Methanolic leaf extract of Gymnema sylvestre augments glucose uptake and ameliorates Insulin resistance by upregulating GLUT-4, PPAR- and #947;, adiponectin and leptin levels in vitro

Some medicinal plants and their purified derivatives have demonstrated beneficial therapeutic potentials for many centuries. They have been reported to exhibit antioxidant activity, reducing the oxidative stress in cells and are therefore useful in the treatment of many human diseases, including diabetes and other non-communicable diseases. This study evaluated antioxidative activity and enzymatic (alpha-amylase and alphaglucosidase) inhibitory potentials of Gymnema sylvestre methanolic leaf extract (GSMLE) using standard methods. Phytochemical screening revealed the presence of alkaloids, tannins, saponins, steroids, terpenoids and flavonoids. The total phenolics and total flavonoids content in the extract were found to be 6.629±0.745 (µg/ml of catechol equivalent) and 0.004±0.0012 (µg/ml of quercetin equivalent) respectively. GSMLE was shown to have radical scavenging activity against DPPH (290.54 ± 39.72 %), hydroxyl radical (86.507 ± 23.55 %) and hydrogen peroxide (45.25 ± 25.23 %). The level of SOD was significantly decreased in H2O2 induced and H2O2+extract induced when compared with normal control (p<0.05); the level of GSH was significantly increased in H2O2 induced control and significantly decreased in H2O2+extract induced test when compared to normal control. GSH was also decreased significantly in H2O2+extract induced when compared to H2O2 induced control (p<0.05). The extract also demonstrated significant inhibition of alpha-glucosidase (IC50 182.26 ±1.05μg/ml) when compared with standard acarbose (IC50 189.52±0.46) and was more potent than the arcarbose on alpha-amylase inhibition with IC50 of 195.3±4.40 and 200.05±7.16 respectively. These findings may therefore, stress the potentiality of using Gymnema sylvestre as a natural remedy for the management of type 2 diabetes.

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Phytochemical evaluation and in vitro antidiabetic efficiency of isopropanolic leaf extract of pimenta racemosa

Kongunadu Research Journal ◽

10.26524/krj.2020.21 ◽

2020 ◽

Vol 7 (2) ◽

pp. 50-55

Author(s):

Anitha T A ◽

Pakutharivu T ◽

Nirubama K ◽

Akshaya V

Keyword(s):

Diabetes Mellitus ◽

Glucose Uptake ◽

Inhibitory Activity ◽

Leaf Extract ◽

Yeast Cells ◽

Antidiabetic Activity ◽

Leaf Extracts ◽

Pimenta Racemosa

The traditional herbal medicines are mainly obtained from plants are used in the management of Diabetes mellitus. The main objective of this work was to assess the presence of phytochemical compounds and to evaluate the in vitro antidiabetic activity of isopropanolic extracts of Pimenta racemosa leaves by studying their α-amylase inhibitory activity and glucose transport across yeast cells. Screening of phytochemicals showed positive results for alkaloids, steroids, cardiac glycosides, terpenoids, reducing sugars, anthraquinones, and results of in vitro α-amylase inhibitory studies demonstrated there was a dose-dependent increase in percentage inhibitory activity by the isopropanolic leaf extracts of Pimenta racemosa. At a concentration of 1 mg/ml, the extract showed a percentage inhibition 33.6 and for 5 mg/ml it was 91.2. The glucose uptake study was also studied through yeast cells by analyzing theamount of glucose remaining in the medium after a specific time intervals. It serves as an indicator for the capability of isopropanolic leaf extracts of Pimenta racemosa to transport the glucose into yeast cells. As a result, we found that the isopropanolic leaf extract of Pimenta racemosa have inhibitory activity against αamylase and also, which is efficient in glucose uptake. This therapeutic potentiality of Pimenta racemosa could be exploited in the treatment of Type 2 Diabetes mellitus. Further studies are also required to elucidate whether the plant have antidiabetic potential by in vivo for corroborating the traditional claim of the plant.

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Immunomodulatory Effect of Gymnema sylvestre (R.Br.) Leaf Extract: An In Vitro Study in Rat Model

PLoS ONE ◽

10.1371/journal.pone.0139631 ◽

2015 ◽

Vol 10 (10) ◽

pp. e0139631 ◽

Cited By ~ 6

Author(s):

Vineet Kumar Singh ◽

Padmanabh Dwivedi ◽

B. R. Chaudhary ◽

Ramesh Singh

Keyword(s):

Rat Model ◽

Leaf Extract ◽

In Vitro Study ◽

Vitro Study ◽

Immunomodulatory Effect ◽

Gymnema Sylvestre

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7-O-Methylaromadendrin Stimulates Glucose Uptake and Improves Insulin Resistance in Vitro

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.33.1494 ◽

2010 ◽

Vol 33 (9) ◽

pp. 1494-1499 ◽

Cited By ~ 34

Author(s):

Wei Yun Zhang ◽

Jung-Jin Lee ◽

In-Su Kim ◽

Yohan Kim ◽

Jeong-Sook Park ◽

...

Keyword(s):

Insulin Resistance ◽

Glucose Uptake

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Interleukin-1β-Induced Insulin Resistance in Adipocytes through Down-Regulation of Insulin Receptor Substrate-1 Expression

Endocrinology ◽

10.1210/en.2006-0692 ◽

2007 ◽

Vol 148 (1) ◽

pp. 241-251 ◽

Cited By ~ 389

Author(s):

Jennifer Jager ◽

Thierry Grémeaux ◽

Mireille Cormont ◽

Yannick Le Marchand-Brustel ◽

Jean-François Tanti

Keyword(s):

Insulin Resistance ◽

Protein Kinase ◽

Insulin Receptor ◽

Glucose Uptake ◽

Insulin Signaling ◽

Protein Kinase B ◽

Transcriptional Level ◽

Insulin Receptor Substrate ◽

Down Regulation ◽

Glut 4

Inflammation is associated with obesity and insulin resistance. Proinflammatory cytokines produced by adipose tissue in obesity could alter insulin signaling and action. Recent studies have shown a relationship between IL-1β level and metabolic syndrome or type 2 diabetes. However, the ability of IL-1β to alter insulin signaling and action remains to be explored. We demonstrated that IL-1β slightly increased Glut 1 translocation and basal glucose uptake in 3T3-L1 adipocytes. Importantly, we found that prolonged IL-1β treatment reduced the insulin-induced glucose uptake, whereas an acute treatment had no effect. Chronic treatment with IL-1β slightly decreased the expression of Glut 4 and markedly inhibited its translocation to the plasma membrane in response to insulin. This inhibitory effect was due to a decrease in the amount of insulin receptor substrate (IRS)-1 but not IRS-2 expression in both 3T3-L1 and human adipocytes. The decrease in IRS-1 amount resulted in a reduction in its tyrosine phosphorylation and the alteration of insulin-induced protein kinase B activation and AS160 phosphorylation. Pharmacological inhibition of ERK totally inhibited IL-1β-induced down-regulation of IRS-1 mRNA. Moreover, IRS-1 protein expression and insulin-induced protein kinase B activation, AS160 phosphorylation, and Glut 4 translocation were partially recovered after treatment with the ERK inhibitor. These results demonstrate that IL-1β reduces IRS-1 expression at a transcriptional level through a mechanism that is ERK dependent and at a posttranscriptional level independently of ERK activation. By targeting IRS-1, IL-1β is capable of impairing insulin signaling and action, and could thus participate in concert with other cytokines, in the development of insulin resistance in adipocytes.

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