Japanese IGT Subjects with High Insulin Response Are Far More Frequently Associated with the Metabolic Syndrome Than Those with Low Insulin Response

Endocrine ◽  
2006 ◽  
Vol 29 (2) ◽  
pp. 351-356 ◽  
Author(s):  
Yutaka Mori ◽  
Kyouko Hoshino ◽  
Kuninobu Yokota ◽  
Yohta Itoh ◽  
Naoko Tajima
2011 ◽  
Vol 2 (5) ◽  
pp. 302-310 ◽  
Author(s):  
I. M. Y. Szeto ◽  
P. S. P. Huot ◽  
S. A. Reza-López ◽  
A. Jahan-mihan ◽  
G. H. Anderson

Rat offspring born to dams fed a high multivitamin diet (HV) are shown to have increased risks of obesity and metabolic syndrome. We hypothesized that a low-vitamin postweaning diet would enhance these characteristics in offspring born to HV dams. During pregnancy, Wistar rats were fed the AIN-93G diet with or without a 10-fold increase in vitamin content. In Experiment 1, at weaning, males were fed the recommended diet (RV) or a diet with 1/3 the vitamin content (1/3 RV) for 12 weeks. In Experiment 2, males and females were fed the RV diet or 1/6 RV diet for 35 weeks. Body weight was measured on a weekly basis, food intake on a daily basis, and for 1 h after an overnight fast following glucose gavage at 6, 12 and 24 weeks. Blood glucose and insulin responses to an oral glucose load were measured at 30 weeks. Males from HV dams, compared with those from RV dams, gained more weight in Experiment 1 (+7%,P< 0.05) and Experiment 2 (+11%,P< 0.0001), along with higher glucose response (+33%,P< 0.05). The 1/6 RV pup diet led to lower weight gain in males (−16%,P< 0.0001) and females (−13%,P< 0.0005), and lower food intake in males (−9%,P< 0.01) independent of the gestational diet. Females on the 1/6 RV diet and from HV dams had higher 1 h food intake (+36%,P< 0.05) and lower insulin response (−25%,P< 0.05) compared with those from RV dams. Exposure of the offspring to low-vitamin diets did not amplify the expression of the metabolic syndrome observed in those born to dams fed an HV diet.


2017 ◽  
Vol 18 (2) ◽  
pp. 147032031770345 ◽  
Author(s):  
Sandro S Almeida ◽  
Flavia C Corgosinho ◽  
Carlos EN Amorim ◽  
Marcos F Gregnani ◽  
Raquel MS Campos ◽  
...  

Introduction: The main purpose of the present study was to investigate whether I/D polymorphism of the ACE gene might affect metabolic changes related to the metabolic syndrome through a long-term interdisciplinary therapy in obese adolescents. Methods: In total, 125 obese adolescents who entered the interdisciplinary obesity programme were assigned to the following two subgroups: metabolic syndrome or non-metabolic syndrome. They were evaluated at baseline and after 1 year. Genomic DNA was extracted from circulating leukocytes. Results: Subjects with the II genotype in the non-metabolic syndrome group were only to increase their fat-free mass after therapy. Regarding lipid profile, subjects with ID and DD genotypes from both groups reduced their low-density lipoprotein cholesterol levels significantly. The metabolic parameters from the ID and DD genotypes of the non-metabolic syndrome group showed a significantly improved insulin response. Conclusion: In the present study, we showed that the ACE polymorphism was able to influence the fat-free mass in the I-carry allele in the non-metabolic syndrome group positively. In addition, the I-carry allele was able to improve the insulin resistance of the metabolic syndrome group significantly. These results suggest that the ACE I/D genotypes can influence, in different ways, the specific parameters of metabolism among obese adolescents submitted for long-term interdisciplinary therapy.


1975 ◽  
Vol 78 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Karin Edström ◽  
Erol Cerasi ◽  
Rolf Luft ◽  
Bengt Persson ◽  
Berlil Thalme

