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Tchernof, André

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CHU de Québec-Université Laval
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  • Publication
    Accès libre
    Effects of the traditional Mediterranean diet on adiponectin and leptin concentrations in men and premenopausal women : do sex differences exist?
    (Nature Publishing Group., 2014-03-05) Bédard, Alexandra; Corneau, Louise; Lamarche, Benoît; Lemieux, Simone; Dodin-Dewailly, Sylvie; Tchernof, André
    Background/Objectives: Most of the interventional studies have investigated the impact of the diet on adiponectin and leptin concentrations only in men or in women. Consequently, it is still unknown whether the consumption of a healthy diet influences in a sex-specific manner these adipocytokines. We examined sex differences in the effects of the Mediterranean diet (MedDiet) on adiponectin and leptin concentrations, and determined whether changes in these adipocytokines are associated with changes in cardiovascular risk factors in both sexes. Subjects/Methods: Participants were 38 men and 32 premenopausal women (24–53 years) with slightly elevated low-density lipoprotein cholestrol concentrations (3.4–4.9¿mmol/l) or total cholesterol/high-density lipoprotein cholestrol (HDL-C)greater than or equal to5.0. Adiponectin, leptin and cardiovascular risk factors were measured before and after a 4-week fully controlled isoenergetic MedDiet. Results: Adiponectin concentration decreased in response to the MedDiet, but this decrease reached statistical significance only in men (P<0.001 for men and P=0.260 for women; sex-by-time interaction, P=0.072). Adjustments for body weight or waist circumference did not change results obtained. Changes in adiponectin were positively associated with concomitant variations in HDL-C in men (r=0.52, P=0.003) and with variations in apolipoprotein A-1 and insulin sensitivity as calculated by both the homeostasis model assessment index for insulin sensitivity and Cederholm indices in women (respectively, r=0.44, P=0.021; r=0.79, P<0.001 and r=0.47, P=0.020). The MedDiet had no impact on leptin and the leptin-to-adiponectin ratio in both sexes. Conclusions: Results suggest a sex difference in adiponectin response to the short-term consumption of the MedDiet, with only men experiencing a decrease. Also sex-specific patterns of associations between changes in adiponectin concentration and changes in cardiovascular risk factors were observed.
  • Publication
    Accès libre
    Interleukin-1β and prostaglandin-synthesizing enzymes as modulators of human omental and subcutaneous adipose tissue function
    (Churchill Livingstone, 2018-11-29) Labrecque, Jennifer; Pelletier, Mélissa; Gauthier, Marie-Frédérique; Michaud, Andréanne; Tchernof, André; Julien, François; Bouvet-Bouchard, Léonie
    IL-1β stimulates expression of prostaglandin (PG)-synthesizing enzymes cyclooxygenase (COX)-2 and aldo-keto reductase (AKR)1B1 in human preadipocytes. We aimed to examine the impact of IL-1β, COX-2 and AKR1B1 on markers of human visceral and subcutaneous adipose tissue function, and to assess whether PG synthesis by these enzymes mediates IL-1β effects. Omental and subcutaneous fat samples were obtained from bariatric surgery patients. PG release and expression of inflammatory and adipogenic markers were assessed in explants treated with COX-2 inhibitor NS-398 or AKR1B1 inhibitor Statil, with or without IL-1β. Preadipocyte differentiation experiments were also performed. IL-1β decreased expression of PPARγ in both fat depots compared to control and increased expression of NF-κB1, IL-6, CCL-5, ICAM-1 and VEGFA, especially in visceral fat for IL-6, CCL-5 and VEGFA. Adding Statil or NS-398 to IL-1β blunted PGF2α and PGE2 release, but did not alter IL-1β effects on adipose tissue function markers. IL-1β down-regulated adipocyte differentiation whereas NS-398 alone increased this process. However, NS-398 did not prevent IL-1β inhibition of adipogenesis. We conclude that IL-1β induces a pro-inflammatory response in human adipose tissues, particularly in visceral fat, and acts independently of concomitant PG release. IL-1β and COX-2 appear to be critical determinants of adipose tissue pathophysiologic remodeling in obesity.
