scholarly journals Hepatic Insulin Extraction in NAFLD Is Related to Insulin Resistance Rather Than Liver Fat Content

2018 ◽  
Vol 104 (5) ◽  
pp. 1855-1865 ◽  
Author(s):  
Kristina M Utzschneider ◽  
Steven E Kahn ◽  
David C Polidori
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Subcutaneous Fat ◽  
Insulin Clearance ◽  
Liver Fat ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Cross Sectional ◽  
Hepatic Insulin Extraction

Abstract Context Total insulin clearance is decreased in nonalcoholic fatty liver disease (NAFLD), but the relationship between liver fat and hepatic insulin extraction (HIE) is unknown. Objective This cross-sectional study addresses the hypothesis that HIE is reduced in NAFLD and investigates metabolic and/or anthropometric characteristics most closely associated with insulin clearance. Participants Nondiabetic subjects with NAFLD (n = 13) and age- and body mass index (BMI)-matched controls with normal liver enzymes (n = 15) underwent abdominal CT, dual-energy X-ray absorptiometry, oral glucose tolerance test (OGTT), and labeled two-step hyperinsulinemic-euglycemic clamps. Outcome Measurements Liver fat was estimated by the CT liver/spleen ratio. Hepatic and extrahepatic insulin clearances were modeled using clamp and OGTT data. Results Extrahepatic insulin clearance and HIE were not different between NAFLD and controls and did not correlate with liver fat. HIE was positively correlated with insulin sensitivity [rate of glucose disposal (Rd; low r = +0.7, P < 0.001; high r = +0.6, P = 0.001), adiponectin (r = +0.55, P = 0.004), and insulin-mediated suppression of clamp nonesterified free fatty acid (NEFA; r = +0.67, P < 0.001)] but was not associated with fasting NEFA, insulin-mediated suppression of glucose production, or measures of adiposity. Extrahepatic insulin clearance was positively associated with percent body fat (r = +0.44, P = 0.02) and subcutaneous fat (r = +0.42, P = 0.03) but not BMI, intra-abdominal fat, liver fat, Rd, adiponectin, or NEFA. Conclusions HIE is not directly associated with hepatic steatosis but is associated with muscle and adipose tissue insulin resistance. The data suggest differential regulation of insulin clearance with extrahepatic insulin clearance being associated with body fat and not insulin sensitivity.

Increased intrahepatic triglyceride is associated with peripheral insulin resistance: in vivo MR imaging and spectroscopy studies

2007 ◽  
Vol 293 (6) ◽  
pp. E1663-E1669 ◽  
Author(s):  
Jong-Hee Hwang ◽  
Daniel T. Stein ◽  
Nir Barzilai ◽  
Min-Hui Cui ◽  
Julia Tonelli ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Magnetic Resonance ◽  
Subcutaneous Fat ◽  
Liver Fat ◽  
Whole Body ◽  
Glucose Disposal ◽  
Resonance Spectroscopy ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Triglyceride Accumulation

Recent studies have indicated that the mass/content of intramyocellular lipid (IMCL), intrahepatic triglyceride (IHTG), visceral fat (VF), and even deep abdominal subcutaneous fat (SF) may all be correlated with insulin resistance. Since simultaneous measurements of these parameters have not been reported, the relative strength of their associations with insulin action is not known. Therefore, the goals of this study were 1) to simultaneously measure IMCL, IHTG, VF, and abdominal SF in the same nondiabetic individuals using noninvasive 1H-magnetic resonance spectroscopy (MRS) and magnetic resonance imaging (MRI) and 2) to examine how these fat stores are correlated with systemic insulin sensitivity as measured by whole body glucose disposal (Rd) during euglycemic-hyperinsulinemic clamp studies. Positive correlations were observed among IMCL, IHTG, and VF. There were significant inverse correlations between whole body Rd and both IMCL and VF. Notably, there was a particularly tight inverse correlation between IHTG and whole body Rd ( r = −0.86, P < 0.001), consistent with an association between liver fat and peripheral insulin sensitivity. This novel finding suggests that hepatic triglyceride accumulation has important systemic consequences that may adversely affect insulin sensitivity in other tissues.

scholarly journals The DGAT2 gene is a candidate for the dissociation between fatty liver and insulin resistance in humans

