Abnormal oral glucose tolerance in genetically obese (fa/fa) rats

1985 ◽  
Vol 248 (5) ◽  
pp. E500-E506 ◽  
Author(s):  
E. Ionescu ◽  
J. F. Sauter ◽  
B. Jeanrenaud
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Oral Glucose ◽  
Base Line ◽  
Oral Glucose Tolerance ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Ingestion ◽  
Obese Rats

The effect of intravenous glucose or tolbutamide administration on plasma glucose and insulin levels was compared with that following spontaneous ingestion of glucose in freely moving 6- to 7-wk- and 13- to 14-wk-old lean and obese (fa/fa) rats. Irrespective of age, the obese rats had a normal blood glucose tolerance when glucose or tolbutamide load was given intravenously, whereas the glucose ingestion [oral glucose tolerance test (OGTT) caused a marked glucose intolerance that became more pronounced with the duration of the syndrome. This suggests that factors other than insulin resistance could play a role in the occurrence of abnormal OGTT in obese rats. When blood insulin levels were expressed as percent change over base line and when compared with age-matched normal rats, the 6- to 7-wk obese rats showed a normal and even higher beta-cell responsiveness to intravenous or oral glucose as well as to tolbutamide. In contrast, the 13- to 14-wk obese rats presented a decreased beta-cell responsiveness to all such stimuli. Thus the beta-cell function of obese rats worsens with time. Inasmuch as 13- to 14-wk-old obese fa/fa rats have insulin resistance, high basal glycemia, and abnormal oral glucose tolerance, they can be viewed as a potential model of type II diabetes.

scholarly journals Plasma calcitonin gene-related peptide is increased prior to obesity, and sensory nerve desensitization by capsaicin improves oral glucose tolerance in obese Zucker rats

2005 ◽  
Vol 153 (6) ◽  
pp. 963-969 ◽  
Author(s):  
Dorte X Gram ◽  
Anker J Hansen ◽  
Michael Wilken ◽  
Torben Elm ◽  
Ove Svendsen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Sensory Nerve ◽  
Zucker Rats ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Nerve Activity ◽  
Calcitonin Gene ◽  
Obese Rats ◽  
Obese Zucker Rats

Objective: It has earlier been demonstrated that capsaicin-induced desensitization improves insulin sensitivity in normal rats. However, whether increased capsaicin-sensitive nerve activity precedes the onset of insulin resistance in diet-induced obesity – and therefore might be involved in the pathophysiology – is not known. Further, it is of relevance to investigate whether capsaicin desensitization improves glycaemic control even in obese individuals and we therefore chose the obese Zucker rats to test this. Design and methods: Plasma levels of calcitonin gene-related peptide (CGRP; a marker of sensory nerve activity) was assessed in 8-week-old Zucker rats. To investigate whether capsaicin desensitization (100 mg/kg at 9 weeks of age) would also ameliorate glycaemia in this non-diabetic model, we assessed oral glucose tolerance at 7 weeks after capsaicin. Results: It was found that plasma CGRP levels were elevated in obese Zucker rats prior to the onset of obesity (16.1±3.4 pmol/l in pre-obese Zucker rats vs 6.9±1.1 pmol/l in lean littermates; P = 0.015) despite similar body weights. Furthermore, capsaicin desensitization reduced both fasting blood glucose (4.3±0.2 mmol/l vs 5.1±0.2 mmol/l in controls; P = 0.050) as well as the mean blood glucose level during an oral glucose tolerance test (OGTT) (6.8±0.3 mmol/l vs 8.6±0.5 mmol/l in control obese rats; P = 0.024) whereas the plasma insulin levels during the OGTT were unchanged. However this did not lead to an improvement in insulin resistance or to a reduction of tissue triglyceride accumulation in muscle or liver. Conclusion: We concluded that capsaicin-induced sensory nerve desensitization improves glucose tolerance in Zucker rats. Since, in this study, plasma CGRP levels, a marker of sensory nerve activity, were increased in the pre-obese rats, our data support the hypothesis that increased activity of sensory nerves precedes the development of obesity and insulin resistance in Zucker rats.

Oral Glucose Tolerance Test with Insulin Assay and the evaluation of Insulin Resistance and Impaired Beta-cell function in primary prevention for Type 2 Diabetes

2020 ◽  
pp. 1-7
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Glucose Tolerance Test ◽  
Cell Function ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Background: Insulin resistance and impaired beta-cell function are associated with type 2 diabetes mellitus (T2DM). Many insulin resistance and beta-cell function indices have been developed using the data from an oral glucose tolerance test (OGTT) with insulin assay. However, insulin assays are not widely used along with the OGTT in primary prevention outpatient clinics. We aimed to evaluate the association of having impaired fasting glucose (IFG), impaired glucose tolerance (IGT), isolated or combined, with insulin resistance and impaired beta-cell function in subjects at risk for T2DM. Methods: This is a cross-sectional study that included 376 subjects who underwent an OGTT who had at least two risk factors for T2DM without any chronic disease. Results: Participants were 51.6±8.2 years old, 71.8% were women, had a mean body mass index (BMI) of 30.1±6.5 kg/m2, 42.4% had obesity and 26.7% hypertension. A HOMA-IR ≥2.5 was independently associated with male sex, BMI>25kg/m2, and with isolatedIFG, isolated-IGT, or combined (p<0.05 for all). On the other hand, only overweight, but not obesity, was independently associated with impaired beta-cell function (disposition index <1.24). Additionally, combined IFG and IGT had 29.7 higher odds to have impaired beta-cell function compared with those that had a normal OGTT. Conclusions: IFG alone, IGT alone, or the presence of both, are associated with higher odds to have insulin resistance and impaired beta-cell function in asymptomatic subjects at risk for T2DM without any chronic disease. Further studies are needed to evaluate this associations with the risk to develop T2DM, cardiovascular events and mortality.

