Maternal quercetin intake during lactation attenuates renal inflammation and modulates autophagy flux in high-fructose-diet-fed female rat offspring exposed to maternal malnutrition

2019 ◽  
Vol 10 (8) ◽  
pp. 5018-5031 ◽  
Author(s):  
Shin Sato ◽  
Toshio Norikura ◽  
Yuuka Mukai
Keyword(s):  
Female Offspring ◽  
Female Rat ◽  
Autophagy Flux ◽  
Maternal Malnutrition ◽  
High Fructose Diet ◽  
Rat Offspring ◽  
Low Protein ◽  
High Fructose ◽  
Protein Diets

Quercetin intake during lactation causes long-term alterations in inflammation and autophagy flux in the kidneys of high-fructose-diet-fed adult female offspring exposed to maternal normal- or low-protein diets.

Early Administration of Angiotensin-Converting Enzyme Inhibitor Captopril, Prevents the Development of Hypertension Programmed by Intrauterine Exposure to a Maternal Low-Protein Diet in the Rat

1998 ◽  
Vol 94 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Rachel C. Sherman ◽  
Simon C. Langley-Evans
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Control Diet ◽  
Female Offspring ◽  
Fetal Exposure ◽  
Early Administration ◽  
Low Protein ◽  
Blood Pressures ◽  
Protein Diets

1. Associations of intrauterine exposure to maternal undernutrition with later hypertension and coronary heart disease in the human population have been duplicated in the rat. Fetal exposure to low protein diets produces offspring that develop raised systolic blood pressure by the age of weaning. This animal model of ‘programmed’ hypertension was used to investigate the role of the renin—angiotensin system in the initiation and maintenance of high blood pressure. 2. Pregnant rats were fed diets containing 18 or 9% casein from conception until littering. The offspring from these pregnancies were administered captopril either between 2 and 4 weeks of age, or from 10 to 12 weeks of age. 3. The feeding of low protein diets in pregnancy had no effect upon the reproductive ability of female rats and the offspring generated were of normal birthweight. By 4 weeks of age the male and female offspring of low-protein-fed dams had systolic blood pressures that were 24–25 mmHg higher than those of rats exposed to a control diet in utero. 4. Treatment of 10-week-old female offspring with captopril for 2 weeks indicated that angiotensin II formation may play a role in the maintenance of high blood pressure in low-protein-exposed rats. While captopril had no significant effect upon systolic pressures of rats exposed to the control diet in intrauterine life, the systolic blood pressures of low-protein animals rapidly declined by 31 mmHg. 5. Administration of captopril to male and female offspring between 2 and 4 weeks of age exerted long-term effects upon systolic blood pressure. Eight weeks after cessation of treatment, at an age where maximal blood pressures are achieved, captopriltreated, low-protein-exposed rats had similar blood pressures to normotensive rats exposed to the protein-replete diet in utero. 6. In conclusion, we have demonstrated that the elevation of adult blood pressure associated with fetal exposure to a maternal low-protein diet, is prevented by early administration of an angiotensin-converting enzyme inhibitor. The actions of angiotensin II in the late suckling period may be a critical determinant of long-term cardiovascular functions in these animals.

Perinatal free‐choice of a high‐calorie low‐protein diet affects leptin signaling through IRS1 and AMPK dephosphorylation in the hypothalami of female rat offspring in adulthood

2019 ◽  
Vol 226 (2) ◽  
pp. e13244 ◽  
Author(s):  
Patricia Rivera ◽  
María T. Ramírez‐López ◽  
Antonio Vargas ◽  
Juan Decara ◽  
Mariam Vázquez ◽  
...  
Keyword(s):  
Free Choice ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Female Rat ◽  
Leptin Signaling ◽  
Rat Offspring ◽  
Low Protein ◽  
High Calorie

Maternal exposure to high-fat and high-fructose diet evokes hypoadiponectinemia and kidney injury in rat offspring

