Research on obesity, weight loss, and food addiction (FA) suggested a strong relationship between use of food additives and the brain's addictive response to food. Previous researchers have examined (FA) and have identified certain food additives such as monosodium glutamate (MSG) and high fructose corn syrup (HFCS) as contributors to food addiction and overeating. Social cognitive theory (SCT) has also been effective in addressing addictive behaviors such as drug addiction, alcohol addiction, and smoking cessation (Bricker et al., 2010). However, researchers had not examined food addiction, social cognitive theory, and obesity in the same study. The purpose of this quantitative, quasi-experimental study was to compare the effects of SCT-based health information and non-SCT-based health information on FA among obese and overweight women. The Yale Food Addiction Scale (YFAS) was used to measure changes in FA and food addiction symptoms among 84 obese and overweight women who received SCT-based health information and non-SCT-based health information. Total scores from pretests and posttests were analyzed using analysis of covariance. Between-group differences on the symptom count posttest scores of the YFAS were analyzed using analysis of variance. Scores were used to determine the difference in FA and FA symptoms between nonrandomized groups. Although the results were not statistically significant, almost 60% (n = 50) of participants experienced a favorable decrease in FA symptoms and experienced weight loss. Findings may provide a basis for determining additional options for health professionals to address obesity and FA patterns.

La prévention nutritionnelle du syndrome métabolique dont l'incidence ne cesse d'augmenter dans les pays industrialisés, entraînant des risques accrus de diabètes et de maladies cardiovasculaires, apparaît comme un enjeu important de Santé publique. La découverte récente des relations étroites entre l'insulinorésistance, signe majeur du syndrome métabolique et le stress oxydant, nous a conduit à considérer les nutriments, à la fois antioxydants et potentiellement insulino-sensibilisateurs, comme des facteurs nutritionnels de choix dans la stratégie de prévention du syndrome métabolique. Trois microconstituants de notre alimentation ont été étudiés: les polyphénols de la cannelle et du thé vert, le chrome III, oligoélément essentiel. Sur un modèle animal de syndrome métabolique, le rat fructose, les extraits de thé vert, riches en épigallocatéchine gallate EGCG, non seulement exercent une protection antioxydante sur les principales cibles impliquées dans les complications oxydatives du diabète (lipides, protéines et acides nucléiques) mais, sont également de puissants modulateurs des métabolismes glucidiques et lipidiques. Les extraits de thé vert activent la cascade de signalisation de l'insuline et modifient l'expression des gènes impliqués dans son métabolisme, et en particulier augmente l'expression des Glut-4 ce qui pourrait expliquer l'amélioration de la glycémie sur notre modèle de syndrome métabolique. Chez l'homme comme chez l'animal, les régimes comportant des extraits aqueux de cannelle, exercent une protection antioxydante, et une corrélation avec la régulation de la glycémie a été trouvée. En ce qui concerne le chrome III, nous apportons, sur cultures cellulaires, les preuves de son absence de génotoxicité à des doses très supérieures à celles utilisées dans les supplémentations chez l'homme, ainsi que des données nouvelles sur son mécanisme d'action antioxydant, impliquant un mécanisme moléculaire d'induction de l'expression de gènes modulant la défense antioxydante et la réparation de l'ADN. Ces premiers résultats sont expérimentaux. Ils démontrent la pertinence d'une association de nutriments antioxydants et insulino potentialisateurs dans la prévention du syndrome métabolique. Cependant, les nombreuses limites dues aux conditions expérimentales imposent de poursuivre ce travail par des études d'intervention chez l'homme, associant dans une supplémentation combinée, extraits de thé vert, extraits aqueux de cannelle et histidinate de chrome.

<p>Methylglyoxal (MG) is a reactive glucose metabolite and a known causative factor for hypertension and diabetes. Hydrogen sulfide (H₂S), on the other hand, is a gasotransmitter with multifaceted physiological functions, including anti-oxidant and vasodilatory properties. The present study demonstrates that MG and H₂S can interact with and modulate each other's functions. Upon <i>in vitro</i> incubations, we found that MG and H₂S can directly interact to form three possible MG-H₂S adducts. Furthermore, the endogenous production level of MG or H₂S was significantly reduced in a concentration-dependent manner in rat vascular smooth muscle cells (A-10 cells) treated with NaHS, a H₂S donor, or MG, respectively. Indeed, MG-treated A-10 cells exhibited a concentration-dependent down-regulation of the protein and activity level of cystathionine &gamma;-lyase (CSE), the main H₂S-generating enzyme in the vasculature. Moreover, H₂S can induce the inhibition of MG-generated ROS production in a concentration-dependent manner in A-10 cells. In 6-22 week-old CSE knockout male mice (CSE^-/-), mice with lower levels of vascular H₂S, we observed a significant elevation in MG levels in both plasma and renal extracts. Renal triosephosphates were also significantly increased in the 6-22 week-old CSE^-/- mice. To identify the source of the elevated renal MG levels, we found that the activity of fructose-1,6-bisphosphatase (FBPase), the rate-limiting enzyme in gluconeogenesis, was significantly down-regulated, along with lower levels of its product (fructose-6-phosphate) and higher levels of its substrate (fructose-1,6-bisphosphate) in the kidney of 6-22 week-old CSE^-/- mice. We have also observed lower levels of the gluconeogenic regulator, peroxisome proliferator-activated receptor-&gamma; coactivator (PGC)-1&alpha;, and its down-stream targets, FBPase-1 and -2, phosphoenolpyruvate carboxykinase (PEPCK), and estrogen-related receptor (ERR)&alpha; mRNA expression levels in renal extracts from 6-22 week-old CSE^-/- mice. Likewise, FBPase-1 and -2 mRNA levels were also significantly down-regulated in aorta tissues from 14-16 week-old CSE^-/- mice. Administration of 30 and 50 &#x00B5;M NaHS induced a significant increase in FBPase-1 and PGC-1&alpha; in rat A-10 cells. We have also observed a significant up-regulation of PEPCK and ERR&alpha; mRNA expression levels in 50 &#x00B5;M NaHS-treated A-10 cells, further confirming the involvement of H₂S in regulating the rate of gluconeogenesis and MG formation. Overall, this unique study demonstrates the existence of a negative correlation between MG and H₂S in the vasculature. Further elucidation of this cross-talk phenomenon between MG and H₂S could lead to more elaborate and effective therapeutic regimens to combat metabolic syndrome and its related health complications.</p>