2009 ◽  
Vol 116 (6) ◽  
pp. 531-537 ◽  
Author(s):  
Konstantinos Kantartzis ◽  
Fausto Machicao ◽  
Jürgen Machann ◽  
Fritz Schick ◽  
Andreas Fritsche ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Body Fat ◽  
Visceral Fat ◽  
Magnetic Resonance Tomography ◽  
Liver Fat ◽  
Oral Glucose ◽  
Total Body Fat ◽  
Total Body

The enzyme DGAT (acyl-CoA:diacylglycerol acyltransferase) catalyses the final step of triacylglycerol (triglyceride) synthesis. Mice overexpressing hepatic DGAT2 fed a high-fat diet develop fatty liver, but not insulin resistance, suggesting that DGAT2 induces a dissociation between fatty liver and insulin resistance. In the present study, we investigated whether such a phenotype also exists in humans. For this purpose, we determined the relationships between genetic variability in the DGAT2 gene with changes in liver fat and insulin sensitivity in 187 extensively phenotyped subjects during a lifestyle intervention programme with diet modification and an increase in physical activity. Changes in body fat composition [MR (magnetic resonance) tomography], liver fat and intramyocellular fat (1H-MR spectroscopy) and insulin sensitivity [OGTT (oral glucose tolerance test) and euglycaemic–hyperinsulinaemic clamp] were determined after 9 months of intervention. A change in insulin sensitivity correlated inversely with changes in total body fat, visceral fat, intramyocellular fat and liver fat (OGTT, all P<0.05; clamp, all P≤0.03). Changes in total body fat, visceral fat and intramyocellular fat were not different between the genotypes of the SNPs (single nucleotide polymorphisms) rs10899116 C>T and rs1944438 C>T (all P≥0.39) of the DGAT2 gene. However, individuals carrying two or one copies of the minor T allele of SNP rs1944438 had a smaller decrease in liver fat (−17±10 and −24±5%; values are means±S.E.M.) compared with subjects homozygous for the C allele (−39±7%; P=0.008). In contrast, changes in insulin sensitivity were not different among the genotypes (OGTT, P=0.76; clamp, P=0.53). In conclusion, our findings suggest that DGAT2 mediates the dissociation between fatty liver and insulin resistance in humans. This finding may be important in the prevention and treatment of insulin resistance and Type 2 diabetes in subjects with fatty liver.

Effect of liver fat on insulin clearance

2007 ◽  
Vol 293 (6) ◽  
pp. E1709-E1715 ◽  
Author(s):  
Anna Kotronen ◽  
Satu Vehkavaara ◽  
Anneli Seppälä-Lindroos ◽  
Robert Bergholm ◽  
Hannele Yki-Järvinen
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Fat Content ◽  
Insulin Clearance ◽  
Liver Fat ◽  
Hepatic Insulin Resistance ◽  
Model Assessment ◽  
Liver Fat Content ◽  
Hepatic Insulin Sensitivity ◽  
Impaired Insulin

A fatty liver is associated with fasting hyperinsulinemia, which could reflect either impaired insulin clearance or hepatic insulin action. We determined the effect of liver fat on insulin clearance and hepatic insulin sensitivity in 80 nondiabetic subjects [age 43 ± 1 yr, body mass index (BMI) 26.3 ± 0.5 kg/m2]. Insulin clearance and hepatic insulin resistance were measured by the euglycemic hyperinsulinemic (insulin infusion rate 0.3 mU·kg−1·min−1for 240 min) clamp technique combined with the infusion of [3-3H]glucose and liver fat by proton magnetic resonance spectroscopy. During hyperinsulinemia, both serum insulin concentrations and increments above basal remained ∼40% higher ( P < 0.0001) in the high (15.0 ± 1.5%) compared with the low (1.8 ± 0.2%) liver fat group, independent of age, sex, and BMI. Insulin clearance (ml·kg fat free mass−1·min−1) was inversely related to liver fat content ( r = −0.52, P < 0.0001), independent of age, sex, and BMI ( r = −0.37, P = 0.001). The variation in insulin clearance due to that in liver fat (range 0–41%) explained on the average 27% of the variation in fasting serum (fS)-insulin concentrations. The contribution of impaired insulin clearance to fS-insulin concentrations increased as a function of liver fat. This implies that indirect indexes of insulin sensitivity, such as homeostatic model assessment, overestimate insulin resistance in subjects with high liver fat content. Liver fat content correlated significantly with fS-insulin concentrations adjusted for insulin clearance ( r = 0.43, P < 0.0001) and with directly measured hepatic insulin sensitivity ( r = −0.40, P = 0.0002). We conclude that increased liver fat is associated with both impaired insulin clearance and hepatic insulin resistance. Hepatic insulin sensitivity associates with liver fat content, independent of insulin clearance.

