scholarly journals The Fasting Serum Insulin and Glucose Levels and the Estimated Insulin Resistance in Clinical and Subclinical Hyperthyroid Patients from Saudi Arabia

2017 ◽  
Vol 05 (03) ◽  
Author(s):  
Abdel Gayoum AA
2019 ◽  
Vol 26 (11) ◽  
pp. 1810-1814
Author(s):  
Sabiha Iqbal ◽  
Syed Imran Ali Shah ◽  
Mirza Zeeshan Sikandar

Obesity is a common clinical disorder featuring excessive buildup of body fat. The bioavailability of vitamin D in obese subjects is lowered because of its sequestration in the superfluous fat tissue. Hypovitaminosis D itself is associated with glucose intolerance, insulin resistance, dyslipidemia and hypertension, which are also linked to obesity. Objectives: To compare and correlate serum vitamin D and insulin resistance in controls and overweight / obese males. Study Design: Cross Sectional, Comparative Study. Setting: The study was conducted in the Department of Physiology, Post – Graduate Medical Institute (PGMI) in collaboration with Lahore General Hospital and Central Park Medical College. Period: From 7th June 2018 to 10th Oct 2018. Material and Methods: Eighty male subjects (age range 35-50 years) included in this cross-sectional comparative study were divided into two groups on the basis of BMI; Group I: non-obese (control) BMI < 25 Kg/m2 (n=40) and Group II: overweight / obese males with BMI ˃25 Kg/m2 (n=40). Fasting serum vitamin D (25 hydroxy cholecalciferol; 25-OH D, serum insulin and blood glucose levels were measured. Insulin resistance (IR) was estimated from fasting serum glucose levels taken in mmol/l and the fasting serum insulin taken in µIU/ml by using Homeostasis Model Assessment-estimated Insulin Resistance (HOMA-IR index). Results: Group II had lower serum 25-OH vitamin D levels and higher HOMA-IR index than control group. Significant negative correlation was present between serum vitamin D and HOMA-IR. Conclusion: Vitamin D deficiency may promote insulin resistance in overweight or obese individuals.


1998 ◽  
Vol 275 (3) ◽  
pp. R788-R792 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Michael R. Ujhelyi ◽  
Margarethe E. Hoenig ◽  
Allison Winecoff Miller

The insulin-resistant (IR) syndrome may be an impetus for the development of hypertension (HTN). Unfortunately, the mechanism by which this could occur is unclear. Our laboratory and others have described impaired endothelium-mediated relaxation in IR, mildly hypertensive rats. The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. Sprague-Dawley rats were randomized to receive a fructose-rich diet for 3, 7, 10, 14, 18, or 28 days or were placed in a control group. The control group received rat chow. After diet treatment, animals were instrumented with arterial cannulas, and while awake and unrestrained, their blood pressure (BP) was measured. Subsequently, endothelium-mediated relaxation to acetylcholine was determined (in vitro) by measuring intraluminal diameter of phenylephrine-preconstricted mesenteric arteries (∼250 μM). Serum insulin levels were significantly elevated in all groups receiving fructose feeding compared with control, whereas there were no differences in serum glucose levels between groups. Impairment of endothelium-mediated relaxation starts by day 14 [mean percent maximal relaxation (Emax): 69 ± 10% of baseline] and becomes significant by day 18 (Emax: 52 ± 11% of baseline; P < 0.01). However, the mean BP (mmHg) does not become significantly elevated until day 28 [BP: 132 ± 1 ( day 28) vs. 116 ± 3 (control); P < 0.05]. These findings demonstrate that both IR and endothelial dysfunction occur before HTN in this model and suggest that endothelial dysfunction may be a mechanism linking insulin resistance and essential HTN.


2015 ◽  
Vol 7 (2) ◽  
pp. 41-46
Author(s):  
S Sultana ◽  
Z Zeba ◽  
A Hossain ◽  
A Khaleque ◽  
R Zinnat ◽  
...  

