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Dr. Christine Demeilliers
Laboratoire TIMC-IMAG, UMR-CNRS 5525 Team : " Environment and Population Health Prevention" Domaine de La Merci 38706 La Tronche Cedex, France

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0 Environmental Health
0 Heavy Metals
0 environmental contaminants
0 Polycyclic aromatic hydrocarbon
0 Persistent organic pollutant

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Journal article
Published: 26 November 2018 in Chemosphere
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Cadmium (Cd) is a metal which may participate in the development of type II diabetes even if Cd exposure levels are mild. However, experimental studies focusing on daily environmentally relevant doses are scarce, particularly for glucose metabolism of the offspring of chronically exposed mothers. The aim is to measure the impact of maternal low level Cd exposure on glucose and lipid metabolism of offspring. Female rats were exposed to 0, 50 or 500 μg kg−1.d−1 of CdCl2, 21 days before mating and during 21 days of gestation and 21 days of lactation. Pups exposure was organized in 3 groups (control, Cd1, Cd2) according to renal dams' Cd burden. Glucose and lipid metabolism's parameters were measured for the pups on post-natal day 21, 26 and 60. Maternal Cd exposure led to significant amounts of Cd in the liver and kidney of pups. At weaning, insulin secretion upon glucose stimulation was unchanged, but the removal of circulating glucose was slower for pups born from the lowest impregnated dams (Cd1). Five days after, glucose tolerance of all groups was identical. Thus, this loss of insulin sensitivity was reversed, in part by increased adiponectin secretion for the Cd1 group. Furthermore, pups from dams accumulating the highest levels of Cd (Cd2) exhibited a compensatory increased insulin pancreatic secretion, together with increased circulating non-esterified fatty acids, indicating the establishment of insulin resistance, 2 months after birth. This study has demonstrated the influence of maternal exposure to low levels of Cd on glucose homeostasis in the offspring that might increase the risk of developing type II diabetes later in life.

ACS Style

Adeline Jacquet; Damien Barbeau; Josiane Arnaud; Samer Hijazi; Florence Hazane-Puch; Frédéric Lamarche; Charline Quiclet; Karine Couturier; Eric Fontaine; Jean-Marc Moulis; Christine Demeilliers. Impact of maternal low-level cadmium exposure on glucose and lipid metabolism of the litter at different ages after weaning. Chemosphere 2018, 219, 109 -121.

AMA Style

Adeline Jacquet, Damien Barbeau, Josiane Arnaud, Samer Hijazi, Florence Hazane-Puch, Frédéric Lamarche, Charline Quiclet, Karine Couturier, Eric Fontaine, Jean-Marc Moulis, Christine Demeilliers. Impact of maternal low-level cadmium exposure on glucose and lipid metabolism of the litter at different ages after weaning. Chemosphere. 2018; 219 ():109-121.

Chicago/Turabian Style

Adeline Jacquet; Damien Barbeau; Josiane Arnaud; Samer Hijazi; Florence Hazane-Puch; Frédéric Lamarche; Charline Quiclet; Karine Couturier; Eric Fontaine; Jean-Marc Moulis; Christine Demeilliers. 2018. "Impact of maternal low-level cadmium exposure on glucose and lipid metabolism of the litter at different ages after weaning." Chemosphere 219, no. : 109-121.

Journal article
Published: 01 September 2018 in Chemosphere
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Several epidemiological and animal studies suggest a positive association between cadmium (Cd) exposure and incidence of type 2 diabetes, but the association remains controversial. Besides, the experimental data have mainly been obtained with relatively high levels of Cd, over various periods of time, and with artificial routes of administration. Do environmental exposures to Cd induce significant disruption of glucose metabolism? Adults Wistar rats were exposed for three months to 0, 5, 50 or 500 μg kg−1 d−1 of CdCl2 in drinking water. Relevant parameters of glucose homeostasis were measured. Cd accumulated in plasma, kidney and liver of rats exposed to 50 and 500 μg kg−1 d−1, without inducing signs of organ failure. In rats drinking 5 μg kg−1 d−1 for 3 months, Cd exposure did not lead to any significant increase of Cd in these organs. At 50 and 500 μg kg−1 d−1 of Cd, glucose and insulin tolerance were unchanged in both sexes. However, females exhibited a significant increase of both fasting and glucose-stimulated plasma insulin that was assigned to impaired hepatic insulin extraction as indicated by unaltered fasting C-peptide plasma levels. Glucose homeostasis is sensitive to chronic Cd exposure in a gender-specific way. Moreover, this study proves that an environmental pollutant such as Cd can have, at low concentrations, an impact on the glucose homeostatic system and it highlights the importance of a closer scrutiny of the underlying environmental causes to understand the increased incidence of type 2 diabetes.