ABSTRACT It has earlier been postulated that a low insulin response to a glucose infusion is characteristic for the prediabetic individual (Cerasi & Luft 1967c). There is also evidence that some infants of individuals with low insulin response might have a carbohydrate metabolism that is in some respects similar to that of newborn infants to diabetic mothers (Edström et al. 1974). In the present study 15 infants to low insulin responders (ILR) and 22 infants to high insulin responders (IHR) were subjected to an intravenous glucose load (IVGTT) at 2–24 h age. A significant difference in glucose tolerance was found between the groups, the mean k-value for the ILR being 1.39 ± 0.41 and that for the IHR 1.05 ± 0.09 (P < 0.05). No mothers were found to have a gestational diabetes (with the possible exception of one low insulin responders) but during late pregnancy the mean k-value at IVGTT in the low responders decreased from nonpregnant values (the mean difference being 0.41 ± 0.20, P < 0.025) while the high responders did not show a corresponding decrease (mean difference 0.12 ± 0.25, P > 0.05). No other differences between the groups of infants that could influence the k-value could be found apart from the mothers being low or high insulin responders. Our findings show that a low insulin response in the mothers might affect the glucose tolerance of the foetus even in the absence of continuous maternal hyperglycaemia in late pregnancy.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jiunn-diann Lin ◽  
Chun-Hsien Hsu ◽  
Yao-Jen Liang ◽  
Wei-Cheng Lian ◽  
Chang-Hsun Hsieh ◽  
...  

Aims. There are two phases of insulin secretion, the first (FPIS) and second phase (SPIS). In this study, we built equations to predict FPIS with metabolic syndrome (MetS) components and fasting plasma insulin (FPI).Methods. Totally, 186 participants were enrolled. 75% of participants were randomly selected as the study group to build equations. The remaining 25% of participants were selected as the external validation group. All participants received a frequently sampled intravenous glucose tolerance test, and acute insulin response after the glucose load (AIRg) was obtained. The AIRg was considered as FPIS.Results. When MetS components were only used, the following equation was built: log (FPIS) = 1.477 − 0.119 × fasting plasma glucose (FPG) + 0.079 × body mass index (BMI) − 0.523 × high-density lipoprotein cholesterol (HDL-C). After FPI was added, the second equation was formulated: log (FPIS) = 1.532 − 0.127 × FPG + 0.059 × BMI - 0.511 × HDL-C + 0.375 × log (FPI), which provided a better accuracy than the first one.Conclusions. Using MetS components, the FPIS could be estimated accurately. After adding FPI into the equation, the predictive power increased further. We hope that these equations could be widely used in daily practice.


1994 ◽  
Vol 87 (2) ◽  
pp. 187-192 ◽  
Author(s):  
Jan Pigon ◽  
Jan Karlsson ◽  
Claes-Göran Östenson

1. We have assessed insulin secretion, insulin sensitivity, exercise capacity and muscle fibre composition in healthy men with a low insulin response to glucose (low insulin responders and endurance-trained subjects) and in healthy men with a normally high insulin response. Low insulin responders have been considered as prediabetic subjects. 2. During glucose infusion, low insulin responders and endurance-trained subjects had acute-phase (0-10 min) insulin responses that were 26% (P < 0.001) and 31% (P < 0.001), and C-peptide responses that were 35% (P < 0.001) and 42% (P < 0.01), respectively of the responses in high insulin responders. Also, the late-phase (10-60 min) insulin and C-peptide responses were lower in low insulin responders and endurance-trained subjects. Endurance-trained subjects, compared with high and low insulin responders, had higher insulin sensitivity (blood glucose concentration during a somatostatin-insulin-glucose infusion test 3.6 ± 0.4 versus 6.3 ± 0.6 mmol/l in high insulin responders, P < 0.01, and 5.5 ± 0.4 mmol/l in low insulin responders, P < 0.01), exercise capacity (4.2 ± 0.2 versus 3.0 ± 0.2 W/kg body weight, P < 0.001, and 2.8 ± 0.1 W/kg body weight, P < 0.001) and a higher percentage of slow-twitch fibres (58.2 ± 5.2 versus 38.5 ± 3.5%, P < 0.01 and 40.9 ± 3.0%, P < 0.001). 3. In conclusion, we demonstrate that low insulin responders exhibited decreased insulin and C-peptide responses to glucose, despite normal insulin sensitivity and exercise capacity. Thus, the low insulin response in low insulin responders reflects a true impairment of insulin release and not a compensatory decrease due to increased insulin sensitivity. The insulin response to glucose in endurance-trained subjects was also decreased, probably due to increased insulin sensitivity.


2019 ◽  
Vol 180 (5) ◽  
pp. 321-328 ◽  
Author(s):  
Hanne L Gulseth ◽  
Ingrid M F Gjelstad ◽  
Audrey C Tiereny ◽  
Danielle McCarthy ◽  
Julie A Lovegrove ◽  
...  

