scholarly journals Metabolic syndrome in Iraqi female patients with major β-thalassemia

2017 ◽  
Vol 27 (4) ◽  
Author(s):  
Shaemaa Hadi Abdulsada ◽  
Aliaa Hashim Farag ◽  
Hassanain Kamil ◽  
Salma Abdul-Rudha ◽  
Ali Abdulrassol Hussein
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
B Cell ◽  
Cell Function ◽  
Atherogenic Index ◽  
Control Group ◽  
Female Patients ◽  
B Cell Function ◽  
Increased Risk

Patients with β-thalassemia may have an increased risk for diabetes mellitus and cardiovascular diseases due to high level of iron which may lead to insulin resistanceand metabolic syndrome. So this study aimed to evaluate the levels of lipids profile in Iraqi female patients with β-thalassemia. Forty twofemale (age 15-30) years were enrolled in this study. Blood was collected and the sera were separated from (22) female patients with β-thalassemia who were attended the Ibn-Al-Baladi hospital from September 2012 to January 2013 and (20) healthy subject as a control group. Body mass index (BMI), lipid profile, FSG, insulin, insulin resistance, insulin sensitivity, B-cell function, iron, atherogenic index of serum were estimated.The results showed the presence of a significant increase in serum iron and significant decrease in insulin, B-cell function, LDL, VLDL, and TC in serum of patients with β-thalassemia when compared with control group. BMI also showed a significant decrease in patients when compared with the controls. Serum Insulin resistance, insulin sensitivity, HDL, TG, AIS, and FSG showed no-significant differences in patients with β-thalassemia when compared with control group. We concluded there was no metabolic syndrome in female patients with β-thalassemia.

Human aging is associated with parallel reductions in insulin and amylin release

1998 ◽  
Vol 275 (5) ◽  
pp. E785-E791 ◽  
Author(s):  
Cynthia J. Dechenes ◽  
C. Bruce Verchere ◽  
Sofianos Andrikopoulos ◽  
Steven E. Kahn
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
B Cell ◽  
Insulin Release ◽  
Cell Function ◽  
B Cell Function ◽  
Increased Risk ◽  
Older Subjects

Aging is associated with an increased risk of type 2 diabetes. To determine whether the insulin resistance of aging is associated with an increase in amylin release or whether amylin release parallels the reduction in insulin release, we studied 10 older (72 ± 2 yr) and 9 young (25 ± 1 yr) subjects. Insulin sensitivity was quantified as the insulin sensitivity index (SI) and B cell function as the acute insulin and amylin responses to iv glucose (AIRg and AARg, respectively) and iv arginine at a glucose level of >25 mM (AIRmax and AARmax). To account for the effect of SIto modulate B cell function, we calculated SI× B cell function. Older subjects were insulin resistant (SI: 4.6 ± 0.8 vs. 8.6 ± 1.4 × 10−5min−1/pM, P < 0.05). Acute responses to glucose [AIRg (older vs. young): 420 ± 106 vs. 537 ± 87 pM; AARg: 6.5 ± 1.7 vs. 9.0 ± 1.5 pM] and arginine (AIRmax: 1,096 ± 203 vs. 1,572 ± 307 pM; AARmax: 14.0 ± 3.5 vs. 16.5 ± 2.4 pM) did not differ despite the difference in SI. When adjusted for SI, insulin responses were reduced in older subjects (SI× AIRg: 1.54 ± 0.29 vs. 4.10 ± 0.63 × 10−2min−1, P = 0.001; SI× AIRmax: 4.03 ± 0.52 vs. 12.7 ± 2.9 × 10−2min−1, P < 0.01), as was amylin release (SI× AARg: 2.46 ± 0.59 vs. 6.85 ± 0.95 × 10−4min−1, P < 0.001; SI× AARmax: 4.71 ± 0.52 vs. 13.5 ± 2.2 × 10−4min−1, P < 0.001). Amylin and insulin release was proportionate, with a molar ratio of 1.5% in older and 1.4% in young subjects. Thus aging is associated with parallel impairments in the adaptation of insulin and amylin release to insulin resistance. It is unlikely that an alteration in amylin release contributes to the increased risk of type 2 diabetes.

Dexamethasone-induced insulin resistance enhances B cell responsiveness to glucose level in normal men

1984 ◽  
Vol 247 (5) ◽  
pp. E592-E596 ◽  
Author(s):  
J. C. Beard ◽  
J. B. Halter ◽  
J. D. Best ◽  
M. A. Pfeifer ◽  
D. Porte
Keyword(s):  
Insulin Resistance ◽  
B Cell ◽  
Glucose Level ◽  
Cell Function ◽  
Insulin Level ◽  
Glucose Levels ◽  
B Cell Function ◽  
Normal Men ◽  
Insulin Responses ◽  
Effect Of Glucose

