scholarly journals Insulin Resistance Induced by Maximal Exercise Correlates With a Post-Exercise Increase in Uridine Concentration in the Blood of Healthy Young Men

2013 ◽  
pp. 163-170 ◽  
Author(s):  
W. DUDZINSKA ◽  
A. LUBKOWSKA ◽  
K. JAKUBOWSKA ◽  
M. SUSKA ◽  
E. SKOTNICKA

Uridine is postulated to participate in the development of insulin resistance. Since exercise is an effective tool in the treatment of insulin resistance it appeared justified to assess the impact of maximal exercise on plasma uridine and insulin sensitivity indices (e.g. insulin and HOMA-IR) in healthy subjects. The study included forty-four healthy males (18.5±2.92 years, VO2max 50.2±6.26 ml kg-1 min-1). Subjects performed a single maximal exercise on a bicycle ergometer. Blood samples were taken three times: immediately before exercise, immediately after exercise and at the 30th min of rest. Uridine concentrations were determined in the whole blood using high-performance liquid chromatography. Serum insulin levels were measured by a specific ELISA method. Insulin sensitivity was assessed by homeostasis model assessment method (HOMA-IR). A maximal exercise-induced increase in the concentration of uridine correlated with post-exercise increases in insulin levels and HOMA-IR. Our results indicate a relationship between the concentration of uridine in the blood and indicators of insulin sensitivity in healthy subjects. We are the first to demonstrate that a maximal exercise-induced increase in the concentration of uridine is correlated with post-exercise increases in insulin levels and HOMA-IR in healthy subjects. It appears that uridine may be an indicator of insulin resistance.

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.


2010 ◽  
Vol 30 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Antonio Cioni ◽  
Caterina Sordini ◽  
Ivo Cavallini ◽  
Roberto Bigazzi ◽  
Vito M. Campese

BackgroundInsulin resistance (IR) is common among patients on dialysis and is worse among patients on peritoneal dialysis (PD) than among patients on hemodialysis. In this study we tested the hypothesis that administration of telmisartan, an angiotensin II type 1 receptor antagonist, might improve insulin sensitivity in patients on PD.MethodThis was a crossover study of 30 nondiabetic patients with end-stage renal disease being treated with PD. Group A patients ( n = 15) received telmisartan and other antihypertensive drugs for 4 months, followed by 4 months without telmisartan. Group B patients ( n = 15) received their usual treatment for 4 months, followed by 4 months of treatment with telmisartan. Blood glucose and serum insulin levels were monitored and homeostasis model assessment method for IR (HOMA-IR) was calculated.ResultsTreatment with telmisartan had no significant impact on serum glucose, potassium, and bicarbonate levels. However, telmisartan significantly reduced serum insulin levels and the HOMA index in groups A and B.ConclusionThis study demonstrated that telmisartan, an angiotensin receptor type 1 antagonist, may effectively improve insulin sensitivity as measured by HOMA in patients treated with PD.


2007 ◽  
Vol 157 (5) ◽  
pp. 655-659 ◽  
Author(s):  
Raffaella Rosso ◽  
Arianna Parodi ◽  
Giuseppe d'Annunzio ◽  
Francesca Ginocchio ◽  
Laura Nicolini ◽  
...  