<p>Methylglyoxal (MG) is a reactive glucose metabolite and a known causative factor for hypertension and diabetes. Hydrogen sulfide (H₂S), on the other hand, is a gasotransmitter with multifaceted physiological functions, including anti-oxidant and vasodilatory properties. The present study demonstrates that MG and H₂S can interact with and modulate each other's functions. Upon <i>in vitro</i> incubations, we found that MG and H₂S can directly interact to form three possible MG-H₂S adducts. Furthermore, the endogenous production level of MG or H₂S was significantly reduced in a concentration-dependent manner in rat vascular smooth muscle cells (A-10 cells) treated with NaHS, a H₂S donor, or MG, respectively. Indeed, MG-treated A-10 cells exhibited a concentration-dependent down-regulation of the protein and activity level of cystathionine &gamma;-lyase (CSE), the main H₂S-generating enzyme in the vasculature. Moreover, H₂S can induce the inhibition of MG-generated ROS production in a concentration-dependent manner in A-10 cells. In 6-22 week-old CSE knockout male mice (CSE^-/-), mice with lower levels of vascular H₂S, we observed a significant elevation in MG levels in both plasma and renal extracts. Renal triosephosphates were also significantly increased in the 6-22 week-old CSE^-/- mice. To identify the source of the elevated renal MG levels, we found that the activity of fructose-1,6-bisphosphatase (FBPase), the rate-limiting enzyme in gluconeogenesis, was significantly down-regulated, along with lower levels of its product (fructose-6-phosphate) and higher levels of its substrate (fructose-1,6-bisphosphate) in the kidney of 6-22 week-old CSE^-/- mice. We have also observed lower levels of the gluconeogenic regulator, peroxisome proliferator-activated receptor-&gamma; coactivator (PGC)-1&alpha;, and its down-stream targets, FBPase-1 and -2, phosphoenolpyruvate carboxykinase (PEPCK), and estrogen-related receptor (ERR)&alpha; mRNA expression levels in renal extracts from 6-22 week-old CSE^-/- mice. Likewise, FBPase-1 and -2 mRNA levels were also significantly down-regulated in aorta tissues from 14-16 week-old CSE^-/- mice. Administration of 30 and 50 &#x00B5;M NaHS induced a significant increase in FBPase-1 and PGC-1&alpha; in rat A-10 cells. We have also observed a significant up-regulation of PEPCK and ERR&alpha; mRNA expression levels in 50 &#x00B5;M NaHS-treated A-10 cells, further confirming the involvement of H₂S in regulating the rate of gluconeogenesis and MG formation. Overall, this unique study demonstrates the existence of a negative correlation between MG and H₂S in the vasculature. Further elucidation of this cross-talk phenomenon between MG and H₂S could lead to more elaborate and effective therapeutic regimens to combat metabolic syndrome and its related health complications.</p>

LA PRINCIPALE SOURCE D'ESPECES REACTIVES DE L'OXYGENE (ROS) EST LA MITOCHONDRIE, PAR L'INTERMEDIAIRE DE SA CHAINE RESPIRATOIRE. DEUX PARAMETRES ESSENTIELS PEUVENT MODULER CETTE PRODUCTION : LA NATURE DES EQUIVALENTS REDUITS (NADH,H+ ET FADH2) ET L'APPORT EN OXYGENE. NOUS NOUS SOMMES INTERESSES AUX EFFETS DE REGIMES ALIMENTAIRES (MODIFIANT LA PROPORTION ENTRE NADH,H+ ET FADH2) ET A L'HYPEROXIE (MODIFIANT L'APPORT EN O2) SUR LA PRODUCTION D'H2O2 PAR LES MITOCHONDRIES DE MUSCLE SQUELETTIQUE ET/OU DE FOIE DE RATS. NOUS AVONS MIS EN EVIDENCE QUE LA CONSOMMATION DE LIPIDES SUPPRIME LES EFFETS BENEFIQUES DE LA RESTRICTION CALORIQUE SUR LA PRODUCTION DE ROS. LE REGIME RICHE EN FRUCTOSE AUGMENTE LA QUANTITE D'H2O2 GENEREE PAR LES MITOCHONDRIES, CELLE-CI POUVANT NEANMOINS ETRE PREVENUE PAR UN TRAITEMENT A LA GLISODIN® (CONSTITUEE DE SOD VEGETALE). LE PRECONDITIONNEMENT HYPEROXIQUE (4 JOURS A 50% D'O2 SUIVI DE 5 JOURS A 80% D'O2) DIMINUERAIT LA PRODUCTION DE ROS EN STIMULANT L'ACTIVITE DE LA COX.

