scholarly journals Glucose tolerance and insulin sensitivity in malnourished children

1972 ◽  
Vol 27 (3) ◽  
pp. 585-592 ◽  
Author(s):  
G. A. O. Alleyne ◽  
P. M. Trust ◽  
H. Flores ◽  
H. Robinson

1. In malnourished, compared with recovered children, fasting blood glucose concentrations were low and there was impaired peripheral glycolysis as shown by a failure of blood lactate to rise after glucose was injected intravenously.2. Homogenates of muscle biopsies from malnourished and recovered children produced equal amounts of lactate when incubated anaerobically with various substrates, but when compared with homogenates of biopsies from normal children the pattern suggested an impairment of glycolysis.3. The rate of glucose disappearance after intravenous glucose was slow in the malnourished child and there was possibly diminished sensitivity to exogenous insulin.4. Isocaloric diets relatively high or low in fat were fed to children who had recovered from malnutrition. Glucose tolerance, insulin sensitivity, fasting plasma insulin and insulin response to intravenous glucose were all the same in children on either diet.

1969 ◽  
Vol 62 (2) ◽  
pp. 242-250 ◽  
Author(s):  
U. Larsson-Cohn ◽  
B. Tengström ◽  
L. Wide

ABSTRACT Intravenous glucose tolerance tests and insulin determinations were performed on 37 women at different stages of the menstrual cycle and after one, three and twelve months of daily continuous treatment with 0.5 mg of norethindrone or 0.5 mg of chlormadinone acetate. The fasting blood glucose concentration, the k-values (percentage disappearance rate of glucose per minute) and the insulin response to glucose administration were compared. No statistically significant differences were found between the values obtained on two occasions before treatment, and during treatment.


1983 ◽  
Vol 55 (6) ◽  
pp. 1660-1664 ◽  
Author(s):  
D. E. James ◽  
K. M. Burleigh ◽  
E. W. Kraegen ◽  
D. J. Chisholm

Physical training causes hypoinsulinemia and enhanced insulin sensitivity. Insulin sensitivity is also enhanced by a single bout of exercise. However, changes in beta-cell responsiveness with acute exercise are ill defined. To clarify these relationships intravenous glucose tolerance tests were performed in 1) physically trained rats (3 different levels), 48 h after the last bout of exercise; 2) untrained rats, 0.5, 4, and 24 h after a single bout of exercise; or 3) sedentary control rats. The total area under the glucose-stimulated insulin response curve (GSIR) was negatively correlated with total distance run during training (r = -0.45, P less than 0.05), whereas glucose tolerance was improved (P less than 0.005 vs. controls) with intensive training. GSIR was suppressed by 38% (P less than 0.01 vs. controls) 0.5 h after a single bout of exercise. This effect persisted for 4 h but was not present after 24 h. These results indicate that a single bout of exercise induces suppression of GSIR which lasts less than 24 h. In contrast, physical training induces prolonged suppression (for at least 48 h) of GSIR, proportional to the intensity of training, and improved glucose tolerance.


1983 ◽  
Vol 104 (1) ◽  
pp. 77-84 ◽  
Author(s):  
A. Wajngot ◽  
R. Luft ◽  
S. Efendić

Abstract. Oral and iv glucose tolerance, insulin response to iv and oral glucose load as well as insulin sensitivity were evaluated in 58 'low insulin responders'. They were selected from a group of 226 healthy subjects with normal fasting blood glucose and normal iv glucose tolerance test on the basis of a low insulin response during a standardized glucose infusion test (GIT). The insulin response to GIT was analysed by parameter identification in a mathematical model (parameter KI). Insulin sensitivity was also measured by computer analysis of GIT (parameter KG) and, in a limited group of subjects, by a somatostatin infusion test. Thirty-three low insulin responders had normal OGTT, whereas 5 demonstrated borderline-1, 16 borderline-2, and 4 decreased OGTT. The first group of subjects demonstrated normal or enhanced insulin sensitivity. Borderline and decreased OGTT, in most instances, was accompanied by decreased insulin sensitivity, implying that a subgroup of low insulin responders exhibited signs of both impaired insulin response to glucose and insulin resistance. Since these defects characterize manifest type-2 diabetes, these subjects possibly may run a high risk to develop this type of diabetes. On the other hand, low insulin response in combination with increased insulin sensitivity may reflect adaptation of the secretory capacity of B-cells to the need of insulin.


PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0262584
Author(s):  
Hannah M. Kinsella ◽  
Laura D. Hostnik ◽  
Hailey A. Snyder ◽  
Sarah E. Mazur ◽  
Ahmed M. Kamr ◽  
...  

