ABSTRACT
AIMS/HYPOTHESIS: Diabetes in pregnancy is linked to development of obesity in the offspring, but the mechanisms are not fully understood. Gestational diabetes mellitus (GDM) occurs when beta cells are unable to compensate for the normal insulin resistance of late pregnancy. In this study, we used a murine model of beta cell dysfunction to examine the effects of maternal GDM on phenotype in male offspring with and without an inherited predisposition for beta cell dysfunction. METHODS: Beta cell-specific aryl-hydrocarbon receptor nuclear translocator-null (ßArnt) mice develop GDM from beta cell dysfunction. ßArnt and control female mice were used to induce GDM and non-diabetic pregnancies, respectively. RESULTS: Offspring from GDM pregnancies became spontaneously obese on a normal-chow diet. They were heavier than offspring from non-diabetic pregnancies, with increased body fat. Respiratory exchange ratio (RER) was higher, indicating decreased capacity to switch to lipid oxidation. Metabolic rate in GDM offspring was decreased prior to onset of obesity. The phenotype was more pronounced in ßArnt GDM offspring than in GDM offspring of control genotype, demonstrating an interaction between genotype and pregnancy exposure. ßArnt GDM offspring had increased hypothalamic neuropeptide Y (Npy) and decreased pro-opiomelanocortin (Pomc) expression. Weight, body fat, insulin sensitivity and RER in all mice, and hypothalamic Npy in ßArnt mice were significantly correlated with AUC of maternal late pregnancy glucose tolerance tests (p < 0.01), but not with litter size, maternal weight, triacylglycerol or pre-pregnancy glycaemia. CONCLUSIONS/INTERPRETATION: In ßArnt mice, exposure to GDM and inheritance of genetic beta cell dysfunction had additive effects on male offspring obesity; severity of the offspring phenotype correlated with maternal glycaemia.
Subject(s)
Diabetes, Gestational/physiopathology , Glucose Intolerance/physiopathology , Insulin-Secreting Cells/pathology , Adiposity/genetics , Adiposity/physiology , Animals , Aryl Hydrocarbon Receptor Nuclear Translocator/genetics , Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism , Birth Weight/genetics , Birth Weight/physiology , Diabetes, Gestational/genetics , Eating/genetics , Eating/physiology , Female , Glucose Intolerance/genetics , Insulin-Secreting Cells/metabolism , Male , Mice , Mice, Knockout , Neuropeptides/metabolism , Obesity/genetics , Pregnancy , Pregnancy ComplicationsSubject(s)
Patient Education as Topic/methods , Renal Dialysis/nursing , Humans , Nursing Assessment , Time FactorsABSTRACT
Orientation of a nephrology nurse in a hemodialysis setting is a complex process; often stressful for the learner and time consuming for the educator. The extent of orientation depends upon individual learning needs and previous clinical experience. The competency-based approach to orientation in hemodialysis is comprehensive, efficient, and cost-effective. Modular in design, it is adaptable to varying levels of orientation needs. Based on andragogical theory, it is goal-oriented and learner-directed. A manual has been developed to facilitate a competency-based orientation in hemodialysis. The manual is an outcome-driven tool designed to integrate the nursing process with dialysis technology. The focus is maximization of nephrology nursing care resulting in enhanced patient outcomes.