ACS Style

Adeline Jacquet; Josiane Arnaud; Isabelle Hininger-Favier; Florence Hazane-Puch; Karine Couturier; Marine Lénon; Frédéric Lamarche; Fayçal Ounnas; Eric Fontaine; Jean-Marc Moulis; Christine Demeilliers. Impact of chronic and low cadmium exposure of rats: sex specific disruption of glucose metabolism. Chemosphere 2018, 207, 764 -773.

AMA Style

Adeline Jacquet, Josiane Arnaud, Isabelle Hininger-Favier, Florence Hazane-Puch, Karine Couturier, Marine Lénon, Frédéric Lamarche, Fayçal Ounnas, Eric Fontaine, Jean-Marc Moulis, Christine Demeilliers. Impact of chronic and low cadmium exposure of rats: sex specific disruption of glucose metabolism. Chemosphere. 2018; 207 ():764-773.

Chicago/Turabian Style

Adeline Jacquet; Josiane Arnaud; Isabelle Hininger-Favier; Florence Hazane-Puch; Karine Couturier; Marine Lénon; Frédéric Lamarche; Fayçal Ounnas; Eric Fontaine; Jean-Marc Moulis; Christine Demeilliers. 2018. "Impact of chronic and low cadmium exposure of rats: sex specific disruption of glucose metabolism." Chemosphere 207, no. : 764-773.

Journal article
Published: 22 March 2018 in Toxics
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The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level. The mitochondria reorganized in response to the challenge by favoring fission as measured by increased circularity at cadmium levels already ten-fold below the median lethal dose. However, the energy charge and respiratory flux devoted to adenosine triphosphate synthesis were only affected at the onset of cellular death. The present data indicate that mitochondria participate in the adaptation of β-cells to even a moderate cadmium burden without losing functionality, but their impairment in the long run may contribute to cellular dysfunction, when viability and β-cells mass are affected as observed in diabetes.

ACS Style

Adeline Jacquet; Cécile Cottet-Rousselle; Josiane Arnaud; Kevin Julien Saint Amand; Raoua Ben Messaoud; Marine Lénon; Christine Demeilliers; Jean-Marc Moulis. Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses. Toxics 2018, 6, 20 .

AMA Style

Adeline Jacquet, Cécile Cottet-Rousselle, Josiane Arnaud, Kevin Julien Saint Amand, Raoua Ben Messaoud, Marine Lénon, Christine Demeilliers, Jean-Marc Moulis. Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses. Toxics. 2018; 6 (2):20.

Chicago/Turabian Style

Adeline Jacquet; Cécile Cottet-Rousselle; Josiane Arnaud; Kevin Julien Saint Amand; Raoua Ben Messaoud; Marine Lénon; Christine Demeilliers; Jean-Marc Moulis. 2018. "Mitochondrial Morphology and Function of the Pancreatic β-Cells INS-1 Model upon Chronic Exposure to Sub-Lethal Cadmium Doses." Toxics 6, no. 2: 20.

Journal article
Published: 01 April 2017 in Clinical Nutrition Experimental
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Background: This study aimed at exploring whether moderate ethanol drinking may have adverse effects on the fatty acids composition and on mitochondrial DNA (mtDNA) of rat brain. A secondary aim was to examine whether dietary antioxidant anthocyanins (ACN) can be protective. Methods: One group of rats received ethanol 12% and another water as an exclusive liquid to drink for 8 weeks. In order to test the impact of ACN consumption, two other groups of rats were fed an ACN-rich diet in combination with either ethanol or water. Brain fatty acids were measured by gas chromatography and mtDNA alterations, markers of mitochondrial suffering, were studied through an original real-time qPCR-based protocol. Results: Linoleic acid (LA, 18:2n-6) and eicosadienoic acid (20:2n-6) were significantly decreased, by 12% and 31% respectively, in the brains of both ethanol groups. The other brain lipids, including arachidonic acid (20:4n-6) and n-3 polyunsaturated fatty acids, were not modified. These changes were associated with a significant increase in deleted mtDNA (by 28%) in the ethanol group, without total mtDNA depletion. The ACN-rich diet prevented the increase in mtDNA common deletion (mtDNA CD). Conclusion: These data demonstrate that moderate ethanol drinking reduces certain brain n-6 and results in mtDNA injury. The antioxidant anthocyanins protect brain mtDNA but do not restore normal n-6 levels. Further studies are required to investigate the consequences of a decrease in n-6 levels in brain

ACS Style

Christine Demeilliers; Marie-Claire Toufektsian; Patricia Salen; François Laporte; Katia Petroni; Michel De Lorgeril. Ethanol drinking, brain mitochondrial DNA, polyunsaturated fatty acids and effects of dietary anthocyanins. Clinical Nutrition Experimental 2017, 12, 11 -19.

AMA Style

Christine Demeilliers, Marie-Claire Toufektsian, Patricia Salen, François Laporte, Katia Petroni, Michel De Lorgeril. Ethanol drinking, brain mitochondrial DNA, polyunsaturated fatty acids and effects of dietary anthocyanins. Clinical Nutrition Experimental. 2017; 12 ():11-19.