The equine neonate is considered to have impaired glucose tolerance due to delayed maturation of the pancreatic endocrine system. Few studies have investigated insulin sensitivity in newborn foals using dynamic testing methods. The objective of this study was to assess insulin sensitivity by comparing the insulin-modified frequently sampled intravenous glucose tolerance test (I-FSIGTT) between neonatal foals and adult horses. This study was performed on healthy neonatal foals (n = 12), 24 to 60 hours of age, and horses (n = 8), 3 to 14 years of age using dextrose (300 mg/kg IV) and insulin (0.02 IU/kg IV). Insulin sensitivity (SI), acute insulin response to glucose (AIRg), glucose effectiveness (Sg), and disposition index (DI) were calculated using minimal model analysis. Proxy measurements were calculated using fasting insulin and glucose concentrations. Nonparametric statistical methods were used for analysis and reported as median and interquartile range (IQR). SI was significantly higher in foals (18.3 L·min-1· μIU-1 [13.4–28.4]) compared to horses (0.9 L·min-1· μIU-1 [0.5–1.1]); (p < 0.0001). DI was higher in foals (12 × 103 [8 × 103−14 × 103]) compared to horses (4 × 102 [2 × 102−7 × 102]); (p < 0.0001). AIRg and Sg were not different between foals and horses. The modified insulin to glucose ratio (MIRG) was lower in foals (1.72 μIUinsulin2/10·L·mgglucose [1.43–2.68]) compared to horses (3.91 μIU insulin2/10·L·mgglucose [2.57–7.89]); (p = 0.009). The homeostasis model assessment of beta cell function (HOMA-BC%) was higher in horses (78.4% [43–116]) compared to foals (23.2% [17.8–42.2]); (p = 0.0096). Our results suggest that healthy neonatal foals are insulin sensitive in the first days of life, which contradicts current literature regarding the equine neonate. Newborn foals may be more insulin sensitive immediately after birth as an evolutionary adaptation to conserve energy during the transition to extrauterine life.


2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Yi-Chyan Chen ◽  
Wei-Win Lin ◽  
Yu-Jung Chen ◽  
Wei-Chung Mao ◽  
Yi-Jen Hung

Growing evidence suggests that mood disorder is associated with insulin resistance and inflammation. Thus the effects of antidepressants on insulin sensitivity and proinflammatory responses will be a crucial issue for depression treatment. In this study, we enrolled 43 non-diabetic young depressed males and adapted standard testing procedures to assess glucose metabolism during 4-week hospitalization. Before and after the 4-week antidepressant treatment, participants underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT). Insulin sensitivity (SI), glucose effectiveness (SG), acute insulin response, and disposition index (DI) were estimated using the minimal model method. The plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α), and adiponectin were measured. The Hamilton depression rating scale (HAM-D) total scores were reduced significantly during the course of treatment. There were no significant changes in the parameters ofSI,SG, and DI. Compared to drug naïve status, the level of plasma IL-6 was significantly elevated (0.77to1.30 pg/ml;P=.001) after antidepressant therapy. However, the concentrations of CRP, TNF-α, and adiponectin showed no differences during the course of treatment. The results suggest that antidepressants may promote stimulatory effect on the IL-6 production in the early stage of antidepressant treatment.


Author(s):  
Gareth J. Dunseath ◽  
Stephen D. Luzio ◽  
Rajesh Peter ◽  
David R. Owens

Abstract Aims The two predominant pathophysiological defects resulting in glucose intolerance are beta-cell dysfunction and insulin insensitivity. This study aimed to re-examine beta-cell function and insulin sensitivity across a continuum from normal glucose tolerance (NGT) to early type 2 diabetes (T2DM) employing highly specific insulin, C-peptide and intact proinsulin assays. Materials and methods A total of 104 persons with NGT, 85 with impaired glucose tolerance (IGT) and 554 with newly diagnosed T2DM were investigated. Following an overnight fast, all underwent a 4-h standardised mixed meal tolerance test (MTT), and on a second day, a sub-group underwent a frequently sampled insulin-modified intravenous glucose tolerance test (FSIVGTT) over a 3-h period. The participants were stratified according to fasting glucose and BMI for analysis. Results The MTT revealed that increasing FPG was accompanied by progressively elevated and delayed postprandial glucose peaks. In parallel, following an initial compensatory increase in fasting and postprandial insulin responses there followed a progressive demise in overall beta-cell secretory capacity. FSIVGTT demonstrated a major reduction in the early insulin response to IV glucose in persons with IGT accompanied by a dramatic fall in insulin sensitivity. Beyond pre-diabetes, ever-increasing fasting and postprandial hyperglycaemia resulted predominantly from a progressively decreasing beta-cell secretory function. Conclusion This study utilising improved assay technology re-affirms that beta-cell dysfunction is evident throughout the spectrum of glucose intolerance, whereas the predominant fall in insulin sensitivity occurs early in its evolution.