scholarly journals Small intestinal metabolism is central to whole-body insulin resistance

Gut ◽  
2020 ◽  
pp. gutjnl-2020-322073
Author(s):  
Giulia Angelini ◽  
Serenella Salinari ◽  
Lidia Castagneto-Gissey ◽  
Alessandro Bertuzzi ◽  
James Casella-Mariolo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Insulin Signalling ◽  
Whole Body ◽  
Glucose Disposal ◽  
Jejunal Loop ◽  
Oral Glucose ◽  
Metabolic Signature ◽  
Jejunal Bypass

ObjectiveTo assess the role of jejunum in insulin resistance in humans and in experimental animals.DesignTwenty-four subjects undergoing biliopancreatic diversion (BPD) or Roux-en-Y gastric bypass (RYGB) were enrolled. Insulin sensitivity was measured at baseline and at 1 week after surgery using oral glucose minimal model.We excluded the jejunum from intestinal continuity in pigs and created a jejunal loop with its vascular and nerve supply intact accessible from two cutaneous stomas, and reconnected the bowel with an end-to-end anastomosis. Glucose stable isotopes were given in the stomach or in the jejunal loop.In vitro studies using primary porcine and human hepatocytes or myoblasts tested the effects of plasma on gluconeogenesis or glucose uptake and insulin signalling.ResultsWhole-body insulin sensitivity (SI∙104: 0.54±0.12 before vs 0.82±0.11 after BPD, p=0.024 and 0.41±0.09 before vs 0.65±0.09/pM/min after RYGB, p=not significant) and Glucose Disposition Index increased only after BPD. In pigs, insulin sensitivity was significantly lower when glucose was administered in the jejunal loop than in the stomach (glucose rate of disappearance (Rd) area under the curve (AUC)/insulin AUC∙10: 1.82±0.31 vs 2.96±0.33 mmol/pM/min, p=0.0017).Metabolomics showed a similar pattern before surgery and during jejunal-loop stimulation, pointing to a higher expression of gluconeogenetic substrates, a metabolic signature of impaired insulin sensitivity.A greater hepatocyte phosphoenolpyruvate-carboxykinase and glucose-6-phosphatase gene expression was elicited with plasma from porcine jejunal loop or before surgery compared with plasma from jejunectomy in pigs or jejunal bypass in humans.Stimulation of myoblasts with plasma from porcine jejunal loop or before surgery reduced glucose uptake, Ser473-Akt phosphorylation and GLUT4 expression compared with plasma obtained during gastric glucose administration after jejunectomy in pigs or after jejunal bypass in humans.ConclusionProximal gut plays a crucial role in controlling insulin sensitivity through a distinctive metabolic signature involving hepatic gluconeogenesis and muscle insulin resistance. Bypassing the jejunum is beneficial in terms of insulin-mediated glucose disposal in obesity.Trial registration numberNCT03111953.

scholarly journals Insulin sensitivity predicts cognitive decline in individuals with prediabetes

2020 ◽  
Vol 8 (2) ◽  
pp. e001741
Author(s):  
Caroline Willmann ◽  
Kathrin Brockmann ◽  
Robert Wagner ◽  
Stephanie Kullmann ◽  
Hubert Preissl ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Cognitive Decline ◽  
Fixed Effects ◽  
Epidemiological Studies ◽  
Oral Glucose ◽  
Dependent Manner ◽  
Prediabetic State ◽  
Cross Sectional

