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1.
Clin Nutr Res ; 11(4): 264-276, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36381473

ABSTRACT

Hemodialysis (HD) patients can experience appetite alterations that affect meals and nutritional status. Few qualitative studies have assessed the chronic impact of HD on the everyday diet. This study aimed to characterise comprehensively the experiences of HD patients adapting to appetite alteration. Semi-structured, face-to-face interviews were conducted in a unit of a tertiary hospital to understand patient experiences with appetite alteration. An interview guide was used to consider adaptive processes developed after reviewing the literature and based on the researchers' clinical experiences. A single researcher conducted all interviews to maintain consistency in data collection. The interview content was analysed using Nvivo 11 based on grounded theory and constant comparison analysis. As a results, the mean age and HD vintage of 14 participants were 60 and 5.8 years, respectively. We developed a self-care model based on HD patient experiences with appetite alteration based on axial and selective coding. Differences in urea sensitivity, taste alteration, and social support could be explained by timing of transitions, life events, and responses to stress. Self-care processes are adapted through the processes of "self-registration" and "self-reconstruction," starting with "disruption." At the stage of adjustment, 4 self-management types were derived based on pattern of self-care: self-initiator, follower, realist, and pessimist. The results of this study provide unique qualitative insight into the lived experiences of HD patients experiencing appetite alteration and their self-care processes. By recognising dietary challenges, health teams can better support HD patients in the transition from dietary education to self-care.

2.
J Nutr Biochem ; 49: 80-88, 2017 11.
Article in English | MEDLINE | ID: mdl-28915389

ABSTRACT

Maternal obesity increases placental transport of macronutrients, resulting in fetal overgrowth and obesity later in life. Choline participates in fatty acid metabolism, serves as a methyl donor and influences growth signaling, which may modify placental macronutrient homeostasis and affect fetal growth. Using a mouse model of maternal obesity, we assessed the effect of maternal choline supplementation on preventing fetal overgrowth and restoring placental macronutrient homeostasis. C57BL/6J mice were fed either a high-fat (HF, 60% kcal from fat) diet or a normal (NF, 10% kcal from fat) diet with a drinking supply of either 25 mM choline chloride or control purified water, respectively, beginning 4 weeks prior to mating until gestational day 12.5. Fetal and placental weight, metabolites and gene expression were measured. HF feeding significantly (P<.05) increased placental and fetal weight in the HF-control (HFCO) versus NF-control (NFCO) animals, whereas the HF choline-supplemented (HFCS) group effectively normalized placental and fetal weight to the levels of the NFCO group. Compared to HFCO, the HFCS group had lower (P<.05) glucose transporter 1 and fatty acid transport protein 1 expression as well as lower accumulation of glycogen in the placenta. The HFCS group also had lower (P<.05) placental 4E-binding protein 1 and ribosomal protein s6 phosphorylation, which are indicators of mechanistic target of rapamycin complex 1 activation favoring macronutrient anabolism. In summary, our results suggest that maternal choline supplementation prevented fetal overgrowth in obese mice at midgestation and improved biomarkers of placental macronutrient homeostasis.


Subject(s)
Choline/therapeutic use , Dietary Supplements , Fetal Macrosomia/prevention & control , Maternal Nutritional Physiological Phenomena , Obesity/physiopathology , Placenta/metabolism , Pregnancy Complications/physiopathology , Animals , Biomarkers/metabolism , Diet, High-Fat/adverse effects , Fatty Acid Transport Proteins/metabolism , Female , Fetal Development , Fetal Macrosomia/etiology , Fetal Weight , Gene Expression Regulation, Developmental , Glucose Transporter Type 1/genetics , Glucose Transporter Type 1/metabolism , Glycogen/metabolism , Mice, Inbred C57BL , Obesity/etiology , Obesity/metabolism , Phosphorylation , Placenta/pathology , Placentation , Pregnancy , Pregnancy Complications/etiology , Pregnancy Complications/metabolism , Pregnancy Complications/pathology , Protein Processing, Post-Translational
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