To determine whether islet adaptation during insulin resistance involves increased responsiveness to the level of plasma glucose, insulin resistance was induced in nine normal men by giving dexamethasone (Dex) (3 mg twice daily for 2 days). Plasma insulin and acute insulin responses (AIR) to isoproterenol were measured at three different glucose levels under control and Dex conditions. During Dex there were elevations above control levels of basal glucose (104 +/- 2 vs. 94 +/- 3 mg/dl) and insulin (21 +/- 3 vs. 13 +/- 2 microU/ml, both P less than 0.03). When glucose levels were raised stepwise by matching amounts using glucose clamps, AIR to isoproterenol rose as a linear function of glucose level under both conditions but rose more steeply during Dex. That is, the potentiating effect of glucose (delta AIR/delta glucose) was greater during Dex: 1.3 +/- 0.2 vs. 0.8 +/- 0.2 (P less than 0.01). Similarly, matched increments in glucose level produced greater increments in prestimulus insulin level during Dex (P less than 0.03). We conclude that 48 h of Dex raises the "gain" of the potentiating effect of glucose. Because the direct effect of glucocorticoids on B cell function has been reported to be inhibitory, the observed stimulation is likely to be a result of the insulin resistance caused by Dex.

scholarly journals Biomarkers of subclinical inflammation and increases in glycaemia, insulin resistance and beta-cell function in non-diabetic individuals: the Whitehall II study

2016 ◽  
Vol 175 (5) ◽  
pp. 367-377 ◽  
Author(s):  
Christian Herder ◽  
Kristine Færch ◽  
Maren Carstensen-Kirberg ◽  
Gordon D Lowe ◽  
Rita Haapakoski ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fasting Insulin ◽  
Subclinical Inflammation ◽  
Increased Risk

Objective Higher systemic levels of pro-inflammatory biomarkers and low adiponectin are associated with increased risk of type 2 diabetes, but their associations with changes in glycaemic deterioration before onset of diabetes are poorly understood. We aimed to study whether inflammation-related biomarkers are associated with 5-year changes in glucose and insulin, HbA1c, insulin sensitivity and beta-cell function before the diagnosis of type 2 diabetes and whether these associations may be bidirectional. Design and methods We used multiple repeat measures (17 891 person-examinations from 7683 non-diabetic participants) from the Whitehall II study to assess whether circulating high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), IL1 receptor antagonist (IL1Ra) and adiponectin are associated with subsequent changes in glycaemia, insulin, insulin resistance and beta-cell function (based on oral glucose tolerance tests). We examined bidirectionality by testing if parameters of glucose metabolism at baseline are associated with changes in inflammation-related biomarkers. Results Higher hsCRP and IL6 were associated with increases in fasting insulin, insulin resistance and, for IL6, with beta-cell function after adjustment for confounders. Higher adiponectin was associated with decreases in fasting glucose, HbA1c, fasting insulin, insulin resistance and beta-cell function. The reverse approach showed that 2-h glucose and insulin sensitivity were associated with changes in IL1Ra. Fasting insulin and insulin resistance showed inverse associations with changes in adiponectin. Conclusions Subclinical inflammation is associated with development of increased glycaemia, insulin resistance and beta-cell function in non-diabetic individuals. These findings are consistent with the hypothesis that inflammation-related processes may increase insulin resistance and lead to a compensatory upregulation of beta-cell function.

scholarly journals Quantitative Linkage Analysis for Pancreatic B-cell Function and Insulin Resistance in a Large Twin Cohort

Diabetes ◽  
2008 ◽  
Vol 57 (4) ◽  
pp. 1120-1124 ◽  
Author(s):  
M. Falchi ◽  
S. G. Wilson ◽  
D. Paximadas ◽  
R. Swaminathan ◽  
T. D. Spector
Keyword(s):  
Insulin Resistance ◽  
Linkage Analysis ◽  
B Cell ◽  
Cell Function ◽  
Pancreatic B Cell ◽  
B Cell Function

Prospective Evaluation of the Effect of Initiating Indinavir-Based Therapy on Insulin Sensitivity and B-Cell Function in HIV-Infected Patients

2001 ◽  
Vol 27 (2) ◽  
pp. 130-134 ◽  
Author(s):  
Michael P. Dubé ◽  
Hannah Edmondson-Melançon ◽  
Dajun Qian ◽  
Rubina Aqeel ◽  
Debra Johnson ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
B Cell ◽  
Cell Function ◽  
Prospective Evaluation ◽  
B Cell Function

scholarly journals Effect of Oral Calcium Supplementation on Insulin Sensitivity in Patients With Metabolic Syndrome

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A468-A468
Author(s):  
Ye Myint ◽  
Mya Thanda Sein ◽  
Khin Saw Than ◽  
Ko Ko ◽  
Tint Swe Latt
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Calcium Supplementation ◽  
Control Group ◽  
Oral Calcium ◽  
Supplement Group ◽  
Serum Pth ◽  
Elemental Calcium ◽  
Pth Level

