scholarly journals Insulin and C-peptide response in healthy persons and individuals with impaired glucose metabolism during oral glucose tolerance test

2005 ◽  
Vol 24 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Olgica Nedic ◽  
Jasminka Miloradovic ◽  
Marija Ratkovic ◽  
Romana Masnikosa
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Oral Glucose ◽  
Diabetic Patients ◽  
Reference Ranges ◽  
Time Intervals ◽  
C Peptide

Serial measurements of blood glucose concentration before and after giving a specific amount of glucose orally provide a standard method to evaluate glucose metabolism. Although the reference ranges for glucose concentration in various disease states that are based on impaired glucose homeostasis have been established, the reference values are not clearly defined for insulin and C-peptide concentrations. The aim of this work was to study the insulin and C-peptide response during OGTT. Healthy individuals exhibited the following profile of insulin and C-peptide levels: 15 ? 4.9 mU/L and 0.5 ? 0.19 nmol/L (0 h), 116 ? 52.8 mU/L and 2.3 ? 0.79 nmol/L (1 h) and 59 ? 26.7 mU/L and 2.0 ? 0.67 nmol/L (2 h). Persons with impaired glucose tolerance had higher C-peptide levels at 0 h, 0.6 ? 0.17 nmol/L, and significantly higher insulin and C-peptide concentrations after 1 h, 209 ? 63.8 mU/L and 3.5 ? 1.00, nmol/L and 2 h, 188 ? 48.8 mU/L and 3.6 ? 0.92 nmol/L. Diabetic patients had higher basal levels of C-peptide, 0.8 ? 0.23 nmol/L, insulin and C-peptide increased after 1 h similarly as in healthy people, but further continued to increase significantly, 181 ? 137.6 mU/L and 3.7 ? 1.49 nmol/L. Subjects that exhibited low blood glucose levels demonstrated lower insulin concentrations at all time intervals, 11 ? 2.5 mU/L (0 h), 63 ? 31.1 mU/L (1 h) and 44 ? 22.9 mU/L (2 h), but the concentration of C-peptide leveled with that of the healthy ones. The results of this work may be useful in establishing reference ranges for insulin and C-peptide concentrations for defined time intervals during OGTT, in health and disease.

CLINICAL SIMULATION OF OGTT GLUCOSE RESPONSE MODEL FOR DIAGNOSIS OF DIABETIC PATIENT

2005 ◽  
Vol 05 (01) ◽  
pp. 123-138
Author(s):  
DHANJOO N. GHISTA ◽  
PATRICK S. K. CHUA ◽  
ANDY UTAMA AULIA ◽  
PETER L. P. YEO
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Clinical Data ◽  
Glucose Concentration ◽  
Glucose Tolerance Test ◽  
Blood Glucose Concentration ◽  
Parametric Identification ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Clinical Simulation

Diagnosis of diabetes is usually achieved by obtaining a single reading of blood-glucose concentration value from the Oral Glucose Tolerance Test (OGTT). However, the result itself is inadequate in providing insight into the glucose-regulatory etiology of diabetes disease disorder, which is important for treatment purposes. The objective of this project was to conduct clinical simulation and parametric identification of OGTT model for diagnosis of diabetic patient, so as to classify diabetic or at-risk patients into different categories, depending on the nature of their blood-glucose tolerance response to oral injestion of a bolus of glucose. In other words, the patient classification depends on how the blood-glucose concentration varies with time; i.e. how much does it peak, how long does it takes to reach its peak value, how fast does it return to the fasting value, etc. during the oral glucose tolerance test. To represent this blood-glucose concentration [y(t)] regulatory dynamics, the model selected is a second-order differential equation, [Formula: see text] of blood-glucose concentration response to a bolus of ingested glucose Gδ(t). This model was then applied to the test subjects by making the model solution-expression for y(t) match the monitored clinical data of blood-glucose concentration at different time intervals, through clinical simulation and parametric identification. The solutions obtained from the model to fit the clinical data were different for normal and diabetic test subjects. The clinical data of "normal" subjects could be simulated by means of an under-damped solution of the model, as: y(t) = (G/ω)e-ωt sin ωt. The data of "diabetic" patients needed to be simulated by means of an over-damped solution of the model, as: y(t) = (G/ω)e-At sin hωt, where G represents the magnitude of the impulse input Gδ(t) to the model (in gms of glucose per litre of blood pool volume), ω is the damped oscillatory frequency of the model, wn is the natural frequency of the system and [Formula: see text]. In order to facilitate differential diagnosis, we developed a non-dimensional diabetic index (DI) expressed as: [Ay max Td/GT max ]. This index can be used to facilitate the diagnosis of diabetes as well as for assessing the risk to becoming diabetic.