  • Publication
    Accès libre
    Oxidative activity of 17β-hydroxysteroid dehydrogenase on testosterone in male abdominal adipose tissues and cellular localization of 17β-HSD type 2
    (North-Holland, 2015-06-26) Fouad Mansour, Mohamed; Boulet, Marie Michèle; Poirier, Donald; Luu The, Van; Brochu, Gaétan; Cianflone, Katherine M.; Lebel, Stefane; Pelletier, Mélissa; Fradette, Julie; Tchernof, André; Mayrand, Dominique
    Testosterone can be converted into androstenedione (4-dione) by 17β-hydroxysteroid dehydrogenase (HSD) activity likely performed by 17β-HSD type 2. Our objective was to evaluate the rate of testosterone conversion to 4-dione as well as expression and localization of 17β-HSD type 2 in omental (OM) vs. subcutaneous (SC) adipose tissues of men. Formation of 4-dione from testosterone was significantly higher in homogenates (p ≤ 0.001) and explants (p ≤ 0.01) of OM than SC tissue. Microscopy analyses and biochemical assays in cell fractions localized the enzyme in the vasculature/endothelial cells of adipose tissues. Conversion of testosterone to 4-dione was weakly detected in most OM and/or SC preadipocyte cultures. Positive correlations were found between 17β-HSD type 2 activity in whole tissue and BMI or SC adipocyte diameter. We conclude that conversion of testosterone to 4-dione detected in abdominal adipose tissue is caused by 17β-HSD type 2 which is localized in the vasculature of the adipose compartment.
  • 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
    Accès libre
    Differential methylation of inflammatory and insulinotropic genes after metabolic surgery in women
    (iMed Pub LLC, 2015-10-03) Guénard, Frédéric; Marceau, Picard; Cianflone, Katherine M.; Deshaies, Yves; Vohl, Marie-Claude; Tchernof, André; Kral, John G.
    Context: Biliopancreatic diversion with duodenal switch (BPD-DS), a metabolic bariatric operation, induces durable loss of excess weight and reduced cardiometabolic risk. Altered epigenetic marks are mechanistically associated with environment-driven phenotypic variations. Objective: The current study aimed to compare gene methylation levels before and after BPD-DS to identify epigenetic marks potentially linked to metabolic improvements induced by BPD-DS. Design and patients: Metabolic risk factors and gene methylation levels of 20 women studied mean 12 years (range 4-22) after BPD-DS were compared to those of 20 severely obese surgical candidates as controls, matched for pre-surgical age, body mass index and dyslipidemia and hypertension prevalences. Whole-genome blood DNA methylation analysis enabled between-group differential methylation analyses. We calculated correlations between methylation levels of the most differentially methylated CpG sites and plasma glucose and insulin levels and HOMA-IR. Results: Differential methylation analysis identified 15,343 genes demonstrating at least one differentially methylated CpG site (p<1.43x10-7). Diabetic and inflammation/immune functions were among the most overrepresented from the 200 genes exhibiting the largest group differences in methylation levels. CpG sites methylation levels of genes related to insulin action correlated significantly with fasting insulin levels and homeostatic model of insulin resistance (p≤0.002 for all). Conclusion: These findings suggest that differential methylation levels in obese controls versus treated women may partially explain the durable metabolic improvements after BPD-DS.
  • Publication
    LINE-1 methylation in visceral adipose tissue of severely obese individuals is associated with metabolic syndrome status and related phenotypes.
    (Springer Nature, 2012-07-02) Biron, Simon; Biertho, Laurent; Pérusse, Louis; Lescelleur, Odette; Bélisle, Alexandre; Turcot, Valérie; Marceau, Simon; Vohl, Marie-Claude; Deshaies, Yves; Tchernof, André
    Background: Epigenetic mechanisms may be involved in the regulation of genes found to be differentially expressed in the visceral adipose tissue (VAT) of severely obese subjects with (MetS+) versus without (MetS-) metabolic syndrome (MetS). Long interspersed nuclear element 1 (LINE-1) elements DNA methylation levels (% meth) in blood, a marker of global DNA methylation, have recently been associated with fasting glucose, blood lipids, heart diseases and stroke. Aim: To test whether LINE-1%meth levels in VAT are associated with MetS phenotypes and whether they can predict MetS risk in severely obese individuals. Methods: DNA was extracted from VAT of 34 men (MetS-: n = 14, MetS+: n = 20) and 152 premenopausal women (MetS-: n = 84; MetS+: n = 68) undergoing biliopancreatic diversion for the treatment of obesity. LINE-1%meth levels were assessed by pyrosequencing of sodium bisulfite-treated DNA. Results: The mean LINE-1%meth in VAT was of 75.8% (SD = 3.0%). Multiple linear regression analyses revealed that LINE-1%meth was negatively associated with fasting glucose levels (β = -0.04; P = 0.03), diastolic blood pressure (β = -0.65; P = 0.03) and MetS status (β = -0.04; P = 0.004) after adjustments for the effects of age, sex, waist circumference (except for MetS status) and smoking. While dividing subjects into quartiles based on their LINE-1%meth (Q1 to Q4: lower %meth to higher %meth levels), greater risk were observed in the first (Q1: odds ratio (OR) = 4.37, P = 0.004) and the second (Q2: OR = 4.76, P = 0.002) quartiles compared to Q4 (1.00) when adjusting for age, sex and smoking. Conclusions: These results suggest that lower global DNA methylation, assessed by LINE-1 repetitive elements methylation analysis, would be associated with a greater risk for MetS in the presence of obesity.
