Abstract
Diet intake in pregnant rats fed a low-protein (LP) diet was significantly reduced during late pregnancy despite elevated plasma levels of ghrelin. In this study, we hypothesized that ghrelin signaling in the hypothalamus is blunted under a low-protein diet condition and therefore, it does not stimulate diet intake during late pregnancy. Female Sprague-Dawley rats were fed a normal (CT) or LP diet from Day 1 of pregnancy. On Day 21, 0.5μg ghrelin was given into the third ventricle (ICV). Diet and water intake at 30, 60, and 120min after ICV injection was measured. Hypothalami were dissected and analyzed for expression of genes related to appetite regulation (Npy, Agrp, Pomc and Cart) and phosphorylation of AMPK and ACC proteins (downstream proteins of ghrelin receptor activation). Results include: In response to ICV injection of ghrelin, (1) diet intake was significantly lower in LP compared to CT rats; (2) water intake was not affected in LP rats; (3) expression of Npy and Agrp, but not Pomc and Cart, were higher in the hypothalamus of LP compared to CT rats; (4) the abundance of phosphorylated AMPK and the ratio of phosphorylated to total AMPK, but not the abundance of total AMPK, were lower in LP compared to CT rats; (5) the abundance of phosphorylated ACC, but not total ACC, was lower in LP rats. These findings suggest that blunted ghrelin signaling in the hypothalamus of pregnant rats fed a LP diet leads to reduced diet intake and exacerbates gestational protein insufficiency.
Highlights
Protein and amino acids are critical for fetal development and growth
In this study, we hypothesized that ghrelin signaling in the hypothalamus is blunted in pregnant rats fed a LP diet and it does not stimulate diet intake during late pregnancy
We investigated the diet and water intake, expression of genes related to appetite regulation (Npy, Agrp, Pomc and Cart), and ghrelin signaling in the hypothalamus of pregnant rats fed a LP diet on day 21 of gestation after intracerebroventricular (ICV) injection of ghrelin
Summary
Protein and amino acids are critical for fetal development and growth. In animals, protein insufficiency during pregnancy causes intrauterine growth restriction (Jansson et al 2006; Gao et al 2012a, 2012b), and programs hypertension, cardiovascular and metabolic diseases in adult offspring (Langley-Evans et al 1996, 1999; Gangula et al 2005; McMullen and Langley-Evans 2005a, 2005b; Sathishkumar et al 2012). Programming of adult health of offspring from pregnant rats fed a low-protein (LP) diet is of clinical significance (Kautzky-Willer and Handisurya 2009) because this model mimics protein insufficiency in the diet in developing countries, due to poverty and in certain ethnic groups in developed countries due to varied socioeconomic limitations. We found that diet consumption by rats fed a LP diet was lower during late gestation compared to that by rats fed normal protein (CT) diet (Gao et al 2015). As a consequence, this reduced diet intake exacerbates nutritional insufficiency during late pregnancy when fetal growth is exponential. Mechanisms for the reduced diet intake in pregnant rats fed a LP diet remain unknown
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