scholarly journals Evaluation of possible mechanisms of three plants for blood glucose control in diabetes

2016 ◽  
Vol 11 (1) ◽  
pp. 224 ◽  
Author(s):  
Damayanthi Dalu ◽  
Satyavati Dhulipala

<p class="Abstract">This study was conducted to provide the evidence for the mechanism of  anti-diabetic activity of <em>Cocculus orbiculatus, Leea indica</em> and <em>Ventilago maderaspatana</em>. This was accomplished by employing methods like uptake of glucose, glycogen synthesis and inhibition of α-glucosidase. For uptake of glucose, diaphragms were dissected out in Tyrode solution with 2% glucose and assayed for glucose content. In glycogen synthesis methodology liver, skeletal muscle and cardiac muscles were isolated, homogenized and glycogen content was analyzed. In α-glucosidase enzyme inhibition procedure involved estimation of α-glucosidase enzyme inhibition. All the three plant extracts exhibited significant (p&lt;0.05 - p&lt;0.01) anti-diabetic activity by increasing glucose uptake, glycogen synthesis and inhibiting α-glucosidase enzyme. Among the three plants, <em>V. maderaspatana</em> (500 mg/kg) exhibited higher glucose uptake, glycogen content and α-glucosidase inhibition activity (IC<sub>50</sub> 145 µg/mL). The present experimental results evidenced the anti-diabetic activity of three plants by all the three mechanisms.</p><p> </p>

2008 ◽  
Vol 294 (1) ◽  
pp. E28-E35 ◽  
Author(s):  
Michale Bouskila ◽  
Michael F. Hirshman ◽  
Jørgen Jensen ◽  
Laurie J. Goodyear ◽  
Kei Sakamoto

Insulin promotes dephosphorylation and activation of glycogen synthase (GS) by inactivating glycogen synthase kinase (GSK) 3 through phosphorylation. Insulin also promotes glucose uptake and glucose 6-phosphate (G-6- P) production, which allosterically activates GS. The relative importance of these two regulatory mechanisms in the activation of GS in vivo is unknown. The aim of this study was to investigate if dephosphorylation of GS mediated via GSK3 is required for normal glycogen synthesis in skeletal muscle with insulin. We employed GSK3 knockin mice in which wild-type GSK3α and -β genes are replaced with mutant forms (GSK3α/βS21A/S21A/S9A/S9A), which are nonresponsive to insulin. Although insulin failed to promote dephosphorylation and activation of GS in GSK3α/βS21A/S21A/S9A/S9Amice, glycogen content in different muscles from these mice was similar compared with wild-type mice. Basal and epinephrine-stimulated activity of muscle glycogen phosphorylase was comparable between wild-type and GSK3 knockin mice. Incubation of isolated soleus muscle in Krebs buffer containing 5.5 mM glucose in the presence or absence of insulin revealed that the levels of G-6- P, the rate of [14C]glucose incorporation into glycogen, and an increase in total glycogen content were similar between wild-type and GSK3 knockin mice. Injection of glucose containing 2-deoxy-[3H]glucose and [14C]glucose also resulted in similar rates of muscle glucose uptake and glycogen synthesis in vivo between wild-type and GSK3 knockin mice. These results suggest that insulin-mediated inhibition of GSK3 is not a rate-limiting step in muscle glycogen synthesis in mice. This suggests that allosteric regulation of GS by G-6- P may play a key role in insulin-stimulated muscle glycogen synthesis in vivo.


1965 ◽  
Vol 208 (2) ◽  
pp. 307-316 ◽  
Author(s):  
J. S. Bishop ◽  
R. Steele ◽  
N. Altszuler ◽  
A. Dunn ◽  
C. Bjerknes ◽  
...  

Glucose-C14 was given intravenously in trace amount, as an initial dose followed by continuous infusion, to measure glucose-C12 release by the liver, and total glucose uptake from plasma by the tissues. The glycogen content of liver and the C14 incorporated into the glycogen and the nonglycogen constituents of liver were measured by analysis of percutaneous biopsy samples. Glucose 6-C14 was used to show that direct uptake and conversion to liver glycogen (without passage through three carbon intermediates) of tagged blood glucose molecules was the source of almost all the C14 of glycogen Insulin infusion at 0 1–0.2 U/kg per hr, iv, along with glucose to limit hypoglycemia, stopped glycogen loss, decreased glucose-C12 release, increased glucose uptake from the plasma by the tissues and brought about the incorporation of plasma glucose-C14 units into liver glycogen. Incorporation of C14 into the nonglycogen constituents of the liver was increased much less. Glucose infusion, presumed to stimulate endogenous insulin secretion, produced similar effects. In earlier periods of insulin infusion the outstanding hepatic effects were decreases in glycogen loss and glucose-C12 release. In later periods the outstanding further effect was a great increase in the use of plasma glucose-C14 for liver glycogen synthesis.


Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 114-126 ◽  
Author(s):  
Ling Zhang ◽  
Guangdong Yang ◽  
Ashley Untereiner ◽  
Youngjun Ju ◽  
Lingyun Wu ◽  
...  

Mounting evidence has established hydrogen sulfide (H2S) as an important gasotransmitter with multifaceted physiological functions. The aim of the present study was to investigate the role of H2S on glucose utilization, glycogen synthesis, as well as gluconeogenesis in both HepG2 cells and primary mouse hepatocytes. Incubation with NaHS (a H2S donor) impaired glucose uptake and glycogen storage in HepG2 cells via decreasing glucokinase activity. Adenovirus-mediated cystathionine γ-lyase (CSE) overexpression increased endogenous H2S production and lowered glycogen content in HepG2 cells. Glycogen content was significantly higher in liver tissues from CSE knockout (KO) mice compared to that from wild type (WT) mice in fed condition. Glucose consumption was less in primarily cultured hepatocytes isolated from WT mice than those from CSE KO mice, but more glucose was produced by hepatocytes via gluconeogenesis and glycogenolysis pathways in WT mice than in CSE KO mice. NaHS treatment reduced the phosphorylation of AMP-activated protein kinase, whereas stimulation of AMP-activated protein kinase by 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside reversed H2S-impaired glucose uptake. H2S-increased glucose production was likely through increased phosphoenolpyruvate carboxykinase activity. In addition, insulin at the physiological range inhibited CSE expression, and H2S decreased insulin-stimulated phosphorylation of Akt in HepG2 cells. CSE expression was increased, however, in insulin-resistant state induced by exposing cells to high levels of insulin (500 nm) and glucose (33 mm) for 24 h. Taken together, these data suggest that the interaction of H2S and insulin in liver plays a pivotal role in regulating insulin sensitivity and glucose metabolism.


1982 ◽  
Vol 52 (2) ◽  
pp. 434-437 ◽  
Author(s):  
R. D. Fell ◽  
S. E. Terblanche ◽  
J. L. Ivy ◽  
J. C. Young ◽  
J. O. Holloszy

This study examined the effects of raising muscle glycogen by carbohydrate feeding and of keeping muscle glycogen low by carbohydrate restriction following exhausting exercise on the ability of perfused skeletal muscle to take up glucose and to synthesize glycogen. Muscle glycogen concentration was more than twice as high in the rats fed carbohydrate as in those not given carbohydrate. Muscle glycogen synthesis during a 30-min perfusion with glucose and insulin was significantly greater in the animals with low muscle glycogen. Furthermore the muscles with low glycogen content converted a greater proportion of the glucose taken up to glycogen and less to lactate than did the muscles with high glycogen content. In rats subjected to exhausting exercise on the preceding day, the rate of glucose uptake by perfused skeletal muscle was significantly higher (60–80%) at the same insulin concentration in animals in which muscle glycogen was kept low than in those in which glycogen was raised by carbohydrate feeding.


2008 ◽  
Vol 294 (3) ◽  
pp. H1266-H1273 ◽  
Author(s):  
Mohamed A. Omar ◽  
Heather Fraser ◽  
Alexander S. Clanachan

Alterations in myocardial glucose metabolism are a key determinant of ischemia-induced depression of left ventricular mechanical function. Since myocardial glycogen is an important source of endogenous glucose, we compared the effects of ischemia on glucose uptake and utilization in isolated working rat hearts in which glycogen content was either replete (G replete, 114 μmol/g dry wt) or partially depleted (G depleted, 71 μmol/g dry wt). The effects of low-flow ischemia (LFI, 0.5 ml/min) on glucose uptake, glycogen turnover (glycogenolysis and glycogen synthesis), glycolysis, adenosine 5′-monophosphate-activated protein kinase (AMPK) activity, and GLUT4 translocation were measured. Relative to preischemic values, LFI caused a time-dependent reduction in glycogen content in both G-replete and G-depleted groups due to an acceleration of glycogenolysis (by 12-fold and 6-fold, respectively). In G-replete hearts, LFI (15 min) decreased glucose uptake (by 59%) and did not affect GLUT4 translocation. In G-depleted hearts, LFI also decreased initially glucose uptake (by 90%) and glycogen synthesis, but after 15 min, when glycogenolysis slowed due to exhaustion of glycogen content, glucose uptake increased (by 31%) in association with an increase in GLUT4 translocation. After 60 min of LFI, glucose uptake, glycogenolysis, and glycolysis recovered to near-preischemic values in both groups. LFI increased AMPK activity in a time-dependent manner in both groups (by 6-fold and 4-fold, respectively). Thus, when glycogen stores are replete before ischemia, ischemia-induced AMPK activation is not sufficient to increase glucose uptake. Under these conditions, an acceleration of glycogen degradation provides sufficient endogenous substrate for glycolysis during ischemia.


