scholarly journals Effect of Chronic Hyperglycemia on Glucose Metabolism in Subjects With Normal Glucose Tolerance

Diabetes ◽  
2018 ◽  
Vol 67 (12) ◽  
pp. 2507-2517 ◽  
Author(s):  
Chris Shannon ◽  
Aurora Merovci ◽  
Juan Xiong ◽  
Devjit Tripathy ◽  
Felipe Lorenzo ◽  
...  
2018 ◽  
Vol 50 (05) ◽  
pp. 408-413 ◽  
Author(s):  
Sema Dogansen ◽  
Gulsah Yalin ◽  
Seher Tanrikulu ◽  
Sema Yarman

AbstractIn this study, we aimed to evaluate the presence of glucose metabolism abnormalities and their impact on IGF-1 levels in patients with acromegaly. Ninety-three patients with acromegaly (n=93; 52 males/41 females) were included in this study. Patients were separated into three groups such as; normal glucose tolerance (n=23, 25%), prediabetes (n=38, 41%), and diabetes mellitus (n=32, 34%). Insulin resistance was calculated with homeostasis model assessment (HOMA). HOMA-IR > 2.5 or ≤2.5 were defined as insulin resistant or noninsulin resistant groups, respectively. Groups were compared in terms of factors that may be associated with glucose metabolism abnormalities. IGF-1% ULN (upper limit of normal)/GH ratios were used to evaluate the impact of glucose metabolism abnormalities on IGF-1 levels. Patients with diabetes mellitus were significantly older with an increased frequency of hypertension (p<0.001, p=0.01, respectively). IGF-1% ULN/GH ratio was significantly lower in prediabetes group than in normal glucose tolerance group (p=0.04). Similarly IGF-1% ULN/GH ratio was significantly lower in insulin resistant group than in noninsulin resistant group (p=0.04). Baseline and suppressed GH levels were significantly higher in insulin resistant group than in noninsulin resistant group (p=0.024, p<0.001, respectively). IGF-1% ULN/GH ratio is a useful marker indicating glucose metabolism disorders and IGF-1 levels might be inappropriately lower in acromegalic patients with insulin resistance or prediabetes. We suggest that IGF-1 levels should be re-evaluated after the improvement of insulin resistance or glycemic regulation for the successful management of patients with acromegaly.


1973 ◽  
Vol 72 (4) ◽  
pp. 727-736 ◽  
Author(s):  
G. Frenkel ◽  
P. F. Kraicer

ABSTRACT The responses of sand rats and rats to disturbances of their glucose metabolism were tested. Despite their latent diabetes, the sand rats had normal glucose tolerance. They did not show signs of starvation diabetes. Their responses to exogenous and endogenous (tolbutamide-stimulated) insulin were greater than those of laboratory rats. Acute insulin deficiency was induced with mannoheptulose. Both species responded with similar levels of hyperglycaemia, although the response of the sand rat was somewhat slower. The only test used here which indicated a metabolic difference related to latent diabetes, was the induction of transient intolerance to glucose by cortisol. These results suggest that latent diabetes is not associated with any marked metabolic abnormality in the unchallenged sand rat, despite the ease of induction of diabetes by caloric loading.


2008 ◽  
Vol 93 (7) ◽  
pp. 2786-2789 ◽  
Author(s):  
Irina Kowalska ◽  
Marek Strączkowski ◽  
Agnieszka Adamska ◽  
Agnieszka Nikolajuk ◽  
Monika Karczewska-Kupczewska ◽  
...  