AbstractObjectiveMetabolic abnormalities, including impairment of glucose homeostasis, have been well characterized in HIV-infected patients. In contrast to adults, insulin resistance and diabetes mellitus appear to be relatively uncommon finding in youth.DesignWe assessed insulin resistance, and associated risk factors, in a population of vertically HIV-infected children and young adults, when compared with a control population of healthy children.MethodsAt the time of enrolment, weeks of pregnancy, birth weight, sex, age, weight, height, body mass index (BMI), pubertal stages, CDC classification, blood pressure, clinical lipodystrophy, hepatitis B or C co-infection, antiretroviral therapy, CD4 T lymphocyte counts, and HIV-RNA levels were recorded. Fasting plasma glucose and insulin levels and homeostatic model assessment-insulin resistance (HOMA-IR) were determined. These parameters were compared between HIV patients and healthy controls with multivariate analyses.ResultsFasting insulin levels (OR=1.21, P<0.001) and glycemia (OR=0.89, P<0.001) were significantly different between HIV-infected patients and controls. Antiretroviral therapy duration (r=0.281, P<0.05), triglyceride levels (r=0.286, P<0.05), age (r=0.299, P<0.05), and BMI SDS (r=0.485, P<0.001) were significant predictor variables of insulin resistance, expressed as HOMA-IR. Moreover, clinical lipodystrophy seems to be strongly correlated to glycemia (P<0.05), triglyceride levels (P<0.05), serum insulin levels (P<0.001), HOMA-IR (P<0.05), and also with therapy duration (P<0.05).ConclusionsBoth HIV infection and antiretroviral therapy demonstrate differential effects on glucose metabolism in HIV-infected children. Targeted prevention of insulin resistance and diabetes mellitus in HIV-infected children and young adults is needed in order to avoid the associated long-term complications that would otherwise occur, given the improvement in life expectancy of HIV-infected individuals.


2021 ◽  
Vol 53 (09) ◽  
pp. 616-624
Author(s):  
Yan Li ◽  
Zhenbin Xu

AbstractInsulin resistance (IR) is a pivotal process in various metabolic diseases. The well-known treatment is lifestyle modification and medication therapy, which may result in poor compliance and side effects. Melatonin has been suggested to have a role in glucose metabolism, yet the results across studies have been inconsistent. Therefore, we performed a systematic review to evaluate the effects of melatonin supplementation on insulin levels and IR. We searched PubMed, Embase, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov, and identified randomized controlled trials (RCTs) published prior to August 2020. Articles were reviewed, selected and extracted by two reviewers independently. In total, 8 RCTs of 376 participants were included. Data were pooled using a random-effects model, with mean differences (MDs) and 95% confidence intervals (CIs). Our results showed that melatonin administration significantly reduced insulin levels and homeostasis model assessment of insulin resistance (HOMA-IR), and increased the quantitative insulin sensitivity check index (QUICKI). We conclude that melatonin ameliorated hyperinsulinemia, insulin resistance, and insulin sensitivity, and the results are an update of a previous meta-analysis. Although more investigations are required, we clearly provide evidence for the use of melatonin as an adjuvant treatment for metabolic disorders involving IR.


2007 ◽  
Vol 114 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Faidon Magkos ◽  
Yannis Tsekouras ◽  
Stavros A. Kavouras ◽  
Bettina Mittendorfer ◽  
Labros S. Sidossis

A single bout of moderate-intensity exercise increases whole-body insulin sensitivity for 12–48 h post-exercise; however, the relationship between exercise energy expenditure and the improvement in insulin sensitivity is not known. We hypothesized that the exercise-induced increase in whole-body insulin sensitivity, assessed with HOMAIR (homoeostasis model assessment of insulin resistance), is directly related to the energy expended during exercise. We studied 30 recreationally active non-obese men (age, 27±5 years; body mass index, 24±2 kg/m2) in the post-absorptive state on two separate occasions: once after exercising at 60% of V̇O22peak (peak oxygen consumption) for 30–120 min on the preceding afternoon (expending a total of 1.28–5.76 MJ) and once after an equivalent period of rest. Blood samples were obtained the following morning. Exercise-induced changes in HOMAIR were curvilinearly related to exercise energy expenditure (r=−0.666, P=0.001) with a threshold of approx. 3.77 MJ (900 kcal) for improvements in HOMAIR to be manifested. In particular, HOMAIR was reduced by 32±24% (P=0.003) in subjects who expended more than 3.77 MJ during exercise, but did not change for those who expended fewer than 3.77 MJ (−2±21%; P=0.301). Furthermore, the magnitude of change in HOMAIR after exercise was directly associated with baseline (i.e. resting) HOMAIR (r=−0.508, P=0.004); this relationship persisted in multivariate analysis. We conclude that improved whole-body insulin resistance after a single bout of exercise is curvilinearly related to exercise energy expenditure, and requires unfeasible amounts of exercise for most sedentary individuals.