2021 ◽  
Vol 13 (1) ◽  
pp. e2021021
Author(s):  
Vincenzo De Sanctis

Summary. Objective: To  study the function of the endocrine pancreas in transfusion-dependent ?-thalassemia (?-TDT) patients with normal oral glucose tolerance test (OGTT) and hypoinsulinemia. Patients and methods: Seven ?-TDT patients  (mean age 22.4 ± 4.2 years) with normal glucose tolerance test (NGT) and poor insulin response (hypoinsulinemia) to OGTT,  not associated with ?-cell autoimmunity, were referred for a second opinion to an Italian Centre, part of the International Network of Clinicians for Endocrinopathies in Thalassemia and Adolescence Medicine (ICET-A). In this pilot study,  the first-phase insulin response (FPIR), expressed as the sum of 1 and  3 minutes insulin, of ?-TDT patients to intravenous glucose tolerance test (IVGTT), was tested. Moreover, the long-term natural history was followed prospectively using an annual OGTT, with the aim of detecting any abnormality of glucose metabolism. Results: The FPIR value  was between the 1st and 3rd percentile in two patients and between the 3rd and 10th percentile in  five. After 43 ± 26 months (range 11 - 80 months) of follow-up, 2 patients developed impaired glucose tolerance (IGT), 3 both IGT and impaired fasting glucose (IFG) and two overt diabetes mellitus (DM). Interestingly, the patients who developed DM had, at baseline the lowest value of insulinogenic index (IGI, 0.08 and 0.25), defined as the ratio of the increment of plasma insulin to plasma glucose during the first 30 minutes after OGTT. Moreover, a significant correlation was found between the IGI at baseline and at follow-up in the patients who developed IGT with or without IFG (R= 0.927; P: 0.023). A significant reduction of Matsuda insulin sensitivity index (ISIM) and Insulin Secretion-Sensitivity Index-2 (ISSI-2) was documented in the study cohort at diagnosis of IFG, IGT and DM. There was a significant inverse correlation between ISSI-2 and area under the curve of plasma glucose (AUC-PG). Conclusions: These data demonstrated, for the first time, a progressive deterioration in glucose homeostasis in ?-TDT subjects with NGT and hypoinsulinemia.  Thus, we consider that variations of insulin sensitivity could possibly have an impact on glucose tolerance in adult patients with TDT. Further investigations should focus on factors that might positively influence insulin sensitivity, including nutrition, drugs and physical activity.  


2010 ◽  
Vol 104 (2) ◽  
pp. 214-221 ◽  
Author(s):  
Adronie Verbrugghe ◽  
Myriam Hesta ◽  
Stephanie Van Weyenberg ◽  
Georgios A. Papadopoulos ◽  
Kris Gommeren ◽  
...  

The present study assessed the effect of separate reduction of each energy-delivering nutrient – protein, fat and carbohydrate – on glucose tolerance and insulin response in a strict carnivore: the domestic cat (Felis catus). Three isoenergetic, home-made diets with the following energetic distribution, low protein (LP): protein 28 % of metabolisable energy; fat 43 %; nitrogen-free extract 29 %; low fat: 47, 27 and 25 %; low carbohydrate (LC): 45, 48 and 7 %, were tested in a 3 × 3 Latin square design. Nine healthy normal-weight cats were randomly assigned to each of the diets in a random order at intervals of 3 weeks. At the end of each testing period, intravenous glucose tolerance tests were performed. Plasma glucose concentrations and area under the glucose curve showed no differences. Area under the insulin curve was lower when cats were fed the LP diet, and the second insulin peak tended to be delayed when the LC diet was fed. In contrast to other studies, in which energy sources were elevated instead of being reduced, the present trial contradicts the often suggested negative impact of carbohydrates on insulin sensitivity in carnivores, and shows that reducing the dietary carbohydrate content below common amounts for commercial foods evokes an insulin-resistant state, which can be explained by the cats' strict carnivorous nature. It even points to a negative effect of protein on insulin sensitivity, a finding that corresponds with the highly gluconeogenic nature of amino acids in strict carnivores.


Sign in / Sign up

Export Citation Format

Share Document