scholarly journals Diabetes mellitus and impaired glucose tolerance in urban adult population

2014 ◽  
Vol 60 (2) ◽  
pp. 118-124 ◽  
Author(s):  
Walter Rodrigues Júnior ◽  
Sandra Cristina Nicodemo Gaban ◽  
Elenir Rose Jardim Cury Pontes ◽  
Celso Correia Souza ◽  
Lilian Patussi Gimenes ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Adult Population ◽  
Oral Glucose ◽  
Diabetic Patients ◽  
Mato Grosso ◽  
Strict Adherence ◽  
Family History Of Diabetes

Objective: Estimating the prevalence of diabetes mellitus (DM) and impaired glucose tolerance (IGT) in the urban population aged between 30 and 69 years in the municipality of Campo Grande, state of Mato Grosso do Sul, Brazil. Methods: Population-based cross-sectional study conducted between October/2009 and February/2011. The investigation included the determination of fasting glucose and participants with blood glucose ≥ 200 mg/dL were considered diabetic. Nondiabetic patients, which showed blood glucose ≥ 100 mg/dL and < 200 mg/dL, underwent an oral glucose tolerance test (OGTT) to investigate whether they had DM or IGT. Results: 1.429 individuals participated in this investigation. The general prevalence, adjusted for sex and age, were: 12.3% for DM (95%CI: 10.5 to 13.9%) and 7.1% for IGT (95%CI: 5.7 to 8.4%). There was a higher prevalence of DM with increasing age in people with low educational level, family history of diabetes, overweight, obesity and central obesity. Among diabetic patients (n = 195), 25% were unaware they had the disease and were diagnosed through investigation. Among patients who already knew they had DM (n = 146), 37% were unaware of the potential chronic complications. Conclusion: This study confirms the increased prevalence of DM in Brazil and emphasizes the need for early diagnosis, as well as the importance of strict adherence to medical treatment in order to prevent its much feared complications.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

Endogenous and Exogenous Insulin Responses in Patients With Cystic Fibrosis

PEDIATRICS ◽  
1975 ◽  
Vol 55 (1) ◽  
pp. 75-82
Author(s):  
Errol G. Wilmshurst ◽  
J. Stuart Soeldner ◽  
Douglas S. Holsclaw ◽  
Robert L. Kaufmann ◽  
Harry Shwachman ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Serum Insulin ◽  
Lower Serum ◽  
Intravenous Glucose ◽  
Family History Of Diabetes ◽  
Insulin Levels