IntroductionEpidemiological studies indicate an association between type 2 diabetes and cognitive dysfunction that appear to start already in the prediabetic state. Although cross-sectional studies have linked insulin resistance to impaired cognition, the potential predictive value of insulin resistance has not yet been sufficiently studied longitudinally without confounding by overt diabetes (and its pharmacological treatment).Research design and methodsWe investigated longitudinal data from participants of the ‘Tübinger Evaluation of Risk Factors for Early Detection of Neurodegeneration’ Study. Subjects underwent a neurocognitive assessment battery (CERAD Plus battery; Consortium to Establish a Registry for Alzheimer’s Disease) at baseline and followed every 2 years (median follow-up 4.0 Q1–3: 2.2–4.3 years). Subjects within a pre-diabetic glycated hemoglobin range of 5.6%–6.5% underwent 5-point 75 g oral glucose tolerance tests (OGTTs) with assessment of insulin sensitivity and insulin secretion (n=175). Subjects with newly diagnosed diabetes mellitus or with major depressivity (Beck Depression Inventory >20) were excluded (n=15). Data were analyzed by mixed models using sex, age and glycemic trait as fixed effects. Subject and time since first measurement were used as random effects.ResultsInsulin sensitivity was positively associated with the CERAD sum score (higher is better) in a time-dependent manner (p=0.0057). This result is mainly driven by a steeper decrease in the memory domain associated with lower insulin sensitivity (p=0.029). The interaction between age and insulin sensitivity was independent of glycemia (p=0.02). There was also no association between insulin secretion and cognition.ConclusionsInsulin resistance rather than sole elevation of blood glucose predicts cognitive decline, specifically in the memory domain, in persons with prediabetes. Treatments of diabetes that improve insulin sensitivity might therefore have the potential to postpone or even prevent cognitive decline in patients with diabetes.

scholarly journals Insulin Resistance Diagnosed by HOMA-IR may be Overestimated in Adults with Greater Fat-Free Mass: The ELSA-Brasil Study

2020 ◽  
Author(s):  
Divanei Zaniqueli ◽  
Rafael de Oliveira Alvim ◽  
Rosane Harter Griep ◽  
Isabela Martins Benseñor ◽  
Sandhi Maria Barreto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Fat ◽  
Bioelectrical Impedance ◽  
Tolerance Test ◽  
Fat Free Mass ◽  
Percent Body Fat ◽  
Oral Glucose ◽  
Model Assessment ◽  
Fasting Insulin ◽  
Cross Sectional

Abstract Background Conflicting results have been reported on the association of fat-free mass (FFM) and insulin resistance (IR). The way of indexing FFM may be a bias. This study sought to test the association of FFM and IR after indexing FFM to avoid collinearity. Methods This cross-sectional study comprised 11,284 volunteers, ages 38-79 years. Body composition was assessed by multi-frequency bioelectrical impedance. FFM indexed to body surface area (FFMbsa) was calculated. Excess body fat was assigned to individuals with percent body fat ≥ 85th percentile for age and sex. Fasting insulin and glucose, and 2h glucose in the oral glucose tolerance test were obtained. Homeostasis model assessment-insulin resistance (HOMA-IR) > 3.0 was set as the cut-off for IR.Results Percent body fat decreased from the 1st to the 5th quintile of FFMbsa in both women (Eta 2 = 0.166) and men (Eta 2 = 0.133). In women, fasting insulin (Eta 2 = 0.002), glucose (Eta 2 = 0.006), and HOMA-IR (Eta 2 = 0.007) increased slightly, whereas 2h glucose did not change towards the highest quintile of FFMbsa. In men, fasting insulin and HOMA-IR were similar across the quintiles of FFMbsa, whereas fasting glucose increased slightly (Eta 2 = 0.002) and 2h glucose decreased (Eta 2 = 0.005) towards the highest quintile of FFMbsa. Greater FFMbsa explained 1.8% of the odds of IR among women and 0.9% among men.Conclusion The lack of association of FFM and 2h glucose contrasted with greater odds of IR (by HOMA-IR) associated with greater FFM. The association of greater FFM and IR may be overestimated when the diagnosis is provided by HOMA-IR.

Plasma bile acids more closely align with insulin resistance, visceral and hepatic adiposity than total adiposity

2020 ◽  
Author(s):  
Ramy H Bishay ◽  
Katherine T Tonks ◽  
Jacob George ◽  
Dorit Samocha-Bonet ◽  
Gideon Meyerowitz-Katz ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Subcutaneous Fat ◽  
Academic Research ◽  
Fat Distribution ◽  
Fat Free Mass ◽  
Liver Fat ◽  
Fibroblast Growth Factor 21 ◽  
Insulin Resistant ◽  
Adult Volunteers

