Exposure of the Pregnant Rat to Low Protein Diet Causes Impaired Glucose Homeostasis in the Young Adult Offspring by Different Mechanisms in Males and Females

2009 ◽  
Vol 234 (12) ◽  
pp. 1425-1436 ◽  
Author(s):  
Astrid Chamson-Reig ◽  
Sandra M. Thyssen ◽  
David J. Hill ◽  
Edith Arany
Endocrine ◽  
2018 ◽  
Vol 63 (1) ◽  
pp. 62-69 ◽  
Author(s):  
Douglas Lopes Almeida ◽  
Fernando Salgueiro Simões ◽  
Lucas Paulo Jacinto Saavedra ◽  
Ana Maria Praxedes Moraes ◽  
Camila Cristina Ianoni Matiusso ◽  
...  

2014 ◽  
Vol 306 (10) ◽  
pp. H1444-H1452 ◽  
Author(s):  
Adam J. Watkins ◽  
Kevin D. Sinclair

Although the association between maternal periconceptional diet and adult offspring health is well characterised, our understanding of the impact of paternal nutrition at the time of conception on offspring phenotype remains poorly defined. Therefore, we determined the effect of a paternal preconception low protein diet (LPD) on adult offspring cardiovascular and metabolic health in mice. Male C57BL/6 mice were fed either normal protein diet (NPD; 18% casein) or LPD (9% casein) for 7 wk before mating. At birth, a reduced male-to-female ratio ( P = 0.03) and increased male offspring weight ( P = 0.009) were observed in litters from LPD compared with NPD stud males with no differences in mean litter size. LPD offspring were heavier than NPD offspring at 2 and 3 wk of age ( P < 0.02). However, no subsequent differences in body weight were observed. Adult male offspring derived from LPD studs developed relative hypotension (decreased by 9.2 mmHg) and elevated heart rate ( P < 0.05), whereas both male and female offspring displayed vascular dysfunction and impaired glucose tolerance relative to NPD offspring. At cull (24 wk), LPD males had elevated adiposity ( P = 0.04), reduced heart-to-body weight ratio ( P = 0.04), and elevated circulating TNF-α levels ( P = 0.015) compared with NPD males. Transcript expression in offspring heart and liver tissue was reduced for genes involved in calcium signaling ( Adcy, Plcb, Prkcb) and metabolism ( Fto) in LPD offspring ( P < 0.03). These novel data reveal the impact of suboptimal paternal nutrition on adult offspring cardiovascular and metabolic homeostasis, and provide some insight into the underlying regulatory mechanisms.


2009 ◽  
Vol 4 (3) ◽  
pp. 189-194 ◽  
Author(s):  
Christopher J. McNeil ◽  
Susan M. Hay ◽  
Garry J. Rucklidge ◽  
Martin D. Reid ◽  
Gary J. Duncan ◽  
...  

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Noriko Sato ◽  
Katsuko Sudo ◽  
Masayo Mori ◽  
Chihiro Imai ◽  
Masaaki Muramatsu ◽  
...  

2014 ◽  
Vol 39 (8) ◽  
pp. 880-887 ◽  
Author(s):  
Luciana Nascimento ◽  
Cristiane M. Freitas ◽  
Reginaldo Silva-Filho ◽  
Ana Catarina R. Leite ◽  
Alessandra B. Silva ◽  
...  

Protein restriction during perinatal and early postnatal development is associated with a greater incidence of disease in the adult, such arterial hypertension. The aim in the present study was to investigate the effect of maternal low-protein diet on mitochondrial oxidative phosphorylation capacity, mitochondrial reactive oxygen species (ROS) formation, antioxidant levels (enzymatic and nonenzymatic), and oxidative stress levels on the heart of the adult offspring. Pregnant Wistar rats received either 17% casein (normal protein, NP) or 8% casein (low protein, LP) throughout pregnancy and lactation. After weaning male progeny of these NP or LP fed rats, females were maintained on commercial chow (Labina-Purina). At 100 days post-birth, the male rats were sacrificed and heart tissue was harvested and stored at −80 °C. Our results show that restricting protein consumption in pregnant females induced decreased mitochondrial oxidative phosphorylation capacity (51% reduction in ADP-stimulated oxygen consumption and 49.5% reduction in respiratory control ratio) in their progeny when compared with NP group. In addition, maternal low-protein diet induced a significant decrease in enzymatic antioxidant capacity (37.8% decrease in superoxide dismutase activity; 42% decrease in catalase activity; 44.8% decrease in glutathione-S-transferase activity; 47.9% decrease in glutathione reductase; 25.7% decrease in glucose-6 phosphate dehydrogenase) and glutathione level (34.8% decrease) when compared with control. From these findings, we hypothesize that an increased production of ROS and decrease in antioxidant activity levels induced by protein restriction during development could potentiate the progression of metabolic and cardiac diseases in adulthood.


2005 ◽  
Vol 289 (6) ◽  
pp. E1115-E1118 ◽  
Author(s):  
K. Morten ◽  
P. Field ◽  
N. Ashley ◽  
K. A. Williams ◽  
D. Harris ◽  
...  

Zidovudine (AZT) lowers the perinatal transmission of HIV but can impair mitochondrial function by depleting mitochondrial DNA (mtDNA). AZT therapy and perinatal nutritional deprivation affect the body fat distribution, which influences glucose tolerance. We sought to model intrauterine exposure to AZT in humans to determine whether it interacts with low-protein diet (LPD) to impact on birth weight and glucose homeostasis in the offspring. Pregnant dams and their offspring were given AZT, an LPD, or AZT and an LPD (LPD + AZT). AZT reduced mtDNA copy number in liver and birth weight in the offspring and increased their fasting glucose and insulin ( P = 0.021, 0.03, 0.001, and 0.011 respectively) at 6–8 wk of age. LPD decreased litter size and birth weight ( P = 0.01 and 0.012). In the LPD + AZT group, birth weight and litter size were reduced compared with untreated controls, and fasting blood glucose and insulin were raised. There was a significant interaction between LPD and AZT on fasting insulin levels ( P = 0.025). Islet size was not significantly affected, but the mean β-cell area/islet was reduced in the LPD + AZT group compared with controls ( P < 0.05). Early exposure to AZT interacts with LPD to impair fetal development in this model. This combination appeared to impair the supply of insulin and, hence, glucose homeostasis, perhaps as a result of impaired mitochondrial function. Although it is not certain that this can be extrapolated to humans, maternal nutritional deprivation combined with AIDS therapy could influence both birth weight and onset of diabetes.


2015 ◽  
Vol 19 (8) ◽  
pp. 369-375 ◽  
Author(s):  
Diorginis Soares Ferreira ◽  
Yuri Liu ◽  
Mariana Pinheiro. Fernandes ◽  
Claudia Jacques Lagranha

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