scholarly journals Abnormal GTT (Glucose Tolerance Test) in Multitransfused β Thalassemia Major Patients –In Vivo Biochemical Reactionary Effect

2018 ◽  
Vol 6 (4) ◽  
Author(s):  
Dr Prachi Gupta (Goyal) ◽  
Keyword(s):  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Thalassemia Major ◽  
Tolerance Test

Status of Glucose Metabolism and the Factors Affecting It, in Children with Thalassemia Major.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3848-3848
Author(s):  
Anupam Sachdeva ◽  
Satya Prakash Yadav ◽  
Subash C. Arya ◽  
Virender K. Khanna ◽  
Archana D. Arya
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Age Of Onset ◽  
Thalassemia Major ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Normal Glucose

Abstract Abnormalities of the glucose metabolism are well documented in patients with Thalassemia Major who are frequently transfused and receiving therapy for chelation, due to excess iron deposition in the pancreas. The incidence of abnormalities in the glucose metabolism increase with age, with peak incidence between 16–20 years. The Indian (Asian) population is genetically predisposed to developing type 2 diabetes mellitus which is an additional risk factor for our Thalassemic population. Chelation is suboptimal in most of the patients due to economic reasons and ignorance. Impaired glucose tolerance (IGT) usually precedes the development of frank diabetes mellitus and intensive chelation in those with impaired glucose tolerance test may delay/prevent the onset of diabetes mellitus. Hence it is important to know the glyco-metabolic status of these children. At our Thalassemia endocrinology clinic, glucose tolerance test (GTT) is performed routinely in all subjects with Thalassemia major who have not already developed diabetes to identify the “at risk” population.GTT is performed by drawing a baseline fasting sample for blood glucose, oral glucose was given in a dose of 1.75mg/kg upto a maximum of 75 gms. Blood glucose level is measured 2 hours after oral glucose. According to the WHO criteria, Fasting plasma glucose between 110–126mg/dl is classified as impaired fasting and above 126mg/dl as diabetes. 2-hour plasma glucose value between 140–200mg/dl is classified as impaired glucose tolerance and above 200 mg/dl as diabetes. The purpose of this study was to analyze the status of the glucose metabolism of children and young adults with Thalassemia major who were attending our Thalassemia endocrinology clinic and to compare the factors affecting subjects with an abnormal glucose metabolism with those who have a normal glucose metabolism. The parameters compared were: effect of mean S. ferritin levels, age of onset of chelation and genetic predisposition. Retrospective analysis of our case records was done to determine the prevalence of diabetes and impaired glucose tolerance in children and young adults between 13 and 25 years of age. Of the 33 subjects evaluated, 16 out of 33 (48.5%) subjects had an abnormality of the glucose metabolism. 14/33 subjects (42.4%) had developed diabetes mellitus and 2 had an impaired GTT. Of the 16 affected subjects 9 were males and 7 were females (M:F = 1.28:1). The mean serum ferritin for this group was 5464ng/ml, 5503ng/ml for the diabetic group and 5425 for those with impaired GTT. (Range 2523–10904ng/ml). History of diabetes in a first or second degree relative was positive in 9 subjects(56.25%), negative in 2 and unknown in 5 subjects. Average age of onset of chelation was 8 years in this group. Oral glucose tolerance test was normal in 17/33(51.5%) subjects of which 10 were males and 7 were females (1.42:1). Average serum ferritin was 4747.4ng/ml in the group with a normal glucose tolerance. (1600–8294ng/ml). Family history of diabetes in a first or second degree relative was positive in 8 subjects(47%), negative in 4 and unknown in 5 subjects. Average age of onset of chelation was 6.5 years in the group with normal glucose metabolism. In conclusion of the 33 subjects evaluated, 48.5% had an abnormal glucose metabolism.