Abstract Context The etiological mechanism of bile acid (BA) effects on insulin resistance and obesity is unknown. Objective To determine if plasma BA are elevated in human obesity and/or insulin resistance. Design Observational study. Setting Academic research center. Participants 71 adult volunteers formed four groups: lean insulin-sensitive (BMI≤25kg/m 2, HOMA-IR&lt;2.0, n=19), overweight/obese non-diabetic who were either insulin-sensitive (Obsensitive, BMI&gt;25kg/m 2, HOMA-IR&lt;1.5, n=11), or insulin-resistant (Obresistant, BMI&gt;25kg/m 2, HOMA-IR&gt;3.0, n=20), and type 2 diabetes (T2D, n=21). Main Outcome Measures Insulin sensitivity by hyperinsulinemic-euglycemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution and liver density by CT and plasma BA. Results In the Obresistant group, glucose infusion rate/fat free mass (GIR/FFM, an inverse measure of insulin resistance) was significantly lower, and visceral and liver fat higher, compared to lean and Obsensitive subjects, despite similar total adiposity in Obresistant and Obsensitive. Total BA concentrations were higher in Obresistant (2.62±1.5mmol/L, p=0.03) and T2D (3.36±2.26mmol/L, p=0.0004) versus Obsensitive (1.16±0.47mmol/L), but were similar between Obsensitive and lean (2.31±1.43mmol/L). Total BA were positively associated with waist circumference (R=0.245, p=0.041), visceral fat (R=0.360, p=0.002) and fibroblast growth factor 21 (R=0.341, p=0.004) and negatively associated with insulin sensitivity (R=-0.395, p=0.001), abdominal subcutaneous fat (R=-0.352, p=0.003), adiponectin (R=-0.375, P=0.001) and liver fat (Hounsfield units, an inverse marker of liver fat, R=-0.245, p=0.04). Conjugated BA were additionally elevated in T2D individuals (p&lt;0.001). Conclusions BA concentrations correlated with abdominal, visceral and liver fat in humans, though an etiological role in insulin resistance remains to be verified.

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance

2000 ◽  
Vol 278 (5) ◽  
pp. E941-E948 ◽  
Author(s):  
David E. Kelley ◽  
F. Leland Thaete ◽  
Fred Troost ◽  
Trina Huwe ◽  
Bret H. Goodpaster
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Subcutaneous Fat ◽  
Area Under The Curve ◽  
Density Lipoprotein ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Central Adiposity ◽  
Cross Sectional ◽  
Arterial Blood

Whereas truncal (central) adiposity is strongly associated with the insulin resistant metabolic syndrome, it is uncertain whether this is accounted for principally by visceral adiposity (VAT). Several recent studies find as strong or stronger association between subcutaneous abdominal adiposity (SAT) and insulin resistance. To reexamine the issue of truncal adipose tissue depots, we performed cross-sectional abdominal computed tomography, and we undertook the novel approach of partitioning SAT into the plane superficial to the fascia within subcutaneous adipose tissue (superficial SAT) and that below this fascia (deep SAT), as well as measurement of VAT. Among 47 lean and obese glucose-tolerant men and women, insulin-stimulated glucose utilization, measured by euglycemic clamp, was strongly correlated with both VAT and deep SAT ( r = −0.61 and −0.64, respectively; both P < 0.001), but not with superficial SAT ( r = −0.29, not significant). Also, VAT and deep SAT followed a highly congruent pattern of associations with glucose and insulin area under the curve (75-g oral glucose tolerance test), mean arterial blood pressure, apoprotein-B, high-density lipoprotein cholesterol, and triglyceride. Superficial SAT had markedly weaker association with all these parameters and instead followed the pattern observed for thigh subcutaneous adiposity. We conclude that there are two functionally distinct compartments of adipose tissue within abdominal subcutaneous fat and that the deep SAT has a strong relation to insulin resistance.