2016 ◽  
Vol 20 (6) ◽  
pp. 853-861 ◽  
Author(s):  
Nana Yamada-Obara ◽  
Sho-ichi Yamagishi ◽  
Kensei Taguchi ◽  
Yusuke Kaida ◽  
Miyuki Yokoro ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Maternal Exposure ◽  
High Fat ◽  
High Fructose Diet ◽  
Rat Offspring ◽  
High Fructose

scholarly journals Chronic Effects of Maternal Low-Protein and Low-Quality Protein Diets on Body Composition, Glucose-Homeostasis and Metabolic Factors, Followed by Reversible Changes upon Rehabilitation in Adult Rat Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4129
Author(s):  
Pandarinath Savitikadi ◽  
Raghu Pullakhandam ◽  
Bharati Kulkarni ◽  
Boiroju Naveen Kumar ◽  
Geereddy Bhanuprakash Reddy ◽  
...  
Keyword(s):  
Body Composition ◽  
Glucose Homeostasis ◽  
Wheat Gluten ◽  
Metabolic Factors ◽  
Adult Rat ◽  
Rat Offspring ◽  
Low Protein ◽  
Plasma Hormones ◽  
Isocaloric Diets ◽  
Protein Diets

Several studies suggest that the maternal protein content and source can affect the offspring’s health. However, the chronic impact of maternal quality and quantity protein restriction, and reversible changes upon rehabilitation, if any, in the offspring, remains elusive. This study examined the effects of maternal low-quality protein (LQP) and low-protein (LP) intake from preconception to post-weaning, followed by rehabilitation from weaning, on body composition, glucose-homeostasis, and metabolic factors in rat offspring. Wistar rats were exposed to normal protein (NP; 20% casein), LQP (20% wheat gluten) or LP (8% casein) isocaloric diets for 7 weeks before pregnancy until lactation. After weaning, the offspring were exposed to five diets: NP, LQP, LQPR (LQP rehabilitated with NP), LP, and LPR (LP rehabilitated with NP) for 16 weeks. Body composition, glucose-homeostasis, lipids, and plasma hormones were investigated. The LQP and LP offspring had lower bodyweight, fat and lean mass, insulin and HOMA-IR than the NP. The LQP offspring had higher cholesterol, T3 and T4, and lower triacylglycerides and glucose, while these were unaltered in LP compared to NP. The majority of the above outcomes were reversed upon rehabilitation. These results suggest that the chronic exposure of rats to maternal LQP and LP diets induced differential adverse effects by influencing body composition and metabolism, which were reversed upon rehabilitation.

Prenatal Dexamethasone Exposure Induced Alterations in Neurobehavior and Hippocampal Glutamatergic System Balance in Female Rat Offspring

2019 ◽  
Vol 171 (2) ◽  
pp. 369-384 ◽  
Author(s):  
Songqiang Huang ◽  
Wanting Dong ◽  
Zhexiao Jiao ◽  
Jie Liu ◽  
Ke Li ◽  
...  
Keyword(s):  
Glucocorticoid Receptors ◽  
Female Offspring ◽  
Abnormal Behavior ◽  
Control Group ◽  
Female Rat ◽  
Glutamatergic System ◽  
Fetal Origins ◽  
Histone Deacetylase 2 ◽  
Rat Offspring

Abstract Epidemiological investigations have suggested that periodic use of dexamethasone during pregnancy is a risk factor for abnormal behavior in offspring, but the potential mechanism remains unclear. In this study, we investigated the changes in the glutamatergic system and neurobehavior in female offspring with prenatal dexamethasone exposure (PDE) to explore intrauterine programing mechanisms. Compared with the control group, rat offspring with PDE exhibited spatial memory deficits and anxiety-like behavior. The expression of hippocampal glucocorticoid receptors (GR) and histone deacetylase 2 (HDAC2) increased, whereas histone H3 lysine 14 acetylation (H3K14ac) of brain-derived neurotrophic factor (BDNF) exon IV (BDNF IV) and expression of BDNF decreased. The glutamatergic system also changed. We further observed that changes in the fetal hippocampus were consistent with those in adult offspring. In vitro, the administration of 0.5 μM dexamethasone to the H19-7 fetal hippocampal neuron cells directly led to a cascade of changes in the GR/HDAC2/BDNF pathway, whereas the GR antagonist RU486 and the HDAC2 inhibitor romidepsin (Rom) reversed changes caused by dexamethasone to the H3K14ac level of BDNF IV and to the expression of BDNF. The increase in HDAC2 can be reversed by RU486, and the changes in the glutamatergic system can be partially reversed after supplementation with BDNF. It is suggested that PDE increases the expression of HDAC2 by activating GR, reducing the H3K14ac level of BDNF IV, inducing alterations in neurobehavior and hippocampal glutamatergic system balance. The findings suggest that BDNF supplementation and glutamatergic system improvement are potential therapeutic targets for the fetal origins of abnormal neurobehavior.

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