Personne :
Weisnagel, John

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Université Laval. Faculté de médecine
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  • Publication
    Accès libre
    Postnatal prevention of childhood obesity in offspring prenatally exposed to gestational diabetes mellitus : where are we now?
    (S. Karger, 2017-08-23) Perron, Julie; Mercier, Roxanne; Weisnagel, John; Kearney, Michèle; Marc-Sériès, Isabelle; Robitaille, Julie; Tchernof, André; Dugas, Camille
    Children exposed to gestational diabetes mellitus (GDM) in utero are at high risk of developing many health problems such as obesity. There is an urgent need to find new strategies to prevent obesity development among high-risk populations such as those children. Accordingly, the aim of this review was to summarize current knowledge on the postnatal prevention of childhood obesity in offspring born from mothers with GDM. Specifically, this review addresses the impact of breastfeeding, complementary feeding practices as well as dietary intake and physical activity during childhood on obesity risk of children exposed to GDM in utero. Furthermore, breast milk composition of diabetic mothers and its potential impact on growth is discussed. According to the available literature, breastfeeding may reduce obesity risk in children exposed to GDM in utero but a longer duration seems necessary to achieve its protective effect against obesity. Detailed analysis of breast milk composition of mothers with GDM will be necessary to fully understand the relationship between breastfeeding and obesity in this specific population. This review highlights the need for more studies addressing the impact of complementary feeding practices and lifestyle habits during childhood on obesity risk of children exposed to GDM in utero.
  • Publication
    Associations between glucose tolerance, insulin sensitivity and insulin secretion phenotypes and polymorphisms in adiponectin and adiponectin receptor genes in the Quebec Family Study
    (Wiley, 2008-02-19) Ruchat, Stéphanie-May; Loos, Ruth; Bouchard, Claude; Rankinen, Tuomo; Pérusse, Louis; Weisnagel, John; Vohl, Marie-Claude; Després, Jean-Pierre
    Aims:  Studies suggest that adiponectin (APM1) and its receptors 1 and 2 (AdipoR1 and AdipoR2) play an important role in the development of insulin resistance (IR). Our objective was to examine associations between APM1 (+45T>G, +276G>T and –3971A>G), AdipoR1 (−100G>T and −3882T>C) and AdipoR2 (−35361A>G and –1352G>A) genes single‐nucleotide polymorphisms (SNPs) and adiponectin plasma levels, indicators of glucose tolerance, insulin sensitivity (IS) and insulin secretion. Methods:  Six hundred and twenty‐two non‐diabetic subjects from the Quebec Family Study (QFS) underwent a 75‐g oral glucose tolerance test (OGTT), with measurement of fasting adiponectin, glucose, insulin and C‐peptide levels. Indices of glucose tolerance, IS and insulin secretion were derived from fasting and OGTT measurements. Results:  Significant evidence of association was found between indices of IS and APM1 and AdipoR1 SNPs. The APM1 –3971G/G homozygotes exhibited a reduced area under the curve of insulin during the OGTT (P = 0.007) and higher Cederholm index (P = 0.01) compared to the A/A homozygotes. The APM1 +45T>G variant was also associated with fasting (P = 0.002) and 2‐h (P = 0.007) glucose values as well as with higher Cederholm index (P = 0.04) and disposition index (P = 0.02). Finally, the AdipoR1 −3882T>C SNP was associated with fasting glucose (P = 0.03), the homeostasis model assessment for insulin resistance (P = 0.04) and an index of insulin secretion (P30/G30, P = 0.02). No evidence of association was found with plasma adiponectin levels. Conclusions:  These results provide evidence for an influence of common SNPs in the APM1 and AdipoR1 genes on different phenotypes of glucose and insulin metabolism associated with increased risk of type 2 diabetes.
  • Publication
    Accès libre
    Influence of physical activity participation on the associations between eating behaviour traits and body mass index in healthy postmenopausal women
    (Hindawi Pub, 2010-09-14) Dubé, Marie-Christine; Doucet, Eric; Riou, Marie-Ève; Piché, Marie-Eve; Lemieux, Simone; Weisnagel, John; Provencher, Véronique; Bergeron, Jean
    We present an overview of fission chamber’s functioning modes, theoretical aspects of the nonnegative matrix factorization methods, and the opportunities that offer neutron data processing in order to achieve neutron flux monitoring tasks. Indeed, it is a part of research project that aimed at applying Blind Source Separation methods for in-core and ex-core neutron flux monitoring while analyzing the outputs of fission chamber. The latter could be used as a key issue for control, fuel management, safety concerns, and material irradiation experiments. The Blind Source Separation methods had been used in many scientific fields such as biomedical engineering and telecommunications. Recently, they were used for gamma spectrometry data processing. The originality of this research work is to apply these powerful methods to process the fission chamber output signals. We illustrated the effectiveness of this tool using simulated fission chamber signals.
