Validation of Simple Indices to Assess Insulin Sensitivity and Pancreatic Beta-Cell Function in Patients with Renal Dysfunction

Kanauchi, Masao; Akai, Yasuhiro; Hashimoto, Takeji

doi:10.1159/000064072

Cited by 15 publications

(6 citation statements)

References 8 publications

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“…Shehab-Eldin et al also did not confirm beta-cell dysfunction, despite the fact that the results of this study were similar to ours [36]. Pancreatic beta-cell function was also established in other studies, in non-diabetic and diabetic patients with normal and impaired renal function using HOMA-%B, plasma glucose, and insulin concentrations obtained at fasting or during 75-gram oral glucose tolerance test (insulin sensitivity index), insulinogenic index, first-phase insulin secretion index, and area under the curve of plasma insulin [12]. In non-diabetic patients, there was no difference in insulin secretion between patients with normal and impaired renal function.…”

Section: Discussionsupporting

confidence: 88%

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Homeostatic model assessment indices in evaluation of insulin resistance and secretion in hemodialysis patients

et al. 2013

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BackgroundSome previous observations suggest that insulin resistance and glucose metabolism disturbances are frequent complications of chronic kidney disease. However, there are no conclusive studies on other indices of the effectiveness of insulin action in end-stage renal disease (ESRD) patients, including chronically hemodialysed (HD) ones.Material/MethodsThe groups comprised 33 non-diabetic ESRD hemodialysed patients and 33 healthy controls matched for age, sex, and body mass index (BMI). In both groups, HOMA-%B, HOMA-%S, HOMA-IR indices, and DI were calculated using HOMA1 and HOMA2 as measures of insulin resistance. The indices were also assessed in subgroups divided according to BMI.ResultsMean fasting plasma glucose concentrations were lower in ESRD patients than in healthy persons (82.4±10.4 vs. 93.9±11.6, p=0.001). Fasting serum insulin concentrations were similar in both groups (median 6.8 vs. 6.0 mU/l, p=0.698). HOMA1-%B values were higher in ESRD patients than controls (median 137.1 vs. 81.6, p=0.002). HOMA1-%S (median 75.6 vs. 71.5) and HOMA1-IR (median 1.3 vs. 1.4) values were not significantly different (p=0.264 and p=0.189, respectively). DI1 levels were higher for HD patients than for healthy subjects (median 1.16 vs. 0.53, p<0.001). In subgroup analysis, all statistically significant differences were restricted mainly to persons with BMI <25 kg/m2. Similar results as for the HOMA1 model were obtained for HOMA2.Conclusions1. HOMA beta-cell function is strongly correlated with HOMA insulin resistance in HD patients. 2. In non-diabetic ESRD hemodialysed patients, the HOMA indices and DI may be useful and important models in interpretation of glucose metabolism disturbances.

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Section: Discussionsupporting

confidence: 88%

“…Not all researchers confirm the increase of insulin resistance in patients with CRF. It is indicated in our study as well (Table 2) [12]. …”

Section: Discussionsupporting

confidence: 72%

Homeostatic model assessment indices in evaluation of insulin resistance and secretion in hemodialysis patients

et al. 2013

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“…Clearly, this may limit the value of the study, and further studies on patients with mild renal impairment are needed. Second, although QUICKI has been reported to be a valid surrogate marker also in this patient group, 44 it may not accurately reflect insulin resistance. However, it has been postulated that resistin is mainly active in modulating hepatic insulin resistance, 40 making use of the euglycemic clamp technique potentially also problematic as it is known to measure mainly peripheral insulin resistance.…”

Section: Discussionmentioning

confidence: 84%

Elevated resistin levels in chronic kidney disease are associated with decreased glomerular filtration rate and inflammation, but not with insulin resistance