  • Publication
    Accès libre
    Characterization and visualization of the liposecretion process taking place during ceiling culture of human mature adipocytes
    (Wistar Institute of Anatomy and Biology, 2019-07-15) Marette, André.; Gauthier, Marie-Frédérique; Bellmann, Kerstin; Ostinelli, Giada; Côté, Julie Anne; Brochu, Dannick; Tchernof, André; Julien, François; Lebel, Stéfane
    Objective To investigate and further characterize the process of mature adipocyte dedifferentiation. Our hypothesis was that dedifferentiation does not involve mitosis but rather a phenomenon of liposecretion. Methods Mature adipocytes were isolated by collagenase digestion of human adipose tissue samples. Ceiling cultures were established using our six-well plate model. Cells were treated with cytosine β-d-arabinofuranoside (AraC) or vincristine (VCR), two agents blocking cell division, and were compared with vehicle. Liposecretion events were visualized by time-lapse microscopy, with and without AraC in adipocytes transducted with a baculovirus. Microscopic analyses were performed after labeling phosphorylated histone 3 and cyclin B1 in ceiling cultures. Results Treatment with AraC almost entirely prevented the formation of fibroblasts up to 12 days of ceiling culture. Similar results were obtained with VCR. The antimitotic effectiveness of the treatment was confirmed in fibroblast cultures from the adipose tissue stromal-vascular fraction by proliferation assays and colony-forming unit experiments. Using time-lapse microscopy, we visualized liposecretion events in which a large lipid droplet was rapidly secreted from isolated mature adipocytes. The same phenomenon was observed with AraC. This was observed in conjunction with histone 3 phosphorylation and cyclin B1 segregation to the nucleus. Conclusion Our results support the notion that dedifferentiation involves rapid secretion of the lipid droplet by the adipocytes with concomitant generation of fibroblast-like cells that subsequently proliferate to generate the dedifferentiated adipocyte population during ceiling culture. The presence of mitotic markers suggests that this process involves cell cycle progression, although cell division does not occur.
  • Publication
    Genetic contribution to C-reactive protein levels in severe obesity
    (Academic Press, 2011-12-01) Turcot, Valérie; Guénard, Frédéric; Faucher, Geneviève; Bouchard, Luigi; Hould, Frédéric-Simon; Garneau, Véronique; Marceau, Picard; Houde, Alain; Vohl, Marie-Claude; Tchernof, André; Deshaies, Yves; Lebel, Stéfane; Bergeron, Jean
    Obese individuals are characterized by a chronic, low-grade inflammatory state. Increased levels of C-reactive protein (CRP), a marker of inflammation, have been observed in subjects with the metabolic syndrome. We have previously reported that genes encoding proteins involved in the anti-inflammatory and immune response are differentially expressed in visceral adipose tissue of obese men with or without the metabolic syndrome. Among these genes, the interferon-gamma-inducible protein 30 (IFI30), CD163 molecule (CD163), chemokine (C-X-C motif) ligand 9 (CXCL9) and thymic stromal lymphopoietin (TSLP), were selected for further genetic analyses. The aim of the study was to verify whether IFI30, CD163, CXCL9 and TSLP gene polymorphisms contribute to explain the inter-individual variability of the inflammatory profile of obesity assessed by plasma high-sensitivity CRP concentrations. A total of 1185 severely obese individuals were genotyped for single nucleotide polymorphisms (SNPs) covering most of the sequence-derived genetic variability at the IFI30, CD163, CXCL9 and TSLP gene loci (total of 27 SNPs). Following measurement of plasma CRP levels, subjects were divided into two groups, low vs. high using the median value of plasma CRP levels (8.31 mg/L) as a cutoff point. Genotype frequencies were compared between groups. Associations between genotypes and plasma CRP levels (continuous variable) were also tested after adjustments for age, sex, smoking and BMI. The rs11554159 and rs7125 IFI30 SNPs showed a significant difference in genotype frequencies (p < 0.05) between subgroups of low vs. high plasma CRP levels (wild type homozygotes: rs11554159 = 47% vs. 55%, rs7125 = 31% vs. 24%, for low vs. high CRP groups, respectively). The association between rs11554159 and CRP levels as a continuous variable remained significant (p = 0.004). Both carriers of the GA and AA genotypes demonstrated, on average, a 13% lower CRP levels in comparison with GG homozygotes. No association was observed between SNPs in the CD163, CXCL9 and TSLP genes and CRP levels. The IFI30 rs11554159 polymorphism could partially explain the inter-individual variability observed in the inflammatory profile associated with obesity.