Muscarinic stimulation maintains in vivo insulin secretion in response to glucose after prolonged hyperglycemia

1995 ◽  
Vol 268 (2) ◽  
pp. R475-R479 ◽  
Author(s):  
B. Balkan ◽  
B. E. Dunning
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Insulin Response ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
General Mechanism ◽  
Intravenous Glucose ◽  
Intravenous Glucose Tolerance

Prolonged hyperglycemia impairs the in vitro insulin release by islets of Langerhans in response to glucose but exaggerates the in vivo insulin response. We hypothesized that this discrepancy results from increased vagal stimulation of the islets. Conscious chronically cannulated rats were infused with glucose (15 mg/min) or saline for 48 h. Three hours thereafter, an intravenous glucose tolerance test was performed with or without prior injection of atropine (0.2 mg). Atropine markedly (> 70%) reduced the insulin response in glucose-infused, but not in saline-infused, rats. Glucose-infused rats displayed basal hypoglycemia but normal glucose excursions during an intravenous glucose tolerance test. It is concluded that prolonged hyperglycemia produces exaggerated muscarinic activation of the beta-cells that will persist > or = 3 h after the termination of the glucose infusion and normalizes in vivo insulin secretion. It is possible that increased parasympathetic activation of the pancreas might constitute a general mechanism to maintain insulin output when the demand for insulin exceeds the inherent beta-cell responsiveness.

scholarly journals BETA THALASSEMIA

2018 ◽  
Vol 25 (09) ◽  
pp. 1402-1405
Author(s):  
Iqbal Ahmed ◽  
Muhammad Ammar Sadiq ◽  
Umair Arshad ◽  
Hafiz Muhammad Anwar ul Haq ◽  
Sobia Tabassum ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Analytical Study ◽  
Glucose Tolerance Test ◽  
Thalassemia Major ◽  
Tolerance Test ◽  
The Other ◽  
Beta Thalassemia ◽  
Blood Transfusions ◽  
Spss Software ◽  
Study Setting

Background: Inadequate Blood Transfusion is responsible for various problemsin children with Thalasseima. On the other hand, repeated transfusions are related with hazards.About 25-50% of the children with thalassemia major have impaired glucose tolerance (IGT)or diabetes. Objectives: To find out the frequency of IGT in children with blood transfusiondependent β thalassemia. Study Design: Descriptive analytical study. Setting: Department ofPediatrics, Shahida Islam Teaching Hospital, Lodhran. Period: 1st July 2017 to 31st December2017. Material and Methods: Known 120 cases of beta Thalassemia major children between3-17 years of age that were regularly transfused. Demographics, disease history and personalinformation regarding all the patients were collected. Glucose tolerance test was performedand Serum ferritin levels were measured. Results were analyzed by SPSS software version20.0. Results: There were 78 (65.0%) children between 3-10 years and 42 (35.0%) between11-17 years. There were 70(58.3) male and 50 (41.7%) female. Frequency of impaired glucosetolerance was noted in 15 (12.5%). Conclusion: Frequency of IGT is high amongst children withthalassemia major having regular blood transfusions.

Glutamate stimulates insulin secretion and improves glucose tolerance in rats

1995 ◽  
Vol 269 (3) ◽  
pp. E551-E556 ◽  
Author(s):  
G. Bertrand ◽  
R. Puech ◽  
M. M. Loubatieres-Mariani ◽  
J. Bockaert
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Dependent Manner ◽  
Intravenous Glucose ◽  
Acid Receptor ◽  
Fasted Rats

