Resistin serum levels are increased but not correlated with insulin resistance in chronic hemodialysis patients

Background/Aims: Insulin resistance is a well-known phenomenon in uremia. Resistin, a recently discovered insulin inhibitor secreted by adipocytes, is associated with obesity and insulin resistance in mice. Adiponectin, also secreted by adipocytes, is known to reduce insulin resistance in humans. The aim of the present study was to address the hypothesis that changes in resistin or adiponectin serum levels may relate to body composition and to insulin resistance in patients with end-stage renal disease. Methods: In a cross-sectional study, 33 non-diabetic patients ( 24 males and 9 females, mean age 61.5 +/- 15.8 years) with end-stage renal disease on chronic hemodialysis (treatment duration 41 +/- 31 months) that lacked signs of infection were enrolled. The control group consisted of 33, matched for age, sex and body mass index (BMI), healthy volunteers ( 22 males, 11 females, mean age 62.6 +/- 12.1 years). BMI (kg/m(2)) was calculated from body weight and height. Body fat (%) was measured by means of bioelectrical impedance. Blood samples were taken always in the morning after a 12-hour fasting period before and after the hemodialysis session. Resistin and adiponectin serum concentrations were measured by enzyme immunoassays and insulin by an electrochemiluminescence immunoassay. The posttreatment values were corrected regarding the hemoconcentration. The homeostasis model assessment index (HOMA-R) was calculated as an estimate of insulin resistance from the fasting glucose and insulin serum levels. Results: Pre-treatment resistin serum levels were significantly increased in hemodialysis patients compared to healthy controls (19.2 +/- 6.2 vs. 3.9 +/- 1.8 ng/ml; p < 0.001). Hemodialysis did not alter resistin levels, as pre- and post-treatment levels were not different when corrected for hemoconcentration (19.2 +/- 6.2 vs. 18.7 +/- 5.0 ng/ml; p = 0.54). Adiponectin levels were also increased in hemodialysis patients compared to healthy controls (25.4 +/- 21.5 vs. 10.5 +/- 5.9 mu g/ml; p < 0.001). A significant inverse correlation was observed between the serum adiponectin levels before the hemodialysis session on the one hand and the BMI ( r = - 0.527, p = 0.002), the HOMA-R ( r = - 0.378, p < 0.05) and the fasting insulin levels ( r = - 0.397, p < 0.05) on the other. However, no significant correlation was observed between serum resistin levels on the one hand versus HOMA-R index (3.2 +/- 3.9 mmol center dot mu IU/ml; r = - 0.098, p = 0.59), insulin levels (13.3 +/- 14.4 mU/l; r = - 0.073, p = 0.69), glucose levels ( 89 +/- 13 mg/dl; r = - 0.049, p = 0.78), BMI (25.6 +/- 3.7 kg/m(2); r = - 0.041, p = 0.82) and body fat content (26.4 +/- 8.4%; r = - 0.018, p = 0.94) on the other hand. Conclusion: Resistin serum levels are significantly elevated in non-diabetic patients with end-stage renal disease that are treated by hemodialysis. The hemodialysis procedure does not affect the resistin levels. Along with previous observations in patients with renal insufficiency in the pre-dialysis stage, our findings implicate an important role of the kidney in resistin elimination. However, increased resistin serum levels in hemodialysis patients are not related to reduced insulin sensitivity encountered in uremia. Copyright (C) 2005 S. Karger AG, Basel

Translanguaging in Multilingual Pre-Primary Classrooms in La Réunion: Reflecting on Inclusion and Social Justice in a French Postcolonial Context

International audienceAbstract This chapter explores the strategies and ideologies of two teachers who, each in their own way, try to mobilize the languages of young plurilingual learners (aged 3–4 and 5–6) in a pre-school situated in a marginalized area in La Reunion, a French island in the Indian Ocean and central hub of migration for families from neighbouring islands. We argue that translanguaging crossed with subaltern studies can be a powerful approach to deconstruct othering processes. Following this analysis, we propose a model for teacher education that includes three main objectives to rethink inclusion and social justice in a French post-colonial context

Pnpla3/Adiponutrin deficiency in mice does not contribute to fatty liver disease or metabolic syndrome[S]

PNPLA3 (adiponutrin, calcium-independent phos­pholipase A2 epsilon [iPLA2ϵ]) is an adipose-enriched, nutritionally regulated protein that belongs to the patatin-like phospholipase domain containing (PNPLA) family of lipid metabolizing proteins. Genetic variations in the human PNPLA3 gene (i.e., the rs738409 I148M allele) has been strongly and repeatedly associated with fatty liver disease. Although human PNPLA3 has triacylglycerol (TAG) hydrolase and transacylase activities in vitro, its in vivo function and physiological relevance remain controversial. The objective of this study was to determine the metabolic consequences of global targeted deletion of the Pnpla3 gene in mice. We found that Pnpla3 mRNA expression is altered in adipose tissue and liver in response to acute and chronic nutritional challenges. However, global targeted deletion of the Pnpla3 gene in mice did not affect TAG hydrolysis, nor did it influence energy/glucose/lipid homoeostasis or hepatic steatosis/injury. Experimental interventions designed to increase Pnpla3 expression (refeeding, high-sucrose diet, diet-induced obesity, and liver X receptor agonism) likewise failed to reveal differences in the above-mentioned metabolic phenotypes. Expression of the Pnpla3 paralog, Pnpla5, was increased in adipose tissue but not in liver of Pnpla3-deficient mice, but compensatory regulation of genes involved in TAG metabolism was not identified. Together these data argue against a role for Pnpla3 loss-of-function in fatty liver disease or metabolic syndrome in mice