Hyperproinsulinemia is commonly present in subjects with impaired glucose tolerance. The present study was undertaken to investigate the proinsulin level in Bangladeshi IGT subjects and to explore its association with insulin resistance. This observational study was conducted under a case-control design with IGT subjects (n=50) and controls (n=44). IGT was diagnosed following the WHO Study Group Criteria. Serum glucose was measured by glucose-oxidase method, serum lipid profile by enzymatic method and serum insulin and serum proinsulin were measured by ELISA method. Insulin secretory capacity (HOMA%B) and insulin sensitivity (HOMA%S) were calculated from fasting serum glucose and fasting serum insulin by homeostasis model assessment. The study subjects were age- and BMI- matched. Mean (±SD) age (yrs) of the control and IGT subjects were 40±6 and 40±5 respectively (p=0.853). Mean (±SD) BMI of the control and IGT subjects were 23±3 and 22±2 respectively (p=0.123). Fasting glucose was not significantly higher in IGT subjects, but serum glucose 2 hours after 75 gm glucose load was significantly higher in IGT subjects. Median (Range) value of fasting serum glucose (mmol/l) of control and IGT subjects were 5.3 (3.8-6) and 5.2 (4-12) respectively; (p=0.297). Median (Range) value of serum glucose (mmol/l) 2 hours after 75 gm glucose load of control and IGT subjects were 6.1 (3-7.8) and 7.9 (5- 21) respectively; (p=0.001). Fasting TG was significantly higher in IGT subjects and LDL-c was significantly lower in IGT subjects. Serum Total cholesterol and HDL-c were not significantly different between the IGT and control subjects. Median (Range) value of fasting serum TG (mg/dl) of control and IGT subjects were 119 (51-474) and 178 (82-540) respectively; (p=0.001). Median (Range) value of fasting serum T chol (mg/dl) of control and IGT subjects were 180 (65-272) and 186 (140-400) respectively; (p=0.191). Median (Range) value of fasting serum HDL-C (mg/dl) of control and IGT subjects were 29 (19-45) and 31 (15-78) respectively; (p=0.914). Median (Range) value of fasting serum LDL-C (mg/dl) of control and IGT subjects were 117(29-201) and 111(41- 320) respectively; (p=0.001). Fasting serum proinsulin was significantly higher in IGT subjects. Median (Range) value of fasting serum proinsulin (pmol/l) of control and IGT subjects were 9.2(1.8-156) and 17(3-51) respectively; (p=0.001). Insulin secretory capacity (HOMA%B) was higher but insulin sensitivity (HOMA%S) was significantly lower in case of IGT subjects. Median (Range) value of HOMA%B of control and IGT subjects were 97(46-498) and 164(17-300) respectively; (p=0.001). Median (Range) value of HOMA%S of control and IGT subjects were 68(19-270) and 39(15-110) respectively (p=0.001). In multiple regression analysis a significant negative association was found between fasting proinsulin and insulin sensitivity (p=0.037). The data led to the following conclusions: a) Insulin resistance is the predominant defect in Bangladeshi IGT subjects. b) Basal proinsulin level is significantly increased in IGT subjects. c) Insulin resistance is negatively associated with serum proinsulin in IGT subjects. DOI: http://dx.doi.org/10.3329/bjmb.v7i2.22411 Bangladesh J Med Biochem 2014; 7(2): 41-46


2017 ◽  
Vol 56 (5) ◽  
pp. 291
Author(s):  
Indra Ihsan ◽  
Eka Agustia Rini ◽  
Rismawati Yaswir

Background Adipose tissue is not merely a site for energy storage, but is also the largest endocrine organ, secreting various adipocytokines. Plasma visfatin, an adipocytokine predominantly secreted from visceral adipose tissue, has insulin-mimetic effects, and has been closely linked to insulin resistance.Objective To compare plasma visfatin levels between obese and non-obese adolescents, as well as between obese adolecents with and without insulin resistance.Methods This cross-sectional study was conducted in students who attended three senior high schools in Padang. Subjects comprised 28 obese and 28 non-obese adolescents. The age of the subjects ranged from 14-18 years. Obesity criteria were based on body mass index (BMI) measurements. Fasting serum glucose level was measured by glucose hexokinase photometry and serum insulin was measured by chemiluminesence immunoassay. Plasma visfatin was measured by enzyme-linked immunosorbent assay (ELISA). The insulin resistance index was estimated from fasting serum insulin and glucose levels using the homeostatic model assessment for insulin resistance (HOMA-IR). Differences in the variables were tested using independent T-test and Mann-Whitney test, depending on the distribution of the variables.Results The mean plasma visfatin level was significantly higher in the obese than in the control group [2.55 (SD 1.54) vs. 1.61 (SD 0.64) ng/mL, respectively; (P=0.005)]. The insulin resistant group had significantly higher mean plasma visfatin level than the non-resistant group [3.61 (SD 1.59) vs. 1.96 (SD 1.18) ng/mL, respectively; (P=0.004)].Conclusion Obese adolescents with insulin resistance have signifcantly higher plasma visfatin levels compared to those without insulin resistance.


