shift the norepinephrine pressor dose-response curve to the right is impaired in these patients. Therefore, impaired insulin-mediated vasodilation could further contribute to the increased prevalence of hypertension observed in states of insulin resistance. Finally, data are presented to indicate that, via a yet unknown interaction with the endothelium, insulin is able to increase nitric oxide synthesis and release and through this mechanism vasodilate. It is interesting to speculate that states of insulin resistance might also be associated with a defect in insulin's action to modulate the nitric oxide system.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Importance of the route of insulin delivery to its control of glucose metabolism

2021 ◽  
Author(s):  
Dale S. Edgerton ◽  
Mary Courtney Moore ◽  
Justin M. Gregory ◽  
Guillaume Kraft ◽  
Alan D. Cherrington
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
The Body ◽  
Whole Body ◽  
Direct Effects ◽  
Pancreatic Insulin ◽  
Hepatic Glucose

Pancreatic insulin secretion produces an insulin gradient at the liver compared to the rest of the body (approximately 3:1). This physiologic distribution is lost when insulin is injected subcutaneously, causing impaired regulation of hepatic glucose production and whole body glucose uptake, as well as arterial hyperinsulinemia. Thus, the hepatoportal insulin gradient is essential to the normal control of glucose metabolism during both fasting and feeding. Insulin can regulate hepatic glucose production and uptake through multiple mechanisms, but its direct effects on the liver are dominant under physiologic conditions. Given the complications associated with iatrogenic hyperinsulinemia in patients treated with insulin, insulin designed to preferentially target the liver may have therapeutic advantages.

scholarly journals IL-15Rα is a determinant of muscle fuel utilization, and its loss protects against obesity

2015 ◽  
Vol 309 (8) ◽  
pp. R835-R844 ◽  
Author(s):  
Emanuele Loro ◽  
Erin L. Seifert ◽  
Cynthia Moffat ◽  
Freddy Romero ◽  
Manoj K. Mishra ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Energy Homeostasis ◽  
Wide Distribution ◽  
Liver Fat ◽  
Acid Oxidation ◽  
Direct Effects ◽  
High Fat ◽  
Binding Partner ◽  
Insulin Resistant ◽  
Diet Induced Obesity

IL-15Rα is the widely expressed primary binding partner for IL-15. Because of the wide distribution in nonlymphoid tissues like skeletal muscle, adipose, or liver, IL-15/IL-15Rα take part in physiological and metabolic processes not directly related to immunity. In fast muscle, lack of IL-15Rα promotes an oxidative switch, with increased mitochondrial biogenesis and fatigue resistance. These effects are predicted to reproduce some of the benefits of exercise and, therefore, improve energy homeostasis. However, the direct effects of IL-15Rα on metabolism and obesity are currently unknown. We report that mice lacking IL-15Rα (IL-15Rα−/−) are resistant to diet-induced obesity (DIO). High-fat diet-fed IL-15Rα−/− mice have less body and liver fat accumulation than controls. The leaner phenotype is associated with increased energy expenditure and enhanced fatty acid oxidation by muscle mitochondria. Despite being protected against DIO, IL-15Rα−/− are hyperglycemic and insulin-resistant. These findings identify novel roles for IL-15Rα in metabolism and obesity.

Sign in / Sign up

Export Citation Format

Share Document