2008 ◽  
Vol 295 (5) ◽  
pp. E1269-E1276 ◽  
Author(s):  
J. Cacho ◽  
J. Sevillano ◽  
J. de Castro ◽  
E. Herrera ◽  
M. P. Ramos

Insulin resistance plays a role in the pathogenesis of diabetes, including gestational diabetes. The glucose clamp is considered the gold standard for determining in vivo insulin sensitivity, both in human and in animal models. However, the clamp is laborious, time consuming and, in animals, requires anesthesia and collection of multiple blood samples. In human studies, a number of simple indexes, derived from fasting glucose and insulin levels, have been obtained and validated against the glucose clamp. However, these indexes have not been validated in rats and their accuracy in predicting altered insulin sensitivity remains to be established. In the present study, we have evaluated whether indirect estimates based on fasting glucose and insulin levels are valid predictors of insulin sensitivity in nonpregnant and 20-day-pregnant Wistar and Sprague-Dawley rats. We have analyzed the homeostasis model assessment of insulin resistance (HOMA-IR), the quantitative insulin sensitivity check index (QUICKI), and the fasting glucose-to-insulin ratio (FGIR) by comparing them with the insulin sensitivity (SIClamp) values obtained during the hyperinsulinemic-isoglycemic clamp. We have performed a calibration analysis to evaluate the ability of these indexes to accurately predict insulin sensitivity as determined by the reference glucose clamp. Finally, to assess the reliability of these indexes for the identification of animals with impaired insulin sensitivity, performance of the indexes was analyzed by receiver operating characteristic (ROC) curves in Wistar and Sprague-Dawley rats. We found that HOMA-IR, QUICKI, and FGIR correlated significantly with SIClamp, exhibited good sensitivity and specificity, accurately predicted SIClamp, and yielded lower insulin sensitivity in pregnant than in nonpregnant rats. Together, our data demonstrate that these indexes provide an easy and accurate measure of insulin sensitivity during pregnancy in the rat.


2009 ◽  
Vol 53 (8) ◽  
pp. 1005-1011 ◽  
Author(s):  
Amanda D. A. Caldas ◽  
Adriana Lofrano Porto ◽  
Lucilia Domingues Casulari da Motta ◽  
Luiz Augusto Casulari

OBJECTIVE: To evaluate the incidence of hypogonadism in men with metabolic syndrome and its correlation with serum insulin levels. METHODS: Observational, transversal study with 80 men with metabolic syndrome. The individuals were divided into two groups: Group 1: 56 patients (70%) with total testosterone > 300 ng/dL (normal gonadal function); Group 2: 24 patients (30%) with total testosterone < 300 ng/dL (hypogonadic). RESULTS: The subjects from Group 2 compared to Group 1 presented higher body mass index (BMI), waist and hip circumferences, insulin, homeostasis model assessment insulin resistance index (Homa-IR) and beta cell (Homa-β), and triglycerides, but lower SHBG and free testosterone values. Inverse correlations between insulin levels and total testosterone and SHBG, as well as between Homa-IR and total testosterone were observed. CONCLUSION: In this series of men with metabolic syndrome, hypogonadism was associated with insulin resistance and may be a marker of metabolic abnormalities.


2016 ◽  
Vol 230 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Adina Maniu ◽  
Graham W Aberdeen ◽  
Terrie J Lynch ◽  
Jerry L Nadler ◽  
Soon O K Kim ◽  
...  

