scholarly journals Fetal exposure to a maternal low-protein diet during mid-gestation results in muscle-specific effects on fibre type composition in young rats

2007 ◽  
Vol 98 (2) ◽  
pp. 292-299 ◽  
Author(s):  
Joanne E. Mallinson ◽  
Dean V. Sculley ◽  
Jim Craigon ◽  
Richard Plant ◽  
Simon C. Langley-Evans ◽  
...  

This study assessed the impact of reduced dietary protein during specific periods of fetal life upon muscle fibre development in young rats. Pregnant rats were fed a control or low-protein (LP) diet at early (days 0–7 gestation, LPEarly), mid (days 8–14, LPMid), late (days 15–22, LPLate) or throughout gestation (days 0–22, LPAll). The muscle fibre number and composition in soleus and gastrocnemius muscles of the offspring were studied at 4 weeks of age. In the soleus muscle, both the total number and density of fast fibres were reduced in LPMid females (P = 0·004 for both, Diet × Sex × Fibre type interactions), while both the total number and density of glycolytic (non-oxidative) fibres were reduced in LPEarly, LPMid and LPLate (but not LPAll) offspring compared with controls (P < 0·001 for both, Diet × Fibre type interaction). In the gastrocnemius muscle, only the density of oxidative fibres was reduced in LPMid compared with control offspring (P = 0·019, Diet × Fibre type interaction), with the density of slow fibres being increased in LPAll males compared with control (P = 0·024, Diet × Sex × Fibre type interaction). There were little or no effects of maternal diet on fibre type diameters in the two muscles. In conclusion, a maternal low-protein diet mainly during mid-pregnancy reduced muscle fibre number and density in 4-week-old rats, but there were muscle-specific differences in the fibre types affected.

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Daniel Tomé ◽  
Joanna Moro ◽  
Anne Blais ◽  
Catherine Chaumontet ◽  
Patrick Even ◽  
...  

Abstract Objectives Low protein diet and essential amino acid deficient-diet have an impact on body weight and growth and different studies also showed an impact of lysine intake on bone metabolism. Lysine has been shown to promote the absorption of intestinal calcium and to participate in the collagen synthesis through its involvement in the reticulation process of the tropocollagen beams. The assembly of tropocollagen bundle into mature collagen fibers is essential for bone formation and remodeling (civitelli et al, 1992; Fini et al, 2001). The objective of this study was to characterize the impact of low protein diet and lysine-deficient diet on bone metabolism of growing rats. Methods Study 1: 6 group of growing rats were fed for 3 weeks different diet with different content of milk protein at levels of 3%, 5%, 8%, 12%, 15% or 20% (% total energy). Study 2: 7 group of growing rats were fed diets with different lysine content (as % of lysine requirement), for 3 weeks: 15%, 25%, 40%, 60%, 75%, 100% or 170% (% Lysine requirement). Body weight was measured daily. At the end of the experiment, the body composition was analyzed and tissues were removed for measurements of the expression of genes involved in protein and bone metabolism. Statistical analysis was done by variance analysis. Results Rats fed low protein diet (3% and 5% of milk protein), compared to control have a lower growth, with a lower body weight and naso-anal length. This weak growth was associated with a lower lean body mass, and also had an impact on bone metabolism. There was a decrease in the bone mineral density, bone mineral content and femur size, associated with a decrease of markers of bone turnover and formation. The same results on bone metabolism were observed on rats fed the 85% lysine deficient diet. Conclusions Low protein diet and lysine-deficient diet reduce growth and bone metabolism. The impact of low protein diet could be related to the lysine deficiency, which have an impact on the calcium intestinal absorption and on collagen synthesis. Funding Sources INRA, AgroParisTech. Supporting Tables, Images and/or Graphs


Parasitology ◽  
1997 ◽  
Vol 115 (3) ◽  
pp. 257-264 ◽  
Author(s):  
M. V. JOHANSEN ◽  
H. O. BØGH ◽  
H. GIVER ◽  
L. ERIKSEN ◽  
P. NANSEN ◽  
...  

The aim of the study was to measure the impact of Schistosoma japonicum and Trichuris suis infections in young growing pigs fed low- or high-protein diets. Thirty-two pigs, 6–10 weeks old, were randomly allocated to 2 groups receiving either a high- or a low-protein diet. After 11 weeks half of the pigs from each group were infected with 1500 S. japonicum cercariae and 4000 T. suis eggs. The weight of the pigs was measured throughout the study, and blood and faecal samples were collected every second week from the time of infection. At the time of infection the low-protein pigs had significantly lower mean body weights, haemoglobin and albumin levels compared with the high-protein pigs, and this pattern continued throughout the study. The serum albumin concentration was further significantly reduced in the infected low-protein pigs compared to the non-infected low-protein pigs. Significantly more S. japonicum worms as well as faecal and tissue eggs were found in the low-protein pigs compared with the high-protein pigs. No differences between the 2 diet groups were observed in T. suis establishment rates or faecal egg excretion. We conclude that this low-protein diet increased the establishment rates of S. japonicum, favoured larger deposits of S. japonicum eggs in the liver and faecal egg excretion, reduced weight gains and caused anaemia and hypoalbuminaemia in young growing pigs as compared with a high-protein diet.


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.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Mark R. Garbrecht ◽  
Fred S. Lamb

The placenta acts as a physiological barrier, preventing the transfer of maternal glucocorticoids to the developing fetus. This is accomplished via the oxidation, and subsequent inactivation, of endogenous glucocorticoids by the 11-β hydroxysteroid dehