scholarly journals GC–MS analysis, toxicological and oral glucose tolerance assessments of methanolic leaf extract of Eucalyptus globulus

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Bamidele Stephen Ajilore ◽  
Tolulope Olamide Oluwadairo ◽  
Olubukola Sinbad Olorunnisola ◽  
Olumide Samuel Fadahunsi ◽  
Peter Ifeoluwa Adegbola
Keyword(s):  
Glucose Tolerance ◽  
Eucalyptus Globulus ◽  
Leaf Extract ◽  
Extraction Procedure ◽  
Toxic Effects ◽  
Gas Chromatography Mass Spectrometry ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Liver And Kidney

Abstract Background Eucalyptus globulus leaf has shown promising potential in its efficacy to manage some diseases but little is known about its safety and its use in the management of diabetes. This study was designed to identify the bioactive compounds present in Eucalyptus globulus leaf extract (EGLEX), assess its toxic effects and its oral glucose tolerance ability. Powdered Eucalyptus globulus leaf was extracted with methanol using standard extraction procedure. Preliminary phytochemistry, gas chromatography–mass spectrometry (GCMS) analysis of the extract, its acute and subacute toxic effects and on its glucose tolerance (in-vivo) capability were assessed using standard laboratory techniques. Results EGLEX was tested positive for the presence of alkaloids, cardiac glycosides, flavonoids, tannins, phlobatannins and terpenoids. Nine compounds were identified by GCMS analysis of the leaf extract. EGLEX (up to 300 mg/kg bwt) showed no toxicity in all the rats dosed for the period of 14 days. The histomorphological study of the liver and kidney tissues harvested from rats dosed with 2000 mg/kg bwt showed features of histoarchitectural distortions in the two tissues. EGLEX (200 mg/kg bwt) further demonstrated effective glucose utilization as insulin and metformin. Conclusions The results obtained deduced that EGLEX is safe at a lower dose of 300 mg/kg bwt but toxic at higher dose of 2000 mg/kg bwt, and that single dose (200 mg/kg bwt) of the plant extract prevented hyperglycemia in normal rats.

scholarly journals Antidiabetic potentials of Syzygium guineense methanol leaf extract

2016 ◽  
Vol 5 (4) ◽  
pp. 150-156
Author(s):  
Ifeoma Chinwude Ezenyi ◽  
◽  
Oluchi Nneka Mbamalu ◽  
Lucy Balogun ◽  
Liberty Omorogbe ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Leaf Extract ◽  
Density Lipoprotein ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Dependent Manner ◽  
Oral Glucose Tolerance ◽  
Control Serum ◽  
Syzygium Guineense ◽  
Alpha Glucosidase

This study examines the effects of a methanol extract of Syzygium guineense leaves in streptozotocin (STZ) - induced diabetes, evaluates its effect on alpha glucosidase and 2, 2-diphenyl-1-picrylhydrazyl radical. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (60 mg/kg). An oral glucose tolerance test was performed after diabetes induction and repeated after 14 days of treatment with the extract. The extract elicited antihyperglycemic action in diabetic rats evidenced by an improved oral glucose tolerance. A dose of 250 mg/kg of extract significantly (P<0.01, 0.001) enhanced glucose clearance at the end of treatment period and was comparable with metformin, the group also showed increase in hepatic glycogen content by 33.9% relative to the diabetic control. Serum biochemical analysis showed that the extract improved indices of renal and hepatic function by reduction in serum albumin, creatinine, liver enzymes, total and direct bilirubin. Similarly, the extract reduced serum cholesterol, triglycerides and high density lipoprotein (HDL) in a non-dose dependent manner; treatment with 250 mg/kg extract caused significant (P<0.05) reduction of HDL. Groups which received 250 and 500 mg/kg of extract showed reversal of glomerular damage compared with the diabetic untreated group. The extract also exhibited concentration-dependent antioxidant activity (EC50= 0.2 mg/ml) and statistically significant (P<0.01, 0.001) alpha glucosidase inhibitory effect (IC50= 6.15 mg/ml). These findings show the antidiabetic potential of S. guineense leaf extract, likely mediated through its ability to inhibit alpha glucosidase, scavenge free radicals and increase intrahepatic glucose uptake and storage.

Egg white hydrolysate enhances insulin sensitivity in high-fat diet-induced insulin-resistant rats via Akt activation

2019 ◽  
Vol 122 (1) ◽  
pp. 14-24 ◽  
Author(s):  
F. Jahandideh ◽  
S. C. de Campos Zani ◽  
M. Son ◽  
S. D. Proctor ◽  
S. T. Davidge ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Egg White ◽  
Oral Glucose ◽  
Protein Abundance ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Insulin Resistant

AbstractAgents that block the renin–angiotensin system (RAS) improve glucoregulation in the metabolic syndrome disorder. We evaluated the effects of egg white hydrolysate (EWH), previously shown to modulate the protein abundance of RAS component in vivo, on glucose homeostasis in diet-induced insulin-resistant rats. Sprague–Dawley rats were fed a high-fat diet (HFD) for 6 weeks to induce insulin resistance. They were then randomly divided into four groups receiving HFD or HFD supplemented with different concentrations of EWH (1, 2 and 4 %) for another 6 weeks in the first trial. In the second trial, insulin-resistant rats were divided into two groups receiving only HFD or HFD+4 % EWH for 6 weeks. Glucose homeostasis was assessed by oral glucose tolerance and insulin tolerance tests. Insulin signalling and protein abundance of RAS components, gluconeogenesis enzymes and PPARγ were evaluated in muscle, fat and liver. Adipocyte morphology and inflammatory markers were evaluated. In vivo administration of EWH increased insulin sensitivity, improved oral glucose tolerance (P < 0·0001) and reduced systemic inflammation (P < 0·05). EWH potentiated insulin-induced Akt phosphorylation in muscle (P = 0·0341) and adipose tissue (P = 0·0276), but minimal differences in the protein abundance of tissue RAS components between the EWH and control groups were observed. EWH treatment also reduced adipocyte size (P = 0·0383) and increased PPARγ2 protein abundance (P = 0·0237). EWH treatment yielded positive effects on the inflammatory profile, glucose tolerance, insulin sensitivity and adipocyte differentiation in HFD-induced insulin resistance rats. The involvement of local RAS activity requires further investigation.