Eight male patients with cystic fibrosis, normal nutrition, normal physical activity, relatively mild pulmonary disease, no evidence of liver disease and no family history of diabetes mellitus underwent a series of carbohydrate tolerance tests in comparison with a group of 18 normal male subjects matched for age and body weight. Compared with the normal group, the patients with cystic fibrosis had significantly impaired glucose tolerance and significantly lower serum immunoreactive insulin levels during oral and intravenous glucose tolerance tests; serum insulin levels were also significantly lower after intravenous administration of tolbutamide in the patients with cystic fibrosis, but the reduction in blood glucose concentration in each group was not significantly different. During an intravenous insulin test, the decrease in blood glucose concentration was the same for both groups, in spite of significantly lower serum insulin levels in the patients with cystic fibrosis. The percentage fall in plasma free fatty acids was at least as great in the patients with cystic fibrosis as in normals during the test procedures, while a significant decrease in plasma alpha-amino nitrogen after intravenously administered insulin was seen only in the patients with cystic fibrosis. These studies suggest that the carbohydrate intolerance of cystic fibrosis is consequent upon an impaired insulin response to glucose, but that this insulin deficiency is partly compensated for by increased peripheral tissue sensitivity to insulin.

Influence of Dihydromyricetin on Lowering Blood Glucose Concentration and Reducing Early Kidney Damage in Imparied Glucose Tolerance Rats

2014 ◽  
Vol 1004-1005 ◽  
pp. 857-863 ◽  
Author(s):  
Yong Qiang Zhou ◽  
Tao Yan Mao
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Early Stage ◽  
Fasting Blood Glucose ◽  
Kidney Damage ◽  
Postprandial Blood Glucose ◽  
Control Groups ◽  
Dose Levels

Diabetic nephropathy (DN) is a common complication of diabetes and it is related to irreversible kidney damages and chronic renal failure. Impaired glucose tolerance (IGT) is an early stage in the development of diabetes and DN. Early detection of IGT and treatment of its associated early kidney damage can effectively prevent the development of DN. In this paper, the influence of dihydromyricetin (DHM) on lowering blood glucose concentration and reducing early kidney damage in IGT rats was studied. Animal model of IGT rats was built by two week intragastric injection of D-galactose and treated with eight weeks of intragastric injection of DHM at two dose levels. The concentrations of fasting blood glucose (FBG), two-hour postprandial blood glucose (2hBG), insulin levels, contents of microalbuminuia (mAlb) and blood urea nitrogen (BUN), and activities of lactate dehydrogenase (LDH) in kidney were analysed and compared with those in control groups. Experimental results indicated that DHM treatment can significantly lower the levels of two-hour postprandial blood glucose and insulin, decrease the content of mAlb and the activities of LDH in kidney, but does not influence the level of BUN. The study suggested that DHM can effectively improve the states of IGT rats and provide a protective effect against early kidney damage.

scholarly journals Glucocorticoid-Induced Preterm Birth and Neonatal Hyperglycemia Alter Ovine β-Cell Development

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3763-3776 ◽  
Author(s):  
Amita Bansal ◽  
Frank H. Bloomfield ◽  
Kristin L. Connor ◽  
Mike Dragunow ◽  
Eric B. Thorstensen ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Preterm Birth ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Cell Mass ◽  
Β Cell ◽  
High Blood Glucose ◽  
Increased Risk

Adults born preterm are at increased risk of impaired glucose tolerance and diabetes. Late gestation fetuses exposed to high blood glucose concentration also are at increased risk of impaired glucose tolerance as adults. Preterm babies commonly become hyperglycemic and are thus exposed to high blood glucose concentration at an equivalent stage of pancreatic maturation. It is not known whether preterm birth itself, or complications of prematurity, such as hyperglycemia, alter later pancreatic function. To distinguish these, we made singleton preterm lambs hyperglycemic (HYPER) for 12 days after birth with a dextrose infusion and compared them with vehicle-treated preterm and term controls and with HYPER lambs made normoglycemic with an insulin infusion. Preterm birth reduced β-cell mass, apparent by 4 weeks after term and persisting to adulthood (12 mo), and was associated with reduced insulin secretion at 4 months (juvenile) and reduced insulin mRNA expression in adulthood. Hyperglycemia in preterm lambs further down-regulated key pancreatic gene expression in adulthood. These findings indicate that reduced β-cell mass after preterm birth may be an important factor in increased risk of diabetes after preterm birth and may be exacerbated by postnatal hyperglycemia.

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