In Vivo and In Vitro Expression of iC1, a Methylation-Controlled J Protein (MCJ) in Bovine Liver, and Response to In Vitro Bovine Fatty Liver Disease Model.

Mitochondrial complex I inhibitor (iC1) is a methylation-controlled J protein (MCJ) that decreases cellular respiration by inhibiting oxidative phosphorylation. Recent rodent studies showed that loss or inhibition of iC1 was associated with preventing lipid accumulation. A common metabolic disorder of dairy cattle is a fatty liver disease (FLD), which often occurs during the periparturient period. In humans and rodents, iC1 is expressed in the liver and acts as a mitochondrial "brake". However, iC1 expression in bovine liver and its possible role in FLD development have not yet been characterized. We hypothesized that iC1 is expressed in the bovine liver and that the expression of iC1 is correlated with FLD in periparturient dairy cattle. To test this hypothesis, we collected bovine liver tissue samples from an abattoir and isolated primary hepatic cells immediately following harvest. Utilizing an in vitro model of bovine FLD developed in our laboratory, we cultured primary hepatic cells in low-glucose DMEM supplemented with 10% FBS. The basal media was made to induce lipid accumulation and cytotoxicity in the primary liver cells with three treatments. To the basal media (control) we added 0.4 mM palmitate (treatment 1) or 20 ng/mL TNFα (treatment 2), or both 0.4 mM palmitate and 20 ng/mL TNFα (treatment 3). Consistent with our hypothesis, we present the novel characterization of iC1 expression in primary bovine liver cells cultured with or without the addition of lipotoxic factors made to emulate bovine FLD. We demonstrate both in situ and in vitro expression of iC1 in bovine liver and mRNA expression in hepatic cells and in the precipitates of conditioned media. The results of RT-qPCR, IHC, and western blot all demonstrated the expression of iC1 in bovine liver. In addition, we isolated precipitates of conditioned media further demonstrated iC1 expression by RT-qPCR. The transcript of iC1 tended to be more concentrated (4-fold; p > 0.05) in TNFα-treated conditioned media when compared with the control. Taken together, we present the novel finding that iC1 transcript and protein are expressed in liver tissue from dairy cattle, primary hepatic cells isolated from that liver tissue, and, finally, in the conditioned media derived from those cells. These novel findings and the prior findings on the role of iC1 in rodents and humans indicate that further investigation of the role of iC1 in the etiology and pathology of FLD in periparturient dairy cows is warranted.

Effect of Walnut Predinner Snack on Mealtime Hunger and Nutrient Intake Among University Students.

Freshman-15 is a phenomenon of first-year university students resulting in weight gain partly due to new cafeteria eating patterns and stress. This study determined if a premeal walnut snack alters planned eating behavior and mealtime nutrient intake during a subsequent buffet-model meal. Healthy university students (n = 36; 18.1 ± 0.5 years; body mass index: 23.6 ± 3.9) received three treatments (90 min premeal) in randomized order on 3 consecutive days: (1) snack of 190 Cal (1 oz) of walnuts (WS), (2) snack of 190 Cal of gummy candy (GS), or (3) no snack (NS; control) before a standard cafeteria dinner (1760 Cal). Visual analog scale (VAS) surveys were administered before and after dinner, and caloric intake was determined. Premeal VAS desire to eat was lower after WS and GS than NS, whereas the sense of hunger and sense of fullness were higher after WS and GS compared with NS. Postmeal VAS was not different between treatments. Mealtime calories, total fat, saturated fat, cholesterol, protein, sodium, fiber, and sugar consumed after WS were significantly less than NS. Total fat and sodium consumed after GS did not significantly differ from NS. Mealtime total fat, sodium, and fiber for WS were significantly less than GC, and a trend was observed for total calories. Differences in calorie intake were not observed between treatments when snack calories were included as part of the mealtime caloric intake. These findings could be helpful for promoting WS and to a lesser degree GS for increased satiety before meals possibly leading to reduced food intake during dinner by university students.

Relationship Between Interpregnancy Interval and Adverse Perinatal and Neonatal Outcomes in Northern Alberta.