Axelsson

Bergsten

Qureshi

et al. 2006

Kidney International

216

158

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In the present study, we explore the role of decreased renal function and a genetic polymorphism on the recently discovered protein resistin, apparently able to inhibit hepatic insulin action in mice. We also investigate possible links with inflammation and the insulin resistance present in patients with chronic kidney disease (CKD). This is a post hoc, cross-sectional study comparing 239 prevalent CKD patients with varying degrees of renal function impairment with an age- and gender-matched randomly selected control group of 25 individuals. Glomerular filtration rate (GFR) was estimated by the mean of urea and creatinine clearance (24-h urine samples) (n=204) or by iohexol clearance (n=60). Plasma analysis of blood lipids, insulin, glucose, inflammatory markers (high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-alpha, vascular cellular adhesion molecule, intercellular adhesion molecule) and resistin (kit from LINCO Research, St Charles, MS) was performed using commercially available assays or routine methods. Insulin resistance was estimated by quantitative insulin-sensitivity check index (QUICKI) and homeostasis model assessment for insulin resistance (HOMA-IR) and body composition by dual-energy X-ray absorptiometry. Genotyping of a C/G promoter single nucleotide polymorphism (n=168) at position -180 of the resistin gene was performed by PyroSequencing. Serum levels of resistin were markedly elevated in the CKD patients with both advanced (39.9+/-1.3 ng/ml) and mild to moderate (23.2+/-1.0 ng/ml) renal function impairment, as compared to controls (8.5+/-0.7 ng/ml; P<0.001). In a multiple linear regression model in patients (adjusted r(2)=0.60), only GFR (beta=3.4; P<0.0001), lean body mass (beta=2.2; P<0.001) and the inflammatory markers were independently associated with circulating resistin levels. There was a weak but significant impact of -180 C/G genotype on plasma levels of resistin (median 43.0+/-2.4 ng/ml in CC, 37.5+/-2.0 ng/ml in CG, and 41.1+/-4.9 ng/ml in GG; P<0.05). Univariate analysis of non-diabetic patients and controls showed that serum resistin was associated with markers of glucose metabolism. However, in a multiple regression model, resistin, as well as all the measured markers of inflammation, was only associated with insulin resistance if GFR was not taken into account. Circulating resistin levels are strongly associated with both GFR and inflammatory biomarkers in CKD. As the significant relationship between plasma resistin levels and insulin resistance was lost following the correction for GFR, resistin is not a likely mediator of insulin resistance in patients with CKD. Renal function is an important factor to take into account in clinical studies relating insulin sensitivity to inflammatory biomarkers in CKD as well as in patients with diabetes mellitus, who often have an impaired renal function.

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“…HOMA-IR was calculated as: Fasting serum insulin (µU/mL) x Fasting serum glucose (mg/dL)/405. [16][17][18][19] Covariates included demographics (age and sex), eGFR, BMI [weight (Kg)/height (m) 2 ], inflammatory markers (hsCRP and IL6), serum osmolality, adiponectin, and leptin. eGFR was calculated using the chronic kidney disease epidemiology collaboration (CKD-EPI) equation 20 .…”

Section: Predictors and Covariatesmentioning

confidence: 99%

Peripheral Insulin Resistance Is Associated with Copeptin in Patients with Chronic Kidney Disease

et al. 2021

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Background - Insulin resistance is associated to cardiovascular disease risk and worsened kidney function. Patients with CKD have higher levels of insulin resistance. Elevated levels of copeptin (a surrogate for vasopressin levels), has been associated to increased incidence and progression of CKD as well as incident diabetes mellitus. The purpose of our study was to study the relationship between insulin resistance, copeptin, and CKD. Methods - We performed a cross-sectional study to investigate if insulin resistance was associated with higher copeptin levels in non-diabetic patients with stage 3-4 CKD vs controls. We measured plasma copeptin levels and utilized data from 52 patients with stage 3-4 CKD and 85 controls (eGFR ≥ 60mL/min/1.73m2) enrolled in The Insulin Resistance in Chronic Kidney Disease (IRCKD) study. We then used a multivariable linear regression model to assess the independent relationship between peripheral or hepatic insulin resistance and copeptin across levels of eGFR. Results - We found that in patients with CKD (eGFR 30-60 mL/min/1.73m2), but not in controls, peripheral insulin resistance was significantly correlated with higher levels of log copeptin (r = -0.21, p = 0.04). In patients with CKD when adjusted for age, sex, BMI, serum osmolality, log IL6, and log leptin-adiponectin ratio, each 1 SD decrease in insulin sensitivity was associated to a 38.9% increase in serum copeptin levels. The relationship between hepatic insulin resistance, copeptin, and eGFR is similar between controls and patients with reduced eGFR. Conclusion -Peripheral insulin resistance is associated with elevated copeptin levels in non-diabetic patients with stage 3-4 CKD. Further research into how the interaction between peripheral insulin resistance and elevated vasopressin impacts CKD progression could be of interest.

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Validation of Simple Indices to Assess Insulin Sensitivity and Pancreatic Beta-Cell Function in Patients with Renal Dysfunction

Cited by 15 publications

References 8 publications

Homeostatic model assessment indices in evaluation of insulin resistance and secretion in hemodialysis patients

Homeostatic model assessment indices in evaluation of insulin resistance and secretion in hemodialysis patients

Elevated resistin levels in chronic kidney disease are associated with decreased glomerular filtration rate and inflammation, but not with insulin resistance

Peripheral Insulin Resistance Is Associated with Copeptin in Patients with Chronic Kidney Disease

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