  • Publication
    Association between metabolic deteriorations and prior gestational diabetes according to weight status
    (Nature Pub. Group, 2014-11-29) Garneau, Véronique; Vigneault, Jessica; Lemieux, Simone; Weisnagel, John; Robitaille, Julie; Tchernof, André
    Objective The aim of the present study is to investigate the effect of prior gestational diabetes mellitus (GDM) on glucose and insulin homeostasis according to weight status. Methods The analysis included 299 women, 216 with [GDM(+)] and 83 without prior GDM [GDM(−)]. The mean time between pregnancy and testing was 3.9 years. Glucose values were obtained from a 2-h 75 g oral glucose tolerance test (OGTT). Body composition was measured by dual-energy X-ray. Results In women with normal BMI, fasting glucose, 2-h post-OGTT glucose, and HbA1 were higher for GDM(+) (P < 0.05). Normal-weight women with GDM(+) presented lower HOMA-IS, insulin secretion, and insulinogenic index (P < 0.05) compared to GDM(−). Body fat and android fat mass were higher, gynoid fat mass was similar, and lean body mass was decreased in GDM(+) vs. GDM(−) with normal weight (P < 0.05). A greater proportion of GDM(+) with overweight/obesity had prediabetes (72.1%) or type 2 diabetes (T2D) (21.7%) vs. GDM(−) and overweight/obesity (17.1 and 2.4%) or GDM(+) and normal weight (60.5 and 14.0%). Conclusions A combination of GDM and overweight/obesity is associated with T2D-related metabolic deteriorations. Nevertheless, normal-weight women with GDM(+) had increased android fat and greater metabolic complications, suggesting that women with prior GDM should benefit from lifestyle intervention, regardless of their weight status.
  • Publication
    Irisin is more strongly predicted by muscle oxidative potential than adiposity in non-diabetic men
    (Springer Science & Business Media B.V., 2015-03-28) Joanisse, Denis R.; Dubois, Marie Julie; Marette, André; Fleury, Pascale; Tremblay, Angelo; Lacaille, Michel; Weisnagel, John; Huth, Claire; Mauriege, Pascale
    Numerous controversies surround the peptide hormone irisin. Although implicated as a myokine promoting the browning of adipose tissue in rodents, its roles in humans remain unclear. Contradictory results have also been found with respect to the relationships between adiposity or metabolic health and plasma irisin levels in humans. We investigated the relationship between irisin levels and body composition (hydrostatic weighing), insulin sensitivity (hyperinsulinemiceuglycemic clamp), fitness level (ergocycle VO2max) and skeletal muscle metabolic profile in 53 men (aged 34–53 years) from four groups: sedentary non-obese controls (body mass index [BMI] <25 kg/m2), sedentary obese (BMI >30 kg/m2), sedentary obese glucose-intolerant, and non-obese highly trained endurance active. Baseline plasma irisin levels were significantly different between groups, being lowest in trained men (140.6±38.2 ng/mL) and highest in metabolically deteriorated glucose-intolerant subjects (204.0±50.5 ng/mL; ANOVA p=0.01). Including all subjects, irisin levels were positively associated with adiposity (e.g. fat mass, r=0.430, p<0.01) and negatively associated with fitness (r=-0.369, p<0.01), insulin sensitivity (M/I, r=-0.355, p<0.01) and muscle citrate synthase (CS) activity (r=-0.482, p<0.01). Most correlations lost statistical significance when excluding active individuals, except for insulin resistance (r=-0.413, p<0.01) and CS (r=-0.462, p<0.01). Multiple regression analyses reveal CS as the strongest independent predictor of irisin levels (r2 range 0.214 to 0.237). We conclude that muscle oxidative potential is an important factor linked to circulating irisin levels. Keywords : Irisin . Myokine . Adipose tissue . Adipokine . Obesity. Insulin sensitivity
  • Publication
    Combined effects of PPARγ2 P12A and PPARα L162V polymorphisms on glucose and insulin homeostasis : the Québec Family Study
    (Springer-Verlag, 2003-11-20) Bouchard, Claude; Pérusse, Louis; Weisnagel, John; Bossé, Yohan; Vohl, Marie-Claude; Després, Jean-Pierre
    Peroxisome proliferator-activated receptors γ2 and α are nuclear factors known to be important regulators of lipid and glucose metabolism. Two polymorphisms, namely PPARγ2 P12A and PPARα L162V, were investigated for their individual and interaction effects on glucose and insulin homeostasis. Genotypes were determined in 663 nondiabetic adults participating in the Québec Family Study and who underwent an oral glucose tolerance test (OGTT). The insulin and C-peptide areas under the curve (AUC) following the OGTT were higher in subjects carrying the PPARα V162 allele compared to homozygous for the L162 allele. When subjects were grouped according to both polymorphisms, higher levels of insulin and C-peptide during the OGTT were observed for those carrying the PPARα V162 allele except when they carry at the same time the PPARγ2 A12 allele. Thus, the PPARγ2 A12 allele seems protective against the deleterious effect of the PPARα V162 allele. Furthermore, a significant gene-gene interaction was observed for the acute (0–30 min) (p<0.001) and the total (p=0.05) C-peptide AUC following the OGTT. These results provide evidence of a gene-gene interaction in the regulation of plasma glucose-insulin homeostasis, and emphasize that these interactions need to be taken into account when dissecting the genetic etiology of complex disorders.
