scholarly journals Orally Administered Whey Proteins Have Comparable Effect on C-Peptide Secretion in Healthy Subjects as Standard C-Peptide Stimulation Tests

2013 ◽  
pp. 179-186
Author(s):  
E. WILDOVÁ ◽  
P. DLOUHÝ ◽  
P. KRAML ◽  
J. RAMBOUSKOVÁ ◽  
V. ŠMEJKALOVÁ ◽  
...  
Keyword(s):  
Cell Function ◽  
Whey Proteins ◽  
Normal Glucose Tolerance ◽  
Individual Variability ◽  
C Peptide ◽  
Glucose Levels ◽  
Normal Glucose ◽  
Stimulation Tests ◽  
Lower Variability ◽  
Peptide Secretion

Our study compared total C-peptide secretion after administration of whey proteins and whey proteins in combination with glucose with results of classical tests assessing beta cell function in the pancreas of healthy individuals. Eight young, healthy (7 males, 1 female; aged 20-26 years), non-obese (BMI: 17-25.9 kg/m2) participants with normal glucose tolerance underwent six C-peptide secretion tests. Three secretion tests measured C-peptide response to orally administered substances: whey proteins only (OWT), whey proteins with glucose (OWGT) and glucose only (OGTT); while three secretion tests measured C-peptide response to intravenously administered substances: arginine (AST), glucagon (GST) and glucose (IVGTT). OWT stimulated a greater (93 %, p<0.05) C-peptide response than AST and a 64 % smaller response (p<0.05) than OGTT. OWT also showed lower variability (p<0.05) in C-peptide responses compared to OWGT and OGTT. The greatest total C-peptide response was induced by OWGT (36 % higher than glucose). OWT consistently increased C-peptide concentrations with lower individual variability, while insignificantly increasing glucose levels. Results of this study suggest that both dietology and beta-cells capacity testing could take advantage of the unique property of whey proteins to induce C-peptide secretion.

scholarly journals Role of C-Peptide in the Regulation of Microvascular Blood Flow

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
T. Forst ◽  
T. Kunt ◽  
B. Wilhelm ◽  
M. M. Weber ◽  
A. Pfützner
Keyword(s):  
Blood Flow ◽  
Beta Cell ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Microvascular Blood Flow ◽  
Diabetic Patients ◽  
C Peptide ◽  
Glucose Levels ◽  
Peptide Secretion

During the recent years, the role of C-peptide, released from the pancreatic beta cell, in regulating microvascular blood flow, has received increasing attention. In type 1 diabetic patients, intravenous application of C-peptide in physiological concentrations was shown to increase microvascular blood flow, and to improve microvascular endothelial function and the endothelial release of NO. C-peptide was shown to impact microvascular blood flow by several interactive pathways, like stimulatingNa+K+ATPase or the endothelial release of NO. There is increasing evidence, that in patients with declining beta cell function, the lack of C-peptide secretion might play a putative role in the development of microvascular blood flow abnormalities, which go beyond the effects of declining insulin secretion or increased blood glucose levels.

scholarly journals Arginine is preferred to glucagon for stimulation testing of β-cell function

2014 ◽  
Vol 307 (8) ◽  
pp. E720-E727 ◽  
Author(s):  
R. Paul Robertson ◽  
Ralph H. Raymond ◽  
Douglas S. Lee ◽  
Roberto A. Calle ◽  
Atalanta Ghosh ◽  
...  
Keyword(s):  
Adverse Events ◽  
Cell Function ◽  
Intraclass Correlation ◽  
Insulin Response ◽  
Normal Glucose Tolerance ◽  
Β Cell ◽  
C Peptide ◽  
Women Subjects ◽  
Normal Glucose ◽  
Β Cell Function

A key aspect of research into the prevention and treatment of type 2 diabetes is the availability of reproducible clinical research methodology to assess β-cell function. One commonly used method employs nonglycemic secretagogues like arginine (arg) or glucagon (glgn). This study was designed to quantify the insulin response to arg and glgn and determine test repeatability and tolerability. Obese overnight-fasted subjects with normal glucose tolerance were studied on 4 separate days: twice using arg (5 g iv) and twice with glgn (1 mg iv). Pre- and postinfusion samples for plasma glucose, insulin, and C-peptide were acquired. Arg and glgn challenges were repeated in the last 10 min of a 60-min glucose (900 mg/min) infusion. Insulin and C-peptide secretory responses were estimated under baseline fasting glucose conditions (AIRarg and AIRglgn) and hyperglycemic (AIRargMAX AIRglgnMAX) states. Relative repeatability was estimated by intraclass correlation coefficient (ICC). Twenty-three (12 men and 11 women) subjects were studied (age: 42.4 ± 8.3 yr; BMI: 31.4 ± 2.8 kg/m2). Geometric means (95% CI) for baseline-adjusted values AIRarg and AIRglgn were 84 (75–95) and 102 (90–115) μU/ml, respectively. After the glucose infusion, AIRargMAX and AIRglgnMAX were 395 (335–466) and 483 (355–658) μU/ml, respectively. ICC values were >0.90 for AIRarg andAIRargMAX. Glucagon ICCs were 0.83, 0.34, and 0.36, respectively, although the exclusion of one outlier increased the latter two values (to 0.84 and 0.86). Both glgn and arg induced mild adverse events that were transient. Glucagon, but not arginine, induced moderate adverse events due to nausea. Taken together, arginine is preferred to glucagon for assessment of β-cell function.

scholarly journals Basal α-Cell Up-Regulation in Obese Insulin-Resistant Adolescents