Abstract Background: Evidence from epidemiological research suggests that dietary calcium may protect against metabolic abnormality in populations at high risk. Observational studies show the relationship between dietary calcium intake and metabolic syndrome. However evidence for beneficial effect of elemental calcium supplementation on metabolic syndrome is limited. Aims: Present studydetermined whether oral calcium supplementation reduced insulin resistance in patients with metabolic syndrome or not. Methods; Hundred patients who have metabolic syndrome without diabetes mellitus, parathyroid disease, chronic renal failure, pregnancy and lactationwere randomly allocated to the group receiving 1500 mg/ day of elemental calcium as calcium carbonate for 8 weeks and the control group. The primary outcome was change in insulin resistance as measured by homeostasis model assessment of insulin resistance (HOMA-IR). Other outcomes were changes of serum free ionized calcium (FiCa) level with accompanying serum parathyroid hormone (PTH) level. Fasting serum glucose was measured by glucose oxidase method. Serum insulin and PTH level were measured by enzyme linked immunoassay. Total serum ionized calcium was analyzed by Atomic Absorption Spectrophotometry. Serum FiCa(mg/dl) level was calculated by using following formula = [6Ca-(K/3)]/(K+6). Results: Mean age of participants was 47.38±13.2 years in calcium supplement group (n = 50) and 49.46±12.9 years in control group (n=50). Mean body mass index was not significant different between two groups (30.91 ±4.23 vs 30.37 ± 4.62 kg/m2). More female were involved in both group, 72% vs 62% respectively. Baseline biochemical parameters of the participants between two groups were not significantly different. After 8 week intervention period, mean serum FiCa increased significantly from 2.64±1.19 mg/dl to 5.82± 5.59 mg/dl, p&lt;0.0001, serum PTH decreased significantly from 57.88 ±17.05 pg/ml to 35.7±23.12 pg/ml, p&lt;0.0001, HOMA-IR decreased significantly from 5.14 ± 3.71 to 2.94±1.51, p&lt;0.0001. None of these parameters were significantly affected in control group. By comparing biochemical changes of calcium supplement group to control group, Mean (SEM) of paired difference changes were observed in serum FiCa level [3.18(0.81) vs 0.81(0.25)mg/dl, p&lt;0.05], serum PTH level [22.18(3.24) vs 3.58(1.99)pg/ml, p&lt;0.0001] and HOMA-IR [2.19(0.45) vs 0.43(0.21), p&lt;0.05]. It indicated that elemental calcium supplementation not only reduced insulin resistance but also decompensated the higher level of PTH to normal range by replenishing FiCa significantly. Conclusion: Eight-week oral elemental calcium supplementation of 1500mg/day showed beneficial effect on insulin sensitivity in patients with metabolic syndrome.

scholarly journals Effect of nicotinic acid-induced insulin resistance on pancreatic B cell function in normal and streptozocin-treated baboons.

1991 ◽  
Vol 87 (4) ◽  
pp. 1395-1401 ◽  
Author(s):  
D K McCulloch ◽  
S E Kahn ◽  
M W Schwartz ◽  
D J Koerker ◽  
J P Palmer
Keyword(s):  
Insulin Resistance ◽  
Nicotinic Acid ◽  
B Cell ◽  
Cell Function ◽  
Pancreatic B Cell ◽  
B Cell Function

scholarly journals Surrogate Measures of Insulin Resistance in Middle-aged Non-diabetic Subjects

2013 ◽  
Vol 59 (6) ◽  
pp. 279-284
Author(s):  
Csép Katalin
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Fasting Insulin ◽  
Middle Aged ◽  
Insulin Levels ◽  
The Metabolic Syndrome ◽  
Sensitivity Indices ◽  
Increased Risk ◽  
Surrogate Measures

Abstract Objective: Insulin resistance has been shown to be a risk factor for type 2 diabetes and cardiovascular disease. The assessment of insulin sensitivity in the clinical practice, however, faces several difficulties. The study proposes to analyze surrogate measures of insulin resistance based on fasting insulin levels in central Romania, and check whether the diagnosis of the metabolic syndrome is an adequate strategy to identify middle-aged persons with reduced insulin sensitivity. Methods: Anthropometric measurements, metabolic profile, and surrogates measures of insulin sensitivity (GIR, HOMA, QUICKI, FIRI, Belfiore, Bennett, Raynaud, McAuley index) based on fasting insulin levels were assessed in 233 non-diabetic middle aged subjects. Results: Cutoff values, determined as the lowest quartile of insulin sensitivity for fasting insulin, HOMA, IRI (1/QUICKI), FIRI and Belfiore's, Bennett's, Raynaud's and McAuley's insulin sensitivity indices were 10.49 mU/L, 2.1, 3.01, 2.32, and 0.03, 1.34, 3.81, 6.29, 5.82. Components of the metabolic syndrome showed moderate but significant correlations with the surrogate measures of insulin resistance (r = 0.22-0.56, p <0.05). HOMA-IR and McAuley indices were the best predictors of clustered cardiometabolic risk factors (AUC - 0.83, 0.81 and 0.82). The metabolic syndrome diagnosis performed well in identifying patients with reduced insulin sensitivity (McAuley 2: sensitivity - 0.78, specificity - 0.84). Conclusion: Fasting insulin derived insulin sensitivity indices may help the recognittion of insulin resistant states predicting cardiometabolic disorders. Actively looking for insulin resistance by these simple indices, or by diagnosing the metabolic syndrome, those at increased risk can be recognized

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