1997 ◽  
Vol 8 (11) ◽  
pp. 683-688 ◽  
Author(s):  
Mostafa Chaour ◽  
Pierre Théroux ◽  
Brian M. Gilfix ◽  
Lucien Campeau ◽  
Jacques Lespérance ◽  
...  

2011 ◽  
Vol 8 (6) ◽  
pp. 820-823 ◽  
Author(s):  
Erik Hemmingsson ◽  
Ulf Ekelund ◽  
Joanna Udden

Background:The impact of walking and bicycling on insulin resistance (IR) in women with abdominal obesity is unclear.Methods:Pooled analysis of data from a randomized trial on physically active commuting (bicycling + walking vs walking only) in women with abdominal obesity [n = 98; age:47.3 ± 7.6 yrs; waist circumference (WC):103.1 ± 7.8 cm]. Bicycling and walking data were collected during 7 consecutive days by trip meters (Trelock FC-410) and pedometers (Yamax digiwalker SW-200) at baseline, 2, 4, and 6 months. Owing to a skew distribution we analyzed bicycling as a binary dummy variable with a 10 km/week cut-off. Fasting serum insulin and homeostatic model assessment – insulin resistance (HOMA-IR) were assessed at baseline and 6 months, as were body mass index (BMI), WC, and dual x-ray absorptiometry (DXA)-assessed % whole-body fat.Results:Increased bicycling by 10 km/wk was associated with reductions in fasting serum insulin at follow-up independent of age, treatment allocation, baseline phenotype, Δ walking, and Δ % body fat (β = −10.9, P = .042), but not HOMA-IR (β = −2.0, P = .13). Increased walking was not associated with fasting serum insulin (P = .33) or HOMA-IR (P = .44) at follow-up, after adjustment for the same covariates and Δ bicycling.Conclusion:Increased bicycling but not walking was associated with reduced insulin levels at follow-up. Bicycling may be more effective than walking for reducing insulin levels in abdominally obese women.


2021 ◽  
Vol 8 (3) ◽  
pp. 305-309
Author(s):  
Sumitra Yadav ◽  
Manisha Gupta

The importance of insulin resistance, compensatory hyperinsulinemia, and its effects, many of which have adverse effects on both the metabolic and reproductive organs. Treatment options for insulin resistance/hyperinsulinemia include lifestyle changes, exercise, weight loss, and or the use of thiazolidinediones (TZDs) or metformin. Weight loss measures are essential to the treatment of this condition. Lifestyle, exercise, and dietary changes, weight loss has been shown to reduce hyperandrogenism, increase ovulation and pregnancy rates, and improve immune conflict. Numerous studies have suggested that metformin plays an important role in the treatment of PCOS including restoring ovulation, weight loss, reducing androgen cycle levels, reducing the risk of miscarriage, and reducing the risk of gestational diabetes (GDM).PCOS patients may develop severe dyslipidemia, such as increased LDL-C and TG levels and decreased HDL-C levels associated with hyperandrogenism, IR, and chronic inflammation. Therefore, statins are widely used in the treatment of PCOS patients to reduce inflammation, oxidative stress, hyperandrogenemia, and other metabolic disorders. Statins have been reported to block HMG-CoA inhibiting mevalonate synthesis, which is a necessary substrate for cholesterol production and can be used to synthesize other important lipid links, therefore, statins can improve lipid status and hyperandrogenism.


2007 ◽  
Vol 40 (13-14) ◽  
pp. 964-968 ◽  
Author(s):  
Michael Vogeser ◽  
Daniel König ◽  
Ingrid Frey ◽  
Hans-Georg Predel ◽  
Klaus Georg Parhofer ◽  
...  

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