scholarly journals Peptide-based GIP receptor inhibition exhibits modest metabolic changes in mice when administered either alone or combined with GLP-1 agonism

2019 ◽  
Author(s):  
Jason A. West ◽  
Soumitra S. Ghosh ◽  
David G. Parkes ◽  
Anastasia Tsakmaki ◽  
Rikke V. Grønlund ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Metabolic Effects ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Gip Receptor

ABSTRACTObjectiveCombinatorial gut hormone therapy is one of the more promising strategies for identifying improved treatments for metabolic disease. Many approaches combine the established benefits of glucagon-like peptide-1 (GLP-1) agonism with one or more additional molecules with the aim of improving metabolic outcomes. Recent attention has been drawn to the glucose-dependent insulinotropic polypeptide (GIP) system due to compelling pre-clinical evidence describing the metabolic benefits of antagonising the GIP receptor (GIPR). We rationalised that benefit might be accrued from combining GIPR antagonism with GLP-1 agonism. To this end we investigated the metabolic effects of co-administration of previously reported peptide-based GIPR antagonists with the GLP-1 agonist liraglutide.MethodsTwo GIPR peptide antagonists, GIPA-1 (mouse GIP(3-30)NH2) and GIPA-2 (NαAc-K10[γEγE-C16]-Arg18-hGIP(5–42)), were pharmacologically characterised in vitro in an assay measuring cAMP production in CHO-K1 cells overexpressing the mouse GIPR. These peptides were then characterised in vivo in lean mice for their effect on oral glucose tolerance, as well as their ability to antagonize exogenous GIP action. Finally, a mouse model of diet-induced obesity (DIO) was used to investigate the potential metabolic benefits of chronic dosing of peptide-based GIPR antagonists, alone or in combination with liraglutide.ResultsIn vitro, both GIPR peptides exhibited potent antagonistic properties, with GIPA-2 being the more potent of the two. Acute in vivo administration of GIPA-1 during an oral glucose tolerance test (OGTT) had negligible effects on glucose tolerance and circulated insulin in lean mice. In contrast, GIPA-2 impaired glucose tolerance and attenuated circulating insulin levels, with offsetting effects on glycemia noted with co-administration with exogenous mouse GIP, suggesting true antagonism via GIPA-2 at the GIP receptor. Chronic administration studies in a DIO mouse model showed expected effects of GLP-1 agonism (via liraglutide), lowering food intake, body weight, fasting blood glucose and plasma insulin concentrations while improving glucose sensitivity, whereas delivery of either GIPR antagonist alone had negligible effects on these parameters. Interestingly, chronic dual therapy with the GIPR antagonists and GLP-1 showed separation from single intervention arms though augmented insulin sensitizing effects (modestly lowering insulin and HOMA-IR) and lowering plasmas triglycerides and free-fatty acids, with more notable effects observed with GIPA-1 compared to GIPA-2.ConclusionWe conclude that, in contrast to the well-documented effects of GLP-1R agonism, systemic administration of peptide-based GIPR antagonists demonstrate minimal benefit on metabolic parameters in DIO mice, exhibiting no major effects on body weight, food intake and glycaemic parameters. However, the co-administration of both a GIPR antagonist together with a GLP1 agonist uncovers interesting synergistic and beneficial effects on measures of insulin sensitivity, circulating lipids and certain adipose stores that seem influenced by the degree or nature of GIP receptor antagonism.

Caffeine-induced impairment of glucose tolerance is abolished by β-adrenergic receptor blockade in humans

2002 ◽  
Vol 92 (6) ◽  
pp. 2347-2352 ◽  
Author(s):  
Farah S. L. Thong ◽  
Terry E. Graham
Keyword(s):  
Glucose Tolerance ◽  
Adrenergic Receptor ◽  
Glucose Tolerance Test ◽  
Potent Inhibitor ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Caffeine Ingestion ◽  
Antagonistic Effects

The caffeine-induced impairment of insulin action is commonly attributed to adenosine receptor (AR) antagonism in skeletal muscle. However, epinephrine, a potent inhibitor of insulin actions, is increased after caffeine ingestion. We tested the hypothesis that the insulin antagonistic effects of caffeine are mediated by epinephrine, and not by AR antagonism, in seven healthy men. On four separate occasions, they received 1) dextrose (placebo, PL), 2) 5 mg/kg caffeine (CAF), 3) 80 mg of propranolol (PR), and 4) 5 mg/kg caffeine + 80 mg of propranolol (CAF + PR) before an oral glucose tolerance test (OGTT). Blood glucose was similar among trials before and during the OGTT. Plasma epinephrine was elevated ( P < 0.05) in CAF and CAF + PR. Areas under the insulin and C-peptide curves were 42 and 39% greater ( P < 0.05), respectively, in CAF than in PL, PR, and CAF + PR. In the presence of propranolol (CAF + PR), these responses were similar to PL and PR. These data suggest that the insulin antagonistic effects of caffeine in vivo are mediated by elevated epinephrine rather than by peripheral AR antagonism.

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