2011 ◽  
Vol 96 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Ram Weiss ◽  
Ebe D'Adamo ◽  
Nicola Santoro ◽  
Karen Hershkop ◽  
Sonia Caprio
Keyword(s):  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
C Peptide ◽  
Insulin Resistant ◽  
Hyperglycemic Clamp ◽  
Secretion Profile ◽  
Normal Glucose ◽  
Peptide Secretion

Context: The aim of this analysis was to evaluate glucagon and c-peptide concentrations in two scenarios: euglycemic hyperinsulinemia and hyperglycemic hyperinsulinemia. We postulated that worsening obesity and insulin resistance will be reflected as an up-regulated (less suppressible) islet secretion profile. Methods: Eighty-two [34 obese with normal glucose tolerance (NGT), 30 obese with impaired glucose tolerance (IGT), and 18 nonobese with NGT] subjects underwent a euglycemic-hyperinsulinemic clamp (EHC) and a hyperglycemic clamp. C-peptide and glucagon were evaluated at basal and steady-state (SS) conditions. Results: Basal glucagon was significantly elevated in obese insulin-resistant and obese IGT subjects as was basal c-peptide. SS glucagon and c-peptide levels during the EHC were lower in the lean and obese insulin-sensitive subjects compared with the obese insulin-resistant subjects with NGT or IGT. Fasting glucagon was the only significant determinant (β = 0.66, P &lt; 0.001) of SS glucagon during the EHC (R2 = 0.57). In a longitudinal follow-up of a subsample, those who converted from normal to IGT significantly increased their fasting glucagon concentration in comparison with those who remained with NGT. Conclusions: Islet up-regulation manifesting as basal elevated glucagon and c-peptide secretion that determines the suppressive effects of hyperinsulinemia appears early in the course of deteriorating glucose tolerance.

STUDIES IN CONGENITAL GENERALIZED LIPODYSTROPHY (SEIP-BERARDINELLI SYNDROME)

1973 ◽  
Vol 72 (3) ◽  
pp. 475-494 ◽  
Author(s):  
Svein Oseid
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Juvenile Form ◽  
Congenital Generalized Lipodystrophy ◽  
Glucose Levels ◽  
Normal Glucose ◽  
Glucose Tolerance Tests ◽  
The One ◽  
Adipose Organ

ABSTRACT Six cases of congenital generalized lipodystrophy have been studied at different ages from infancy to adolescence with regard to glucose tolerance, insulin secretion, and insulin sensitivity. During the first few years of life there is normal glucose tolerance. The fasting immuno-reactive insulin (IRI) levels are either slightly elevated or normal. The IRI response to glucose is exaggerated and prolonged, at least from the third year of life. Some degree of insulin resistance is already present in infancy. From the age of 8–10 years glucose tolerance decreases rapidly. The fasting IRI levels are usually grossly elevated, while fasting plasma glucose levels are only moderately elevated or normal. The IRI responses to oral and iv administered glucose, and to tolbutamide are exaggerated; the insulinogenic indices are high. Cortisone primed glucose tolerance tests become abnormal. Insulin resistance is marked, and increases with age. After cessation of growth at approximately 12 years of age, frank diabetes with fasting hyperglycaemia and diabetic glucose tolerance curves developed in the one patient followed beyond this age. Her fasting IRI was increased, but there was a poor IRI response to glucose stimulation, suggesting a partial exhaustion of the β-cells. Her initial IRI response to tolbutamide was still good, but not as brisk as in the younger patients. This type of diabetes is quite different from the juvenile form, and also from the diabetes of older age. It may be causally related to the lack of an adequate adipose organ necessary for the disposal of excesses of glucose, or possibly related to another anti-insulin mechanism.

Effect of High ß-Glucan Barley on Postprandial Plasma Glucose Levels in Subjects with Normal Glucose Tolerance and Patients with Type 2 Diabetes

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 772-P
Author(s):  
MARIKO HIGA ◽  
AYANA HASHIMOTO ◽  
MOE HAYASAKA ◽  
MAI HIJIKATA ◽  
AYAMI UEDA ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Normal Glucose Tolerance ◽  
Postprandial Plasma Glucose ◽  
Glucose Levels ◽  
Normal Glucose

Liraglutide Therapy in a Prediabetic State: Rethinking the Evidence

2020 ◽  
Vol 16 (7) ◽  
pp. 699-715 ◽  
Author(s):  
Georgios S. Papaetis
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Current Evidence ◽  
Β Cell ◽  
Prediabetic State ◽  
New Therapeutic Approaches ◽  
Normal Glucose

Background: Prediabetes is defined as a state of glucose metabolism between normal glucose tolerance and type 2 diabetes. Continuous β-cell failure and death are the reasons for the evolution from normal glucose tolerance to prediabetes and finally type 2 diabetes. Introduction: The necessity of new therapeutic approaches in order to prevent or delay the development of type 2 diabetes is obligatory. Liraglutide, a long-acting GLP-1 receptor agonist, has 97% homology for native GLP-1. Identification of the trophic and antiapoptotic properties of liraglutide in preclinical studies, together with evidence of sustained β-cell function longevity during its administration in type 2 diabetes individuals, indicated its earliest possible administration during this disease, or even before its development, so as to postpone or delay its onset. Methods: Pubmed and Google databases have been thoroughly searched and relevant studies were selected. Results: This paper explores the current evidence of liraglutide administration both in humans and animal models with prediabetes. Also, it investigates the safety profile of liraglutide treatment and its future role to postpone or delay the evolution of type 2 diabetes. Conclusion: Liralgutide remains a valuable tool in our therapeutic armamentarium for individuals who are overweight or obese and have prediabetes. Future well designed studies will give valuable information that will help clinicians to stratify individuals who will derive the most benefit from this agent, achieving targeted therapeutic strategies.

Sign in / Sign up

Export Citation Format

Share Document