Publications by authors named "Katherine M Kennedy"

Identifying sources of variance that contribute to residual feed intake (RFI) can aid in improving feed efficiency. The objectives of this study were to investigate immune cells phenotype and bioenergetic measures in CD4 T cells in low feed efficient (LE) and high feed efficient (HE) dairy cows. Sixty-four Holstein cows were enrolled at 93 ± 22 days in milk (DIM) and monitored for 7 weeks to measure RFI.

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Dysregulation of maternal adaptations to pregnancy due to high pre-pregnancy BMI (pBMI) or excess gestational weight gain (GWG) is associated with worsened health outcomes for mothers and children. Whether the gut microbiome contributes to these adaptations is unclear. We longitudinally investigated the impact of pBMI and GWG on the pregnant gut microbiome.

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It is clear that the gastrointestinal tract influences metabolism and immune function. Most studies to date have used male test subjects, with a focus on effects of obesity and dietary challenges. Despite significant physiological maternal adaptations that occur across gestation, relatively few studies have examined pregnancy-related gut function.

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Article Synopsis
  • Scientists are debating whether a fetus and its surroundings are home to stable groups of tiny living things called microbes during a healthy pregnancy.
  • Recent studies suggest that when they find these microbes, it could be because of mistakes during the testing process, not that the fetus actually has them.
  • Understanding these findings is important for learning how our immune system develops and shows that studying tiny living things in places with very few of them can be really tricky, so we need to use different science methods to get it right.
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Conceptual models developed over the past century describe 2 key constraints to feed intake (FI) of healthy animals: gut capacity and metabolic demand. Evidence that greater energy demands (e.g.

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Paternal obesity predisposes offspring to metabolic dysfunction, but the underlying mechanisms remain unclear. We investigated whether this metabolic dysfunction is associated with changes in placental vascular development and is fueled by endoplasmic reticulum (ER) stress-mediated changes in fetal hepatic development. We also determined whether paternal obesity indirectly affects the in utero environment by disrupting maternal metabolic adaptations to pregnancy.

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Microbial colonization of the human intestine impacts host metabolism and immunity; however, exactly when colonization occurs is unclear. Although many studies have reported bacterial DNA in first-pass meconium samples, these samples are typically collected hours to days after birth. Here, we investigated whether bacteria could be detected in meconium before birth.

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Our objective was to determine the effects of uncouplers of oxidative phosphorylation on the metabolism of propionate in liver tissue of dairy cows in the postpartum period. A total of 8 primiparous dairy cows were biopsied for liver tissue explants in 2 block-design experiments. Cows were 5.

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Key Points: The prevalence of obesity and non-alcoholic fatty liver disease in children is dramatically increasing at the same time as consumption of foods with a high sugar content. Intake of high fructose corn syrup (HFCS) is a possible aetiology as it is thought to be more lipogenic than glucose. In a mouse model, HFCS intake during adolescence increased fat mass and hepatic lipid levels in male and female mice.

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Our objective was to determine the temporal effects of increasing supply of propionate on propionate metabolism in liver tissue of dairy cows in the postpartum (PP) period. A total of 6 dairy cows [primiparous: n = 3, 9.00 ± 1.

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The placenta is a metabolically active interfacial organ that plays crucial roles in fetal nutrient delivery, gas exchange and waste removal reflecting dynamic maternal and fetal interactions during gestation. There is growing evidence that the sex of the placenta influences fetal responses to external stimuli in utero, such as changes in maternal nutrition and exposure to environmental stressors. However, the exact biochemical mechanisms associated with sex-specific metabolic adaptations during pregnancy and its link to placental function and fetal development remain poorly understood.

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Our objective was to determine the effects of uncouplers of oxidative phosphorylation on feeding behavior of lactating dairy cows. We hypothesized that uncouplers of oxidative phosphorylation would increase meal size and meal length and performed 2 experiments to test our hypothesis. In experiment 1, 4 late-lactation cows (345 ± 48.

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A faster rate of infusion of propionic acid into the rumen of cows in the postpartum period increased meal size compared with a slower rate of infusion in a previous experiment. Because propionate is anaplerotic and stimulates oxidation of acetyl coenzyme A (CoA) in the liver, and hepatic oxidation has been linked to satiety, this result was opposite to our expected response. We then hypothesized that the faster rate of infusion might have saturated the pathway for propionate metabolism in hepatocytes resulting in lower first-pass extraction by the liver.

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The objective of this research was to identify potential short-term metabolic bottlenecks of propionate metabolism in the liver of dairy cows in the postpartum (PP) period and how such bottlenecks are affected by feeding status. Propionate, produced primarily from the fermentation of starch, decreases dry matter intake for cows in the postpartum period, likely by stimulating oxidation of acetyl-CoA in the liver. In this study, 8 dairy cows [2 blocks of 4 cows each, 6.

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Key Points: Maternal obesity has been associated with shifts in intestinal microbiota, which may contribute to impaired barrier function Impaired barrier function may expose the placenta and fetus to pro-inflammatory mediators We investigated the impacts of diet-induced obesity in mice on maternal and fetal intestinal structure and placental vascularization Diet-induced obesity decreased maternal intestinal short chain fatty acids and their receptors, impaired gut barrier integrity and was associated with fetal intestinal inflammation. Placenta from obese mothers showed blood vessel immaturity, hypoxia, increased transcript levels of inflammation, autophagy and altered levels of endoplasmic reticulum stress markers. These data suggest that maternal intestinal changes probably contribute to adverse placental adaptations and also impart an increased risk of obesity in the offspring via alterations in fetal gut development.

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The U.S. Department of Agriculture's Food Safety and Inspection Service compliance guideline known as Appendix B specifies chilling time and temperature limits for cured and uncured meat products to inhibit growth of spore-forming bacteria, particularly Clostridium perfringens.

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