scholarly journals QOL-43. ENDOCRINE AND METABOLIC CHANGES IN CHILDREN TREATED FOR MEDULLOBLASTOMA

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii439-iii439
Author(s):  
Alexey Kalinin ◽  
Natalia Strebkova ◽  
Olga Zheludkova
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Impaired Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Hormone Deficiency ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

Abstract We examined 63 patients (40 males/23 females) after complex treatment of medulloblastoma. Patients had a median age (range) of 11.3 (5.5 ÷ 17.9) years. The median time after the end of treatment was 3.7 (1.5 ÷ 11.6) years. Endocrine disorders were detected with the following frequency: growth hormone deficiency - 98.41% (62 of 63 patients), thyroid hormone deficiency – 69.8% (44/63), adrenal hormone deficiency - 17.4% (11/63). Three cases (4.7%) of premature sexual development were also detected. Lipids levels, beta-cell function and insulin resistance (IR) during 2-h oral glucose tolerance test were evaluated. A mono frequent bioelectrical impedanciometer was used to measure body composition. Overweight (SDS BMI&gt; 1) was observed only in 16 patients (3 girls and 13 boys), obesity (SDS BMI&gt; 2) in 1 boy. Dyslipidemia was found in 34 patients (54%). All patients underwent oral glucose tolerance test. Insulin resistance (ISI Matsuda &lt;2.5 and/or HOMA-IR&gt; 3.2) was detected in 7 patients (11/1%), impaired glucose tolerance (120 min glucose ≥7.8 mmol / l) was observed in 2 patients with IR and in 2 patients without IR. At the same time, IR and impaired glucose tolerance were encountered in only 5 children with overweight and no one with obesity. All patients with impaired glucose tolerance had normal values of fasting glucose (4.3 ÷ 5.04 mmol / l) and HbA1c (4.8 ÷ 5.8%). A bioelectrical impedanciometer was used to measure body composition in 49 cases, the percentage of adipose tissue was increased in 14 patients (28%) with normal BMI.

The Effect of D-Norgestrel, 30 Micrograms, on The Oral Glucose Tolerance Test, Including Insulin Levels, in Thai Women

1976 ◽  
Vol 27 (5) ◽  
pp. 523-527 ◽  
Author(s):  
Suparporn Vongvinyoutragan ◽  
Orapan Matangkasombut ◽  
Vichai Poshyachinda ◽  
Nikorn Dusitsin ◽  
Monthira Tankeyoon ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Thai Women ◽  
Insulin Levels

scholarly journals The Role of Insulin-Like Growth Factor (IGF) Binding Protein-2 in the Insulin-Mediated Decrease in IGF-I Bioactivity

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 5192-5192
Author(s):  
Ayman M. Arafat ◽  
Martin O. Weickert ◽  
Jan Frystyk ◽  
Joachim Spranger ◽  
Christof Schöfl ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Igf System ◽  
Igf I ◽  
Igf Binding

ABSTRACT Context: Insulin interacts with the GH-IGF system by a reciprocal regulation of IGF-binding proteins (IGFBP) and GH, which in turn regulate insulin sensitivity via bioactive IGF-I. This network is linked to metabolic syndrome and cardiovascular diseases. Objective: We evaluated the effect of glucose and insulin on IGFBP-1-4, particularly IGFBP-2, in the regulation of bioactive IGF-I and its relation to insulin resistance. Setting: The study was conducted at an endocrinology center. Research Design and Methods: Twenty-four healthy subjects (12 men; aged 21–72 yr; body mass index 25.9 ± 0.9 kg/m2) and 19 subjects with impaired glucose tolerance (IGT; eight men; aged 26–71 yr; body mass index 28.9 ± 1.2 kg/m2 ) were prospectively studied using oral glucose tolerance test and hyperinsulinemic euglycemic clamp. Results: During the clamp, insulin decreased IGF-I bioactivity in both IGT subjects and controls (−16.2 ± 2.8 and −13.9 ± 3.3%, respectively; P &lt; 0.01). In addition, insulin increased IGFBP-2 and GH and decreased IGFBP-1 and -4 but did not alter total IGF-I, IGF-II, or IGFBP-3 levels. During the oral glucose tolerance test, GH and IGFBP-1 were markedly suppressed. Subjects with IGT showed more pronounced insulin resistance and lower GH, IGFBP-1, and IGFBP-2 levels (P &lt; 0.05). In multiple regression analysis, IGFBP-2 was an independent predictor of insulin sensitivity (β = 0.36, P &lt; 0.05) and IGF-I bioactivity (β = −0.5, P &lt; 0.05). Conclusions: Our data indicate that insulin acutely decreases IGF-I bioactivity through differential modulation of IGFBPs. Furthermore, IGFBP-2 plays a central role in the insulin-IGF system cross talk and is closely linked to insulin resistance, thereby providing a further explanation for its association with the metabolic syndrome.

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