We previously showed in vitro that glutamate stimulates insulin release via an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Here we address a more physiological question concerning the in vivo effect of intravenously or orally administered glutamate on insulinemia and glycemia in fed and fasted rats. In anesthetized fed rats, the intravenous administration of glutamate at 9 and 30 mg/kg transiently increased insulinemia in a dose-dependent manner. The insulin-secretory effect of glutamate (9 mg/kg) was blocked by an antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. In anesthetized fasted rats, glutamate at 9 mg/kg was ineffective, but during an intravenous glucose tolerance test (0.5 g/kg), glutamate markedly potentiated insulin release and increased the glucose disappearance rate. In conscious rats, the intragastric administration of glutamate at 200 mg/kg elicited a transient insulin response in fed animals and had no effect in fasted animals but, during an oral glucose tolerance test (1 g/kg), enhanced insulin secretion and reduced the hyperglycemia. Glutamate was effective at plasma concentrations of 200-300 microM. In conclusion, intravenously and orally administered glutamate stimulates insulin secretion in vivo via an excitatory amino acid receptor and improves glucose tolerance.

scholarly journals THE ICET-A RECOMMENDATIONS FOR THE DIAGNOSIS AND MANAGEMENT OF DISTURBANCES OF GLUCOSE HOMEOSTASIS IN THALASSEMIA MAJOR PATIENTS

2016 ◽  
Vol 8 ◽  
pp. 2016058 ◽  
Author(s):  
Vincenzo De Sanctis
Keyword(s):  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Glucose Tolerance Test ◽  
Laboratory Data ◽  
Thalassemia Major ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Model Assessment ◽  
Intravenous Glucose ◽  
Diagnosis And Management

Iron overload in patients with thalassemia major (TM) affects glucose regulation, and is mediated by several mechanisms. These include the oxidative damage inflicted by iron on the pancreatic ß -cells and liver cells leading to pancreatic and hepatic dysfunction and insulin resistance. These disturbances have been identified by oral glucose tolerance test (OGTT), euglycemic insulin clamp, homeostatic model assessment (HOMA), intravenous glucose tolerance test (IVGT) and continuous glucose monitoring system (CGMS). A group of endocrinologists, hematologists and paediatricians, members of the International Network of Clinicians for Endocrinopathies in Thalassemia and Adolescence Medicine (ICET-A) convened to formulate recommendations for the diagnosis and management of abnormalities of glucose homeostasis in thalassemia major patients on the basis of available evidence from clinical and laboratory data and consensus practice. The results of their work and discussions are described in this article.Key words: Thalassemia major; Glucose homeostasis; Diagnosis; Management; Guidelines 

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.

scholarly journals AMPK Phosphorylation Effect of Genistein Is Independent of GPR30

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 484-484
Author(s):  
Sarai Vásquez-Reyes ◽  
Ariana Vargas-Castillo ◽  
Jose C Crispin ◽  
Florencia Rosetti ◽  
Nimbe Torres ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Composition ◽  
Oxygen Consumption ◽  
Weight Gain ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Wild Type ◽  
Ampk Phosphorylation

Abstract Objectives Genistein promotes fatty acid oxidation, improves glucose tolerance and increases energy expenditure. These effects are associated with AMPK phosphorylation in skeletal muscle. However, the molecular mechanism by which genistein activates the signaling pathway to activate AMPK phosphorylation is not yet known. Several target proteins have been suggested, one o them is GPR30, but it has not been studied. Thus, the aim of this study was to determine if AMPK phosphorylation by genistein is activated by GPR30. Methods To determine if GPR30 is involved in the mechanism that promotes AMPK phosphorylation we used C2C12 GPR30 KD (knock down) myotubes obtained by transduction with a shRNA, and also GPR30 −/− primary myotubes. AMPK phosphorylation was determined via western blot in the presence of genistein after 1 hour in both cultures. Furthermore, in order to establish in vivo if the beneficial effects of genistein were associated to GPR30, C57BL/6 mice (wild type WT) and GPR30 −/− mice were fed with both control and high fat sucrose diets (HFSD) containing genistein for 2 months. During two months of treatment, weight gain, food consumption, and body composition were measured as well as a glucose tolerance test (GTT), indirect calorimetry and AMPK phosphorylation by western blot in skeletal muscle of all of groups. Results Genistein at concentrations of 0.3,1,3 and 10µM increased AMPK phosphorylation in GPR30 KD, and GPR30 −/− primary myotubes, indicating that GPR30 is not directly involved in AMPK phosphorylation by genistein in an in vitro model. The in vivo study showed that the effect of genistein in GPR30 −/− mice on weight gain, body composition, GTT and indirect calorimetry was similar compared to wild type mice. The mice that consumed a HFSD with genistein gained less weight and less body fat, regardless of genotype (WT or GPR30 −/−). Similar effects were observed in the glucose tolerance test, oxygen exchange coefficient and oxygen consumption. Wild type and GPR30 −/− mice that consumed genistein had a better glucose tolerance than those that did not consume genistein. Conclusions This study showed that GPR30 its not directly involved in promoting AMPK phosphorylation by genistein. In addition, genistein reduced weight gain, increased glucose tolerance and increased oxygen consumption even in the absence of GPR30. Funding Sources INCMNSZ.