BACKGROUND: Birth outcomes are known to be associated with birth spacing, but there are population differences. The purpose of this study was to examine the association between interpregnancy intervals and perinatal and neonatal outcomes in a Canadian population during the era of mandatory folate fortification of food. METHODS: We conducted a study of 46 243 women who had two consecutive singleton births in northern Alberta between 1999 and 2007, using a linked provincial dataset. Perinatal outcomes of interest were preterm birth, low birth weight (LBW), small for gestational age, and perinatal death. Neonatal outcomes were low Apgar score, low arterial blood gas pH, need for neonatal resuscitation or admission to NICU, and neonatal death. Multivariable logistic regression was used to control for maternal demographic and obstetrical characteristics. RESULTS: The risk of preterm birth was increased for multiple interpregnancy intervals: for an interval of 0 to 5 months, the adjusted odds ratio (aOR) was 1.37 (95% CI 1.18 to 1.59), for 6 to 11 months the aOR was 1.18 (95% CI 1.04 to 1.34), for 24 to 35 months the aOR was 1.16 (95% CI 1.02 to 1.31), and for 36+ months the aOR was 1.36 (95% CI 1.20 to 1.53), compared with the reference interval of 12 to 17 months. The risk of LBW was increased with interpregnancy intervals of 0 to 5 months (aOR 1.48; 95% CI 1.23 to 1.80), 6 to 11 months (aOR 1.21; 95% CI 1.03 to 1.42), 24 to 35 months (aOR 1.21; 95% CI 1.03 to 1.41) and 36+ months (aOR 1.48; 95% CI 1.27 to 1.73). The risk of SGA was increased with intervals 0 to 5 months (aOR 1.29; 95% CI 1.09 to 1.52), 24 to 35 months (aOR 1.15; 95% CI 1.01 to 1.31), and 36+ months (aOR 1.26; 95% CI 1.11 to 1.44). The risk of perinatal death was increased with an interval of 36+ months (aOR 1.60; 95% CI 1.06 to 2.43). Similar associations were also observed for neonatal outcomes. CONCLUSION: This study suggests that both short and long interpregnancy intervals are associated with adverse perinatal and neonatal outcomes, and it provides risk estimates for a Canadian population in the era of folate fortification of food.

Contexte : Bien qu'il soit reconnu que les issues de grossesse sont associées aux intervalles intergrossesses, certaines différences sont constatées d'une population à l'autre. Cette étude avait pour objectif d'examiner l'association entre les intervalles intergrossesses et les issues périnatales et néonatales au sein d'une population canadienne, au cours des années suivant la décision qui a rendu obligatoire l'enrichissement des aliments en folate. Méthodes : Nous avons mené une étude auprès de 46 243 femmes qui ont mené deux grossesses monofœtales consécutives à terme dans le nord de l'Alberta entre 1999 et 2007, en utilisant un ensemble de données liées provinciales. L'accouchement préterme, le faible poids de naissance (FPN), l'hypotrophie fœtale et le décès périnatal ont été les issues périnatales sur lesquelles nous nous sommes penchés. Pour ce qui est des issues néonatales, nous nous sommes penchés sur le faible indice d'Apgar, le faible pH mis au jour par gazométrie du sang artériel, la nécessité de procéder à une réanimation néonatale ou à une admission à l'UNSI et le décès néonatal. Une régression logistique multivariée a été utilisée pour neutraliser l'effet des caractéristiques démographiques et obstétricales maternelles. Résultats : Nous avons constaté que de multiples intervalles intergrossesses ont été marqués par une hausse du risque d'accouchement préterme : un intervalle de 0 à 5 mois était associé à un rapport de cotes corrigé (RCc) de 1,37 (IC à 95 %, 1,18 - 1,59), un intervalle de 6 à 11 mois était associé à un RCc de 1,18 (IC à 95 %, 1,04 - 1,34), un intervalle de 24 à 35 mois était associé à un RCc de 1,16 (IC à 95 %, 1,02 - 1,31) et un intervalle de plus de 36 mois était associé à un RCc de 1,36 (IC à 95 %, 1,20 - 1,53), par comparaison avec l'intervalle de référence (de 12 à 17 mois). Le risque de FPN a connu une hausse dans le cas des intervalles intergrossesses de 0 à 5 mois (RCc, 1,48; IC à 95 %, 1,23 - 1,80), de 6 à 11 mois (RCc, 1,21; IC à 95 %, 1,03 - 1,42), de 24 à 35 mois (RCc, 1,21; IC à 95 %, 1,03 - 1,41) et de plus de 36 mois (RCc, 1,48; IC à 95 %, 1,27 - 1,73). Le risque d'hypotrophie fœtale a connu une hausse dans le cas des intervalles intergrossesses de 0 à 5 mois (RCc, 1,29; IC à 95 %, 1,09 - 1,52), de 24 à 35 mois (RCc, 1,15; IC à 95 %, 1,01 - 1,31) et de plus de 36 mois (RCc, 1,26; IC à 95 %, 1,11 - 1,44). Le risque de décès périnatal a connu une hausse dans le cas de l'intervalle intergrossesse de plus de 36 mois (RCc, 1,60; IC à 95 %, 1,06 - 2,43). Des associations semblables ont également été constatées pour ce qui est des issues néonatales. Conclusion : Cette étude laisse entendre que les intervalles intergrossesses tant courts que longs sont associés à des issues indésirables périnatales et néonatales, et elle offre des estimations du risque pour une population canadienne au cours des années suivant la décision qui a rendu obligatoire l'enrichissement des aliments en folate.