Abstract Context: Retinol-binding protein (RBP) 4 is secreted by adipose tissue and is postulated to be a determinant of insulin sensitivity. The mechanisms of RBP4 insulin desensitizing action remain unclear. Objective: The aim of the present study was to estimate the relationships between serum RBP4 concentration with insulin sensitivity and oxidative and nonoxidative glucose metabolism in lean and obese women. Design and Participants: The study group consisted of 67 women with normal glucose tolerance, 27 lean and 40 overweight or obese. Insulin sensitivity was estimated with the euglycemic hyperinsulinemic clamp. Glucose and lipid oxidation was measured with indirect calorimetry in the basal state and during the last 30 min of the clamp. Nonoxidative glucose metabolism was calculated in insulin-stimulated conditions by subtracting glucose oxidation from total glucose metabolism. Results: There was no difference in serum RBP4 concentration between lean and obese women. Serum RBP4 was inversely related to insulin sensitivity and nonoxidative glucose metabolism in the entire group (r = −0.36, P =0.003 in both cases) and within the subgroups of lean (r = −0.41, P =0.034 and r = −0.41, P =0.031) and obese women (r = −0.41, P =0.009 and r = −0.40, P =0.01, respectively). These relationships were independent of potential confounding factors. RBP4 levels were not associated with oxidative metabolism of glucose or lipid. Conclusions: Our data indicate that serum RBP4 is related to decreased insulin sensitivity, mostly through its association with nonoxidative glucose metabolism.


2021 ◽  
pp. 193229682110269
Author(s):  
Manuel M. Eichenlaub ◽  
Natasha A. Khovanova ◽  
Mary C. Gannon ◽  
Frank Q. Nuttall ◽  
John G. Hattersley

Background: Current mathematical models of postprandial glucose metabolism in people with normal and impaired glucose tolerance rely on insulin measurements and are therefore not applicable in clinical practice. This research aims to develop a model that only requires glucose data for parameter estimation while also providing useful information on insulin sensitivity, insulin dynamics and the meal-related glucose appearance (GA). Methods: The proposed glucose-only model (GOM) is based on the oral minimal model (OMM) of glucose dynamics and substitutes the insulin dynamics with a novel function dependant on glucose levels and GA. A Bayesian method and glucose data from 22 subjects with normal glucose tolerance are utilised for parameter estimation. To validate the results of the GOM, a comparison to the results of the OMM, obtained by using glucose and insulin data from the same subjects is carried out. Results: The proposed GOM describes the glucose dynamics with comparable precision to the OMM with an RMSE of 5.1 ± 2.3 mg/dL and 5.3 ± 2.4 mg/dL, respectively and contains a parameter that is significantly correlated to the insulin sensitivity estimated by the OMM ( r = 0.7) Furthermore, the dynamic properties of the time profiles of GA and insulin dynamics inferred by the GOM show high similarity to the corresponding results of the OMM. Conclusions: The proposed GOM can be used to extract useful physiological information on glucose metabolism in subjects with normal glucose tolerance. The model can be further developed for clinical applications to patients with impaired glucose tolerance under the use of continuous glucose monitoring data.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2126
Author(s):  
Masanobu Hibi ◽  
Sayaka Hari ◽  
Tohru Yamaguchi ◽  
Yuki Mitsui ◽  
Sumio Kondo ◽  
...  

Effects of meal frequency on blood glucose levels and glucose metabolism were evaluated over 3 days in adult males with normal glucose tolerance (NGT, n = 9) or impaired fasting glucose (IFG, n = 9) in a randomized, crossover comparison study. Subjects were provided with an isocaloric diet 3 times daily (3M) or 9 times daily (9M). Blood glucose was monitored on Day 3 using a continuous glucose monitoring system, and subjects underwent a 75-g oral glucose tolerance test (OGTT) on Day 4. Daytime maximum blood glucose, glucose range, duration of glucose ≥180 mg/dL, and nighttime maximum glucose were significantly lower in the NGT/9M condition than in the NGT/3M condition. Similar findings were observed in the IFG subjects, with a lower daytime and nighttime maximum glucose and glucose range, and a significantly higher daytime minimum glucose in the 9M condition than in the 3M condition. The OGTT results did not differ significantly between NGT/3M and NGT/9M conditions. In contrast, the incremental area under the curve tended to be lower and the maximum plasma glucose concentration was significantly lower in the IFG/9M condition than in the IFG/3M condition. In IFG subjects, the 9M condition significantly improved glucose metabolism compared with the 3M condition. Higher meal frequency may increase glucagon-like peptide 1 secretion and improve insulin secretion.


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