scholarly journals In-Vitro α-amylase, α-glucosidase Inhibitory Activities and In-Vivo Anti-Hyperglycemic Potential of Different Dosage Forms of Guduchi (Tinospora Cordifolia [Willd.] Miers) Prepared With Ayurvedic Bhavana Process

2021 ◽  
Vol 12 ◽  
Author(s):  
Rohit Sharma ◽  
Rajesh Bolleddu ◽  
Jayanta K. Maji ◽  
Galib Ruknuddin ◽  
Pradeep K. Prajapati
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Dosage Forms ◽  
Tinospora Cordifolia ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Guduchi (Tinospora cordifolia [Willd.] Miers) is a flagship rejuvenating herb of Ayurveda with reported anti-diabetic potential. In the present study, different dosage forms of Guduchi stem (growing on neem tree) were developed by adopting Ayurvedic pharmaceutical process of Bhavana (levigation). Guduchi Churna (GC) was subjected to 07 times Bhavana separately with its own extracted juice, decoction and potable water, and dosage forms namely Svarasa Bhavita Guduchi Churna (SBGC), Kwatha Bhavita Guduchi Churna (KBGC), and Jala Bhavita Guduchi Churna (JBGC) were prepared. The present study was aimed to evaluate the role of Bhavana on the potentiation of therapeutic properties of Guduchi. Sequential solvent extracts (5, 10, 15 and 25%) of GC, SBGC, KBGC and JBGC were prepared in different solvents [phosphate buffer, hexane, dichloromethane (DCM), chloroform] and screened for the α-amylase and α-glucosidase inhibitory activity. The results revealed that phosphate buffer and DCM extracts of SBGC exhibited strong α-amylase inhibitory potential (&gt;80% inhibition at 25% concentration) followed by KBGC, JBGC and GC with reference to the standard acarbose. In α-glucosidase inhibitory activity, maximum inhibition was observed in DCM and chloroform extracts of SBGC (&gt;85% inhibition at 25% concentration), followed by KBGC (&gt;80% inhibition at 25% concentration), JBGC and GC. In vivo anti-hyperglycemic studies were carried out by oral glucose tolerance test in Swiss albino mice. Test drugs (JBGC, KBGC, SBGC) treated groups showed marginal decrease of blood glucose levels in normo glycemic mice. However, the blood glucose level in test drug JBGC, KBGC and SBGC treated groups was still within normal range in overnight fasted mice. In oral glucose tolerance test, among all dosage forms SBGC (51.08%) produced pronounced anti-hyperglycemic effect followed by KBGC (42.57%) at a dose of 520 mg/kg. The GC, JBGC, KBGC and SBGC samples were also standardized using berberine (a well established anti-diabetic compound) as a marker compound by HPTLC fingerprint analysis. Findings of the present study indicate that SBGC and KBGC can be used in the treatment of diabetes mellitus and gives supporting evidence to Ayurvedic claims that the Bhavana process has pharmaceutico-therapeutic significance in Ayurvedic drug development.

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