  • Publication
    Accès libre
    Transcriptomic profiles of skeletal muscle tissue following an euglycemic-hyperinsulinemic clamp in insulin-resistant obese subjects
    (Springer Link, 2012-05-08) Rudkowska, Iwona; Weisnagel, John; Vohl, Marie-Claude; Jacques, Hélène; Marette, André
    Insulin resistance in skeletal muscle is an early phenomenon in the pathogenesis of type 2 diabetes. Muscle is mainly responsible for insulin-stimulated glucose clearance from the bloodstream. Thus, regulation of gene expression in muscle tissue may be involved in the pathogenesis of insulin resistance. The objective was to investigate gene expression and metabolic pathways alterations in skeletal muscle tissue following an euglycemic-hyperinsulinemic clamp in obese insulin-resistant subjects. We carried out a transcriptome comparison of skeletal muscle tissue before and after a 3-h euglycemic-hyperinsulinemic clamp following 8-week supplementation with n-3 polyunsaturated fatty acid (PUFA) (1.8 g/day) with or without a supplement of fish gelatin (FG) (25 % of daily protein intake) in 16 obese insulin-resistant subjects. Results indicate that approximately 5 % (1932) of expressed transcripts were significantly changed after the clamp in both n-3 PUFA and n-3 PUFA + FG supplementation periods. Of these differentially expressed transcripts, 1394 genes associated with enzymes, transcription and translation regulators, transporters, G protein-coupled receptors, cytokines, and ligand-dependent nuclear receptors were modified. Metabolic pathways that were significantly modified included liver X receptor/retinoid X receptors (RXR) activation, vitamin D receptor/RXR activation, interleukin (IL)-8, acute phase response, IL10, triggering receptor expressed on myeloid cells 1, peroxisome proliferator-activated receptor, G-beta/gamma and hepatocyte growth factor and IL6 signaling. Taken together, results suggest that mainly inflammatory and transcription factors are modified following clamp in obese insulin-resistant subjects. Overall, understanding the changes in metabolic pathways due to insulin may be a potential target for the management of insulin resistance.
  • Publication
    Human resistin gene polymorphism is associated with visceral obesity and fasting and oral glucose stimulated C-peptide in the Québec Family Study
    (Kurtis, 2004-12-01) Bouchard, Claude; Pérusse, Louis; Engert, James; Weisnagel, John; Hudson, Thomas J.; Vohl, Marie-Claude; Bouchard, Luigi
    Obesity and insulin resistance are common features of Type 2 Diabetes. A new protein called resistin has been shown to be secreted by adipocytes in mice and to influence insulin sensitivity. The goal of the present study was to investigate the associations between one polymorphism (g-420C>G) of the human resistin gene and phenotypes related to adiposity and glucose metabolism. We genotyped 725 (including 42 diabetics) adult subjects participating in the Québec Family Study (QFS) by a minisequencing method. Forty-two were diabetic subjects. Phenotypes measured were: body mass index (BMI) and waist circumference (WC), % body fat (PFAT) and fat mass (FM) assessed by under water weighing, abdominal total, subcutaneous and visceral fat assessed by computed tomography and fasting plasma glucose, insulin and C-peptide and their responses to an oral glucose tolerance test (OGTT). Comparisons between genotypes were performed in non-diabetic men (no.=280) and women (no.=403) separately by analyses of covariance (ANCOVA). Among men, g-420 G homozygotes had less visceral fat (p<0.05), lower levels of acute insulin responses to an OGTT and lower levels of C-peptide in a fasting state and in responses to an OGTT than carriers of the C allele (p<0.01). These associations were independent of age and adiposity but were not observed in women. These results suggest that in men, the human resistin gene is associated with reduced amount of visceral obesity and lower insulin secretory responses to a glucose load.
