Abstract
The low birth weight (LBW) individual had greater risk of developing metabolic dysfunction in adulthood. The aim of this study was to test whether the LBW individual is more prone to glucose intolerance on a high nutrient dense (HND) diet, and to investigate the associated hypothalamic gene expressions using pigs as model. The intake of digestible energy intake, if calculated on a body weight basis, was greater in LBW pigs than that of normal birth weight (NBW) pigs. The LBW pigs fed the HND diet had greater digestible energy intake than those fed the NND diet at adulthood, which did not occur for NBW pigs. Notably, up-regulated hypothalamic toll-like receptor 4, interleukin 6 and phospho-NFκB p65 expressions, and the altered expressions of hypothalamic leptin receptor, suppressor of cytokine signaling 3, agouti-related protein and proopiomelanocortin predicted the overconsumption of energy intake and development of glucose intolerance in LBW pigs fed the HND diet. Collectively, pigs born with LBW had a distinct hypothalamic leptin signaling to a high nutrient dense diet, which contributed to greater energy intake and glucose intolerance.
Highlights
Low birth weight (LBW), a consequence of insufficient nutrient transfer during the intrauterine phase, affects several important physiological processes involved in energy metabolism, cellular signaling, redox balance, and stress response in a variety of tissues including intestine, liver and muscle[1], contributing to increased morbidity and mortality during the neonatal phase, and poor postnatal growth rates and health status throughout life[2,3]
The high nutrient dense (HND) diet did not affect the intake of digestible energy from d 1 to 30, 31 to 60, 61 to 90 and 91 to of the experiment, except that there was greater digestible energy intake in pigs fed the HND diet compared with pigs fed the nutrient dense (NND) diet from d to 150 of experiment (P < 0.05)
The intake of digestible energy from d 121 to 150 of the experiment was greater in low birth weight (LBW) pigs fed the HND diet as compared with pigs fed the NND diet (P < 0.05), but not for normal birth weight (NBW) pigs
Summary
Low birth weight (LBW), a consequence of insufficient nutrient transfer during the intrauterine phase, affects several important physiological processes involved in energy metabolism, cellular signaling, redox balance, and stress response in a variety of tissues including intestine, liver and muscle[1], contributing to increased morbidity and mortality during the neonatal phase, and poor postnatal growth rates and health status throughout life[2,3]. Low birth weight pigs provided with a high quality and expensive dietary regime might ensure maximum growth and increased profitability[7]. These results indicated that sufficient nutrient intake was necessary for the LBW individual to compensate for their early growth restriction. While the link between impaired fetal growth and the risk of developing postnatal metabolic syndromes is undoubtedly strong, the underlying mechanisms involved in this process remained ill-defined. Some of these mechanisms include epigenetics, alterations in transcription factor activity, mitochondrial dysfunction and impaired organogenesis[10,11]. In the present study, the LBW and NBW pigs were fed a normal- or high nutrient dense diet to test the hypothesis that whether hypothalamic genes and proteins were differentially expressed in LBW pigs to alter their postnatal energy intake level and the glucose tolerance
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