Glucose-induced insulin secretion in uremia: Effects of aminophylline infusion and glucose loads

Allegra, V.; Mengozzi, Giacomo; Martimbianco, Lucia; Vasile, A.

doi:10.1038/ki.1990.325

Cited by 27 publications

(31 citation statements)

References 19 publications

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“…However, type 2 diabetes arises from an imbalance between insulin sensitivity and secretion (42). That β cell dysfunction plays a role in CKD is supported by several studies describing a prediabetic state in uremia that is characterized by both increased insulin resistance and defective insulin secretion (43)(44)(45)(46)(47)(48).…”

Section: Increased Protein O-glcnacylation Alters Glucose Metabolism mentioning

confidence: 83%

Urea impairs β cell glycolysis and insulin secretion in chronic kidney disease

Koppe¹,

Nyam²,

Vivot³

et al. 2016

Journal of Clinical Investigation

122

105

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of the Rodent Metabolic Phenotyping core facility of the CRCHUM for metabolic studies in mice; M. Guévremont, J. Morin, and the Cellular Physiology Service core of the CRCHUM for quantification of β cell mass and αLISA assay; C. Tremblay (CRCHUM) for valuable technical assistance; E. Joly for technical advice; and M. Ferdaoussi for fruitful discussions.Address correspondence to: Vincent Poitout, CRCHUM, 900 Saint-Denis Street, Montreal, Quebec, H2X 0A9, Canada. Phone: 514.890.8044; E-mail: vincent.poitout@umontreal.ca.the CHUM (protocols ND-05-035 and 16-048, respectively). Written consent for research was obtained from all donors.

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Section: Increased Protein O-glcnacylation Alters Glucose Metabolism mentioning

confidence: 83%

Urea impairs β cell glycolysis and insulin secretion in chronic kidney disease

Koppe¹,

Nyam²,

Vivot³

et al. 2016

Journal of Clinical Investigation

122

105

View full text Add to dashboard Cite

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“…Other than the high prevalence of risk factors for IR in our population, CKD-specific causes of IR have also been reported, including post-translational defects, specific uremic toxins, metabolic acidosis, and vitamin D deficiency (32,33). Using the common belief (7), we assume in this study that CKD leads to the development of IR.…”

Section: Discussionmentioning

confidence: 99%

Clinical Correlates of Insulin Sensitivity and Its Association with Mortality among Men with CKD Stages 3 and 4

Huang

Ärnlöv

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Insulin resistance participates in the pathogenesis of multiple metabolic and cardiovascular diseases. CKD patients have impaired insulin sensitivity, but the clinical correlates and outcome associations of impaired insulin sensitivity in this vulnerable population are not well defined.Design, setting, participants, & measurements The prospective cohort study was from the third examination cycle of the Uppsala Longitudinal Study of Adult Men, a population-based survey of elderly men ages 70-71 years; insulin sensitivity was assessed by glucose disposal rate as measured with euglycemic clamps. Inclusion criterion was eGFR,60 ml/min per 1.73 m 2 (n=543). Exclusion criteria were incomplete data on euglycemic clamp and diabetes (n=97), leaving 446 men with CKD stages 3 and 4 (eGFR median=51.9 ml/min per 1.73 m 2 ; range=20.2-59.5 ml/min per 1.73 m 2 ).Results The mean of glucose disposal rate was 5.461.9 mg/kg per minute. In multivariable analysis, the independent clinical correlates of glucose disposal rate were eGFR (slope, 0.02; 95% confidence interval, 0.01 to 0.04), hypertension (20.48; 95% confidence interval, 20.86 to 20.11), hyperlipidemia (20.51; 95% confidence interval, 20.84 to 20.18), and body mass index (20.32; 95% confidence interval, 20.37 to 20.27). During follow-up (median=10.0 years; interquartile range=8.7-11.0 years), 149 participants died. In Cox regression models, glucose disposal rate was not associated with all-cause or cardiovascular mortality. Multiplicative interactions (P,0.05) were observed between glucose disposal rate and physical activity or smoking in total mortality association. After subsequent stratification, glucose disposal rate was an independent correlate of all-cause mortality in smokers (adjusted hazard ratio, 0.72; 95% confidence interval, 0.54 to 0.96 per 1 mg/kg per minute glucose disposal rate increase) and physically inactive individuals (hazard ratio, 0.77; 95% confidence interval, 0.61 to 0.97) but not their counterparts.Conclusion eGFR, together with various components of the metabolic syndrome, contributed to explain the variance of insulin sensitivity in men with CKD stages 3 and 4. Insulin sensitivity was associated with a lower mortality risk in individuals who smoked and individuals who were physically inactive.

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“…Prior studies suggest variable response in ESRD, resulting in glucose intolerance in some patients (35,36). We hypothesized that CKD-related insulin resistance would lead to glucose intolerance and increased risk of overt diabetes among older adults, who are already at increased risk of these disorders.…”

Section: Discussionmentioning

confidence: 99%

Chronic Kidney Disease, Insulin Resistance, and Incident Diabetes in Older Adults

Pham

Robinson‐Cohen

Biggs

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Insulin resistance is a complication of advanced CKD. Insulin resistance is less well characterized in earlier stages of CKD. The response of the pancreatic b cell, effects on glucose tolerance, and risk of diabetes are not clear.Design, setting, participants, & measurements The Cardiovascular Health Study included 4680 adults without baseline diabetes. The Chronic Kidney Disease Epidemiology Collaboration creatinine equation was used to obtain the estimated GFR (eGFR). Insulin resistance was evaluated as fasting insulin concentration. The insulin sensitivity index, b cell function, and glucose tolerance were assessed by oral glucose tolerance testing. Incident diabetes was defined as fasting glucose $126 mg/dl, nonfasting glucose $200 mg/dl, or use of glucose-lowering medications.Results Mean age was 72.5 years (range, 65-98 years). Mean eGFR was 72.2 (SD 17.1) ml/min per 1.73 m 2 . After adjustment, each 10 ml/min per 1.73 m 2 lower eGFR was associated with a 2.2% higher fasting insulin concentration (95% confidence interval [CI], 1.4%, 2.9%; P,0.001) and a 1.1% lower insulin sensitivity index (95% CI, 0.03%, 2.2%; P=0.04). Surprisingly, eGFR was associated with an augmented b cell function index (P,0.001), lower 2-hour glucose concentration (P=0.002), and decreased risk of glucose intolerance (P=0.006). Over a median 12 years' follow-up, 437 participants (9.3%) developed diabetes. eGFR was not associated with the risk of incident diabetes.Conclusions Among older adults, lower eGFR was associated with insulin resistance. However, with lower eGFR, b cell function was appropriately augmented and risks of impaired glucose tolerance and incident diabetes were not increased.

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Glucose-induced insulin secretion in uremia: Effects of aminophylline infusion and glucose loads

Cited by 27 publications

References 19 publications

Urea impairs β cell glycolysis and insulin secretion in chronic kidney disease

Urea impairs β cell glycolysis and insulin secretion in chronic kidney disease

Clinical Correlates of Insulin Sensitivity and Its Association with Mortality among Men with CKD Stages 3 and 4

Chronic Kidney Disease, Insulin Resistance, and Incident Diabetes in Older Adults

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