  • Publication
    Evidence for interaction between PPARG Pro12Ala and PPARGC1A Gly482Ser polymorphisms in determining type 2 diabetes intermediate phenotypes in overweight subjects
    (Thieme, 2009-06-17) Ruchat, Stéphanie-May; Bouchard, Claude; Pérusse, Louis; Rankinen, Tuomo; Weisnagel, John; Vohl, Marie-Claude
    Background: The peroxisome proliferator-activated receptor-γ (PPARG) Pro12Ala and the PPARG co-activator-1α (PPARGC1A) Gly482Ser polymorphisms (SNPs) have been associated with type 2 diabetes mellitus (T2DM) risk. We hypothesized that independent and interactive effects of the PPARG Pro12Ala and PPARGC1A Gly482Ser polymorphisms influence T2DM intermediate phenotypes. Material and Methods: PPARG Pro12Ala and PPARGC1A Gly482Ser SNPs were studied in 680 non diabetic subjects who underwent a 75 g oral glucose tolerant test (OGTT). Glucose and insulin plasma levels in the fasting state and derived from the OGTT were included in the present study. Results: We found significant independent effects of the PPARG and PPARGC1A variants on fasting insulin levels (p=0.02 for both), HOMA-IR (p=0.03 and p=0.02, respectively), insulin area under the curve (AUC) (p=0.007 and p=0.006, respectively) and 2-h glucose levels (p=0.02 for PPARGC1A). Furthermore, significant gene-gene interactions were found for fasting insulin, HOMA-IR and insulin AUC (p=0.03 for all). Carriers of the PPARGC1A Gly allele who were also PPARG Ala-carriers had higher fasting insulin levels (p=0.02), HOMA-IR (p=0.01) and insulin AUC (p=0.01) compared to the Ser/Ser-Ala+genotype combination, whereas no differences between the PPARGC1A genotypes among the PPARG Pro/Pro carriers were observed. Conclusion: Together, these results showed that PPARG Pro12Ala and PPARGC1A Gly482Ser variants are associated, alone and in interaction, with insulin and glucose homeostasis and suggest that gene-gene interactions should be taken into account in candidate gene studies of T2DM to identify subjects with markedly different risks of developing the disease.
  • Publication
    Evidence of interaction between type 2 diabetes susceptibility genes and dietary fat intake for adiposity and glucose homeostasis-related phenotypes
    (S. Karger, 2010-03-09) Ruchat, Stéphanie-May; Elks, Cathy E.; Bouchard, Claude; Loos, Ruth; Pérusse, Louis; Weisnagel, John; Vohl, Marie-Claude; Rankinen, Tuomo
    Background/Aims: Genome-wide association studies have led to the identification of several susceptibility genes for type 2 diabetes mellitus (T2DM). The objective of this study was to test the hypothesis that the associations between single nucleotide polymorphisms (SNPs) in these genes and adiposity and glucose homeostasis-related phenotypes are influenced by dietary fat intake. Methods: Thirty-three SNPs in 9 T2DM genes (CDKAL1, CDKN2A/B, HHEX, HNF1B, IGF2BP2, KCNJ11, SLC30A8, TCF7L2 and WFS1) were tested in a maximum of 669 subjects from the Quebec Family Study. Subjects were measured for several adiposity indices and underwent a 75-gram oral glucose tolerance test. Total fat intake was estimated from a 3-day dietary record. Results: We observed 13 significant (p ^ 0.01) SNP-dietary fat interactions. Among them, IGF2BP2 rs4402960, alone or in interaction with dietary fat intake, influenced abdominal total fat (ATF: SNP effect, p = 0.006, interaction effect, p = 0.009) and abdominal visceral fat (AVF: SNP effect, p = 0.007, interaction effect, p = 0.01). Similarly, TCF7L2 rs12573128 alone or in interaction with dietary fat intake, influenced insulin sensitivity (SNP effect and interaction effect, p ^ 0.008) and glucose tolerance (SNP effect p ^ 0.009 and interaction effect, p ^ 0.01). Conclusion: These results suggest that gene-dietary fat interactions may influence glucose homeostasis-related phenotypes and play an important role in determining the increased risk of diabetes associated with the T2DM susceptibility genes.