Objective Impaired insulin secretion and action contribute to the development of type 2 diabetes. Dietary fat modification may improve insulin sensitivity, whereas the effect on insulin secretion is unclear. We investigated the effect of dietary fat modification on insulin secretion in subjects with the metabolic syndrome. Design In a 12-week pan-European parallel, randomized controlled dietary intervention trial (LIPGENE), 486 subjects were assigned to four isoenergetic diets: high-fat diets rich in saturated fat (HSFA) or monounsaturated fat (HMUFA) or low-fat, high-complex carbohydrate diets with (LFHCC n-3) or without (LFHCC control) 1.2 g/day of n-3 PUFA supplementation. Insulin secretion was estimated as acute insulin response to glucose (AIRg) and disposition index (DI), modeled from an intravenous glucose tolerance test. Results There were no overall effect of the dietary intervention on AIRg and DI in the total cohort, in neither the high-fat nor LFHCC groups. We observed significant diet*fasting glucose category interactions for AIRg (P = 0.021) and DI (P = 0.001) in the high-fat groups. In subjects with normal fasting glucose and preserved first phase insulin secretion, the HMUFA diet increased, whereas the HSFA diet reduced AIRg (P = 0.015) and DI (P = 0.010). Conclusions The effects of dietary fat modification on insulin secretion were minor, and only evident in normoglycemic subjects. In this case, the HMUFA diet improved AIRg and DI, as compared to the HSFA diet.


2017 ◽  
Vol 88 (3-4) ◽  
pp. 265-273 ◽  
Author(s):  
Christiane S. Hampe ◽  
Michele L. Shaffer ◽  
Christian L. Roth

Background: Obesity is strongly associated with insulin resistance, hypertension, dyslipidemia, and therefore risk for metabolic syndrome (MetS), which is an increasing problem in youth. The potential role of elevated liver enzyme levels in this context needs to be further investigated. Methods: This paper provides a post hoc analysis of a cross-sectional study of 77 obese nondiabetic children (51% female; median age 11.7 years; BMI >97th percentile) enrolled at the University of Bonn, Bonn, Germany. Anthropometric parameters, lipid profiles, glycemic control, and liver enzyme levels were evaluated. Glucose and insulin levels were determined during an oral glucose tolerance test (OGTT). Gender- and age-specific cutoff values were used to assess MetS. Results: A high prevalence of hypertension (51%), dyslipidemia (52%), elevated liver enzyme levels (51%), and hyperglycemia (24%) was found. There was considerable overlap between the presence of different MetS risk factors in individuals, and 40% of the participants had ≥3 of a maximum of 5 MetS risk factors. Elevated liver enzyme levels were significantly associated with reduced insulin sensitivity, as the OGTT-insulin response was significantly higher in participants with elevated transaminases (p = 0.01). This association was independent of hyperglycemia and dyslipidemia (p = 0.03). Conclusions: We conclude that liver enzyme levels are related to insulin sensitivity in obese children and could therefore be an indirect indicator for MetS. Testing for disturbed glucose metabolism should be considered for obese children with elevated liver enzymes.


1974 ◽  
Vol 75 (1) ◽  
pp. 87-104 ◽  
Author(s):  
Karin Edström ◽  
Erol Cerasi ◽  
Rolf Luft

ABSTRACT A decreased insulin response to glucose administration has been suggested to be a prerequisite for the development of diabetes mellitus. Factors that increase the demand for insulin in the organism may precipitate diabetes in subjects with a low insulin response to a glucose infusion test (GIT). Since it is well-known that pregnancy is a diabetogenic factor, its effect on the carbohydrate metabolism of subjects with a low insulin response was studied. During pregnancy, the insulin response of the low responders was enhanced as in the controls, but at all stages the insulin response was significantly less than in the controls. None of the subjects developed glucose intolerance during pregnancy. The fasting blood glucose and plasma insulin levels and the k-value in intravenous glucose tolerance tests (IVGTT) were modified according to similar patterns in both groups. The sensitivity to endogenous insulin was significantly greater in the low insulin responders but was reduced to a greater extent than in the controls towards the end of pregnancy. In four of the 11 low insulin responders the initial insulin response to glucose in the last trimester was lower than in mid-pregnancy. This occurred only in one out of 14 high insulin responders. It is suggested that gestational diabetes occurs in those low insulin responders who demonstrate either a dramatic decrease in insulin sensitivity, or limitations in the enhancement of insulin release, or, more likely both conditions.


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