Chicago/Turabian Style

Christine Demeilliers; Marie-Claire Toufektsian; Patricia Salen; François Laporte; Katia Petroni; Michel De Lorgeril. 2017. "Ethanol drinking, brain mitochondrial DNA, polyunsaturated fatty acids and effects of dietary anthocyanins." Clinical Nutrition Experimental 12, no. : 11-19.

Journal article
Published: 01 October 2016 in Chemosphere
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Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants present in dietary fats. Most studies evaluating PCB effects have been conducted with a single compound or a mixture of PCBs given as a single acute dose. The purpose of this study was to evaluate in vivo PCB toxicity in a realistic model of exposure: a low daily dose of PCBs (twice the tolerable daily intake (TDI)), chronically administered (8 weeks) to rats in contaminated goat milk. Liver and brain PCB toxicities were investigated by evaluating oxidative stress status and mitochondrial function. PCB toxicity in the liver was also estimated by transaminase enzymatic activity. This study shows that even at low doses, chronic PCB exposure resulted in a statistically significant reduction of mitochondrial function in liver and brain. In the liver, oxygen consumption in the condition of adenosine triphosphate (ATP) production (state 3) decreased by 22-29% (p < 0.01), according to the respiratory substrates. In the brain, respiratory chain complexes II and III were reduced by 24% and 39%, respectively (p < 0.005). The exposed rats presented higher lipid peroxidation status (+20%, p < 0.05) and transaminase activity (+30%, p < 0.05) in the blood. Thus, our study showed that exposure of rats to a daily realistic dose of PCBs (twice the TDI in a food complex mixture of environmental origin) resulted in multiple disruptions in the liver and brain.

ACS Style

Fayçal Ounnas; Florence Privé; Fréderic Lamarche; Patricia Salen; Isabelle Favier-Hininger; Philippe Marchand; Bruno Le Bizec; Anais Venisseau; Cécile Batandier; Eric Fontaine; Michel de Lorgeril; Christine Demeilliers. A relevant exposure to a food matrix contaminated environmentally by polychlorinated biphenyls induces liver and brain disruption in rats. Chemosphere 2016, 161, 80 -88.

AMA Style

Fayçal Ounnas, Florence Privé, Fréderic Lamarche, Patricia Salen, Isabelle Favier-Hininger, Philippe Marchand, Bruno Le Bizec, Anais Venisseau, Cécile Batandier, Eric Fontaine, Michel de Lorgeril, Christine Demeilliers. A relevant exposure to a food matrix contaminated environmentally by polychlorinated biphenyls induces liver and brain disruption in rats. Chemosphere. 2016; 161 ():80-88.

Chicago/Turabian Style

Fayçal Ounnas; Florence Privé; Fréderic Lamarche; Patricia Salen; Isabelle Favier-Hininger; Philippe Marchand; Bruno Le Bizec; Anais Venisseau; Cécile Batandier; Eric Fontaine; Michel de Lorgeril; Christine Demeilliers. 2016. "A relevant exposure to a food matrix contaminated environmentally by polychlorinated biphenyls induces liver and brain disruption in rats." Chemosphere 161, no. : 80-88.

Journal article
Published: 26 March 2015 in International Journal of Food Sciences and Nutrition
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The main aim of this study was to compare the effects of two wheat aleurone (WA) fractions on circulating n-3 fatty acids in rats. We demonstrated that only the fraction able to induce the highest urinary excretion of polyphenol metabolites (>1µmol) resulted in a significant increase in plasma level of Eicosapentanoic acid (+22%, p < 0.05). While other constituents of whole wheat can be involved in this response, our data suggest that cereals containing high levels of phenolic compounds can increase blood n-3 without affecting n-6 fatty acids. Further studies are required to confirm this hypothesis and explore the underlying biological mechanisms.

ACS Style

Fayçal Ounnas; Patricia Salen; Christine Demeilliers; Luca Calani; Francesca Scazzina; Florence Hazane-Puch; François Laporte; Camilla Melegari; Daniele Del Rio; Michel De Lorgeril. Wheat aleurone fractions and plasman−3 fatty acids in rats. International Journal of Food Sciences and Nutrition 2015, 66, 391 -394.

AMA Style

Fayçal Ounnas, Patricia Salen, Christine Demeilliers, Luca Calani, Francesca Scazzina, Florence Hazane-Puch, François Laporte, Camilla Melegari, Daniele Del Rio, Michel De Lorgeril. Wheat aleurone fractions and plasman−3 fatty acids in rats. International Journal of Food Sciences and Nutrition. 2015; 66 (4):391-394.

Chicago/Turabian Style

Fayçal Ounnas; Patricia Salen; Christine Demeilliers; Luca Calani; Francesca Scazzina; Florence Hazane-Puch; François Laporte; Camilla Melegari; Daniele Del Rio; Michel De Lorgeril. 2015. "Wheat aleurone fractions and plasman−3 fatty acids in rats." International Journal of Food Sciences and Nutrition 66, no. 4: 391-394.