1966 ◽  
Vol 51 (2) ◽  
pp. 193-202
Author(s):  
J. A. Antonioli ◽  
A. Vannotti

ABSTRACT 1. The metabolism of suspensions of circulating leucocytes has been studied after intramuscular injection of a dose of 50 mg/kg of a corticosteroid (cortisone acetate). The suspensions were incubated under aerobic conditions in the presence of a glucose concentration of 5.6 mm. Glucose consumption, lactate production, and variations in intracellular glycogen concentration were measured. After the administration of the corticosteroid, the anabolic processes of granulocyte metabolism were reversibly stimulated. Glucose consumption and lactate production increased 12 hours after the injection, but tended to normalize after 24 hours. The glycogen content of the granulocytes was enhanced, and glycogen synthesis during the course of the incubation was greatly stimulated. The action of the administered corticosteroid is more prolonged in females than in males. The injection of the corticosteroid caused metabolic modifications which resemble in their modulations and in their chronological development those found in circulating granulocytes of guinea-pigs suffering from sterile peritonitis. These results suggest, therefore, that, in the case of acute inflammation, the glucocorticosteroids may play an important role in the regulation of the metabolism of the blood leucocytes.


2020 ◽  
Vol 14 (3) ◽  
pp. 196-202
Author(s):  
Atul Kaushik ◽  
Teamrat S. Tesfai ◽  
Daniel K. Barkh ◽  
Furtuna K. Ghebremeskel ◽  
Habtom G. Zerihun ◽  
...  

Background: A snake bite is fundamentally an injury often resulting in puncture wounds meted out by the animal's fangs and occasionally resulting in envenomation. Rate of snake bites around 5,400,000 bites per year leads to over 2,500,000 envenomings and around 125,000 fatal cases annually. Snake venom enzymes are rich in metalloproteinases, phospholipaseA2, proteinases, acetylcholinesterases and hyaluronidases. Objective: Cyphostemma adenocoule is traditionally being used for the treatment of snake bites in Eritrea. The present research was aimed at evaluating the snake venom enzyme inhibition activity of C. adenocoule against puff adder venom and developing a base for the traditional use of the plant against snakebites in Eritrea. Methods: The anti-venom activity of C. adenocoule was assessed in-vitro through phospholipaseA2 enzyme inhibition assay using egg yolk as a cell. The ethanol and chloroform extracts of C. adenocoule showed in vitro anti phospholipase A2 activity, whereas the water extracts of the plant showed no activity. Results: Among the extracts of C. adenocoule, the highest percentage of inhibition was obtained from chloroform extract (95.55% at 100mg/ml). The extract showed prominent activity at different concentrations (34.7% at10mg/ml, 48.8% at 20mg/ml, 54.8% at 40mg/ml, 60.9% at 60mg/ml, 80.5% at 80mg /ml). The ethanol extract also showed certain activity at various concentrations (25.22% at10mg/ml, 14.78% at 20mg/ml, 2.6% at40mg/ml). The activity of the chloroform extracts increases as concentration increases, whereas the activity of the ethanol extracts decreases as concentration increases. The aqueous extract of C. adenocoule did not show any activity at all concentrations. Conclusion: In this study, the chloroform and ethanol extracts of the plant inhibited the enzyme of interest and thus proved the efficacy of anti-snake venom activity of the plant.


2021 ◽  
Vol 36 (1) ◽  
pp. 618-626 ◽  
Author(s):  
Fatema R. Saber ◽  
Rehab M. Ashour ◽  
Ali M. El-Halawany ◽  
Mohamad Fawzi Mahomoodally ◽  
Gunes Ak ◽  
...  

2003 ◽  
Vol 285 (2) ◽  
pp. R413-R419 ◽  
Author(s):  
Paul Franken ◽  
Phung Gip ◽  
Grace Hagiwara ◽  
Norman F. Ruby ◽  
H. Craig Heller

Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by ∼40% in the cortex of B6 mice, while glycogen significantly decreased by 20–38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.


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