  • Publication
    Accès libre
    Body mass index is associated with epigenetic age acceleration in the visceral adipose tissue of subjects with severe obesity
    (Springer, 2019-12-02) Guénard, Frédéric; Toro Martin, Juan de; Hould, Frédéric-Simon; Vohl, Marie-Claude; Lebel, Stéfane; Tchernof, André; Julien, François; Marceau, Simon
    Background There is solid evidence that obesity induces the acceleration of liver epigenetic aging. However, unlike easily accessible blood or subcutaneous adipose tissue, little is known about the impact of obesity on epigenetic aging of metabolically active visceral adipose tissue (VAT). Herein, we aimed to test whether obesity accelerates VAT epigenetic aging in subjects with severe obesity. Results A significant and positive correlation between chronological age and epigenetic age, estimated with a reduced version of the Horvath’s epigenetic clock, was found in both blood (r = 0.78, p = 9.4 × 10−12) and VAT (r = 0.80, p = 1.1 × 10−12). Epigenetic age acceleration, defined as the residual resulting from regressing epigenetic age on chronological age, was significantly correlated with body mass index (BMI) in VAT (r = 0.29, p = 0.037). Multivariate linear regression analysis showed that, after adjusting for chronological age, sex and metabolic syndrome status, BMI remained significantly associated with epigenetic age acceleration in VAT (beta = 0.15, p = 0.035), equivalent to 2.3 years for each 10 BMI units. Binomial logistic regression showed that BMI-adjusted epigenetic age acceleration in VAT was significantly associated with a higher loss of excess body weight following biliopancreatic diversion with duodenal switch surgery (odds ratio = 1.21; 95% CI = 1.04–1.48; p = 0.03). Conclusions Epigenetic age acceleration increases with BMI in VAT, but not in blood, as previously reported in liver. These results suggest that obesity is associated with epigenetic age acceleration of metabolically active tissues. Further studies that deepen the physiological relevance of VAT epigenetic aging will help to better understand the onset of metabolic syndrome and weight loss dynamics following bariatric surgery.
  • Publication
    Molecular screening of the 11β-HSD1 gene in men characterized by the metabolic syndrome
    (Wiley, 2012-09-06) Brouillette, Charles; Houde, Alain; Vohl, Marie-Claude; Després, Jean-Pierre; Robitaille, Julie; Tchernof, André
    Adipose tissue type 1 11β‐hydroxysteroid dehydrogenase (11β‐HSD1), which generates hormonally active cortisol from inactive cortisone, has been shown to play a central role in adipocyte differentiation and abdominal obesity‐related metabolic complications. The objective was to investigate whether genetic variations in the human 11 β‐HSD1 gene are associated with the metabolic syndrome among French‐Canadian men. We sequenced all exons, the exon‐intron splicing boundaries, and 5′ and 3′ regions of the human 11 β‐HSD1 gene in 36 men with the metabolic syndrome, as defined by the National Cholesterol Education Program‐Adult Treatment Panel III, and two controls. Three intronic sequence variants were identified: two single‐nucleotide polymorphisms in intron 3 (g.4478T>G) and intron 4 (g.10733G>C) and one insertion in intron 3 (g.4437‐4438insA). The relative allele frequency was 19.6%, 22.1%, and 19.6% for the g.4478G, g.10733C, and g.4438insA alleles, respectively. One single‐nucleotide polymorphism was identified in exon 6 (c.744G>C or G248G). The frequency of the c.744C allele was only 0.46% in a sample of 217 men. Variants were not associated with components of the metabolic syndrome except for plasma apolipoprotein B levels. In conclusion, molecular screening of the 11 β‐HSD1 gene did not reveal any sequence variations that can significantly contribute to the etiology of the metabolic syndrome among French‐Canadians.