This study tested the hypothesis that estrogen programs mechanisms within the primate fetus that promote insulin sensitivity and glucose homeostasis in offspring. Glucose tolerance tests were performed longitudinally in prepubertal offspring of baboons untreated or treated on days 100 to 165/175 of gestation (term is 184 days) with the aromatase inhibitor letrozole, which decreased fetal estradiol levels by 95%. Basal plasma insulin levels were over two-fold greater in offspring delivered to letrozole-treated than untreated animals. Moreover, the peak 1min, average of the 1, 3, and 5min, and area under the curve blood glucose and plasma insulin levels after an i.v. bolus of glucose were greater (P<0.05 and P<0.01, respectively) in offspring deprived of estrogen in utero than in untreated animals and partially or completely restored in letrozole plus estradiol-treated baboons. The value for the homeostasis model assessment of insulin resistance was 2.5-fold greater (P<0.02) and quantitative insulin sensitivity check index lower (P<0.01) in offspring of letrozole-treated versus untreated animals and returned to almost normal in letrozole plus estradiol-treated animals. The exaggerated rise in glucose and insulin levels after glucose challenge in baboon offspring deprived of estrogen in utero indicates that pancreatic beta cells had the capacity to secrete insulin, but that peripheral glucose uptake and/or metabolism were impaired, indicative of insulin resistance and glucose intolerance. We propose that estrogen normally programs mechanisms in utero within the developing primate fetus that lead to insulin sensitivity, normal glucose tolerance, and the capacity to metabolize glucose after birth.


2015 ◽  
pp. 467-477 ◽  
Author(s):  
W. DUDZINSKA ◽  
A. LUBKOWSKA ◽  
B. DOLEGOWSKA ◽  
M. SUSKA ◽  
M. JANIAK

Studies have shown that uridine concentration in plasma may be an indicator of uric acid production in patients with gout. It has been also postulated that uridine takes part in blood pressure regulation. Since physical exercise is an effective tool in treatment and prevention of cardio-vascular diseases that are often accompanied by hyperuricemia and hypertension, it seemed advisable to attempt to evaluate the relationship between oxypurine concentrations (Hyp, Xan and UA) and that of Urd and BP after physical exercise in healthy subjects. Sixty healthy men (17.2±1.71 years, BMI 23.2±2.31 kg m−2, VO2max 54.7±6.48 ml kg−1 min−1) took part in the study. The subjects performed a single maximal physical exercise on a bicycle ergometer. Blood for analyses was sampled three times: immediately before exercise, immediately after exercise, and in the 30th min of rest. Concentrations of uridine and hypoxanthine, xanthine and uric acid were determined in whole blood using high-performance liquid chromatography. We have shown in this study that the maximal exercise-induced increase of uridine concentration correlates with the post-exercise increase of uric acid concentration and systolic blood pressure. The results of our study show a relationship between uridine concentration in blood and uric acid concentration and blood pressure. We have been the first to demonstrate that a maximal exercise-induced increase in uridine concentration is correlated with the post-exercise and recovery-continued increase of uric acid concentration in healthy subjects. Thus, it appears that uridine may be an indicator of post-exercise hyperuricemia and blood pressure.


2021 ◽  
pp. 1-9
Author(s):  
Narges Ghorbani Bavani ◽  
Parvane Saneei ◽  
Ammar Hassanzadeh Keshteli ◽  
Ahmadreza Yazdannik ◽  
Ebrahim Falahi ◽  
...  

Abstract Objective: We investigated the association of dietary Mg intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated FFQ. Dietary Mg intake was calculated by summing up the amount of Mg in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI). Participants: Iranian female nurses (n 345) selected by a multistage cluster random sampling method. Results: The Mg intake across energy-adjusted quartiles was 205 (se 7), 221·4 (se 8), 254·3 (se 7) and 355·2 (se 9) mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of Mg intake (Q1: 0·34 (se 0·02), Q2: 0·36 (se 0·01), Q3: 0·40 (se 0·01), and Q4: 0·39 (se 0·02), P = 0·02); however, this association disappeared after considering markers of endothelial function, indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, Mg intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239 (se 17), Q2: 214 (se 12), Q3: 196 (se 12), and Q4: 195 (se 17), P = 0·29). There was no other significant association between dietary Mg intake and other indicators of glucose homoeostasis or endothelial markers. Conclusions: Higher dietary Mg intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.


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