Aggregatibacter actinomycetemcomitans is a Gram negative bacterium found exclusively in the mammalian oral cavity where it resides in the gingival crevice, the space between the tooth and gum tissue. Though it has historically been considered a common commensal organism, it is now appreciated that A. actinomycetemcomitans is an opportunistic pathogen associated with the diseases periodontitis and endocarditis. To cause infection, A. actinomycetemcomitans must interact and compete with neighboring bacteria for space and nutrients, though little is known about the physiology it employs within the gingival crevice. Using A. actinomycetemcomitans grown in a chemically defined medium containing carbon sources found in vivo, I use transcriptome analyses and growth studies to show that A. actinomycetemcomitans preferentially utilizes lactate over the phosphotransferase system (PTS) sugars glucose and fructose. Additionally, the presence of lactate or pyruvate inhibits the transport and metabolism of these sugars in a post-transcriptionally controlled process I have termed PTS substrate exclusion. Since lactate is an energetically inferior carbon source, PTS substrate exclusion appears to be a carbon resource partitioning mechanism that allows A. actinomycetemcomitans to avoid competition for energetically favorable sugars with other species, and I propose a model to describe this phenomenon. To begin to understand the mechanism of PTS substrate exclusion, I examine the first step of the proposed model by purifying and characterizing the L-lactate dehydrogenase (LctD) from A. actinomycetemcomitans. I demonstrate that, unlike other studied lactate dehydrogenases, the LctD from A. actinomycetemcomitans does not exhibit feedback inhibition in the presence of physiologically relevant concentrations of pyruvate, which supports my hypothesis that elevated intracellular pyruvate levels inhibit the PTS. The results of my studies provide insight into a new regulatory mechanism governing carbon utilization in this bacterium. / text

Nectarivorous hummingbirds subsist almost exclusively on a mixture of sucrose, glucose and fructose found in floral nectar. Previous studies have shown that hummingbirds can fuel hovering flight almost exclusively using recently ingested sucrose. However, the relative capacities for the direct utilization of glucose and fructose by hovering hummingbirds remain unknown. 13C-enriched solutions of glucose and fructose were administered separately. Exhaled breath samples were collected using feeder-mask respirometry and sent for subsequent mass spectrometric analysis. I found hovering hummingbirds transition from exclusively oxidizing endogenous fatty acids when fasted, to oxidizing newly ingested carbohydrates when given access to either glucose or fructose solutions. Interestingly, the amount ingested, fractional turnover of stable carbon isotope signatures, amount oxidized, energy expended and proportion of hovering metabolism supported by each hexose, were each similar between glucose and fructose. These results demonstrate hovering hummingbirds’ ability to utilize fructose and glucose equally.

Nectarivorous hummingbirds subsist almost exclusively on a mixture of sucrose, glucose and fructose found in floral nectar. Previous studies have shown that hummingbirds can fuel hovering flight almost exclusively using recently ingested sucrose. However, the relative capacities for the direct utilization of glucose and fructose by hovering hummingbirds remain unknown. 13C-enriched solutions of glucose and fructose were administered separately. Exhaled breath samples were collected using feeder-mask respirometry and sent for subsequent mass spectrometric analysis. I found hovering hummingbirds transition from exclusively oxidizing endogenous fatty acids when fasted, to oxidizing newly ingested carbohydrates when given access to either glucose or fructose solutions. Interestingly, the amount ingested, fractional turnover of stable carbon isotope signatures, amount oxidized, energy expended and proportion of hovering metabolism supported by each hexose, were each similar between glucose and fructose. These results demonstrate hovering hummingbirds’ ability to utilize fructose and glucose equally.

Glycerol and fructose are molecules that are readily available in substantial quantities fromthe biomass. In this work dehydration routes for valorization of these compounds wereinvestigated. Therefore, zirconia and titania based catalysts, and calcium phosphate materialswere prepared and evaluated in the glycerol dehydration in gas phase. Niobia-ceria mixedoxides and mesoporous Nb2O5-MeO2 (M = Ce, Zr, Ti) mixed oxides were prepared andtested in fructose dehydration reaction in aqueous phase. The surface acid-base properties ofthe studied catalysts were correlated to their catalytic performance.

Universiẗat, Diss.--Osnabrück, 1994.