Normal insulin sensitivity and IMCL content in overweight humans are associated with higher fasting lipid oxidation

2002 ◽  
Vol 283 (3) ◽  
pp. E556-E564 ◽  
Author(s):  
Gianluca Perseghin ◽  
Paola Scifo ◽  
Massimo Danna ◽  
Alberto Battezzati ◽  
Stefano Benedini ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Lipid Oxidation ◽  
Body Fat ◽  
Resting Energy Expenditure ◽  
Plasma Free Fatty Acid ◽  
Whole Body ◽  
Glucose Disposal ◽  
Family History Of Diabetes ◽  
History Of

Intramyocellular lipid (IMCL) storage is considered a local marker of whole body insulin resistance; because increments of body weight are supposed to impair insulin sensitivity, this study was designed to assess IMCL content, lipid oxidation, and insulin action in individuals with a moderate increment of body fat mass and no family history of diabetes. We studied 14 young, nonobese women with body fat <30% ( n = 7) or >30% ( n = 7) and 14 young, nonobese men with body fat <25% ( n = 7) or >25% ( n = 7) by means of the euglycemic-insulin clamp to assess whole body glucose metabolism, with indirect calorimetry to assess lipid oxidation, by localized1H NMR spectroscopy of the calf muscles to assess IMCL content, and with dual-energy X-ray absorptiometry to assess body composition. Subjects with higher body fat had normal insulin-stimulated glucose disposal ( P = 0.80), IMCL content in both soleus ( P = 0.22) and tibialis anterior ( P = 0.75) muscles, and plasma free fatty acid levels ( P = 0.075) compared with leaner subjects in association with increased lipid oxidation ( P < 0.05), resting energy expenditure ( P = 0.046), resting oxygen consumption ( P = 0.049), and plasma leptin levels ( P < 0.01) in the postabsorptive condition. In conclusion, in overweight subjects, preservation of insulin sensitivity was combined with increased lipid oxidation and maintenance of normal IMCL content, suggesting that abnormalities of these factors may mutually determine the development of insulin resistance associated with weight gain.

scholarly journals Measurement and Correlation of Indices of Insulin Resistance in Patients on Peritoneal Dialysis

2016 ◽  
Vol 36 (4) ◽  
pp. 433-441 ◽  
Author(s):  
Kelli R. King-Morris ◽  
Serpil Muge Deger ◽  
Adriana M. Hung ◽  
Phyllis Ann Egbert ◽  
Charles D. Ellis ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Peritoneal Dialysis ◽  
Glucose Tolerance ◽  
Large Scale ◽  
Tolerance Test ◽  
Glucose Disposal ◽  
Maintenance Hemodialysis ◽  
Oral Glucose ◽  
Model Assessment ◽  
Cross Sectional

BackgroundInsulin resistance (IR) is common in maintenance dialysis patients and is associated with excess mortality. Hyperinsulinemic euglycemic glucose clamp (HEGC) is the gold standard for measuring IR. There are limited studies using HEGC for comparison to other indirect indices of IR in peritoneal dialysis (PD) patients, nor have there been direct comparisons between patients receiving PD and those on maintenance hemodialysis (MHD) with regard to severity of IR, methods of measurement, or factors associated with the development of IR.MethodsThis is a cross-sectional, single-center study performed in 10 prevalent PD patients of median age 48 years (range 41 – 54); 50% were female and 60% were African American. Insulin resistance was assessed by HEGC (glucose disposal rate [GDR]), homeostatic model assessment of IR (HOMA-IR), HOMA-IR corrected by adiponectin (HOMA-AD), leptin adiponectin ratio (LAR), quantitative insulin sensitivity check index (QUICKI), McAuley's index, and oral glucose tolerance test (OGTT) at each time point for a total of 18 studies. Retrospective analysis compared this cohort to 12 hemodialysis patients who had previously undergone similar testing.ResultsThe median GDR was 6.4 mg/kg/min (interquartile range [IQR] 6.0, 7.8) in the PD cohort compared with the MHD group, which was 5.7 mg/kg/min (IQR 4.3, 6.6). For both the PD and MHD cohorts, the best predictors of GDR by HEGC after adjusting for age, gender, and body mass index (BMI), were HOMA-AD (PD: r = -0.69, p = 0.01; MHD: r = -0.78, p = 0.03) and LAR (PD: r = -0.68, p < 0.001; MHD: r = -0.65, p = 0.04). In both groups, HOMA-IR and QUICKI failed to have strong predictive value. Eight of 10 PD patients had at least 1 abnormal OGTT, demonstrating impaired glucose tolerance.ConclusionsInsulin resistance is highly prevalent in PD patients. The adipokine based formulas, HOMA-AD and LAR, correlated well in both the PD and MHD populations in predicting GDR by HEGC, outperforming HOMA-IR. The use of these novel markers could be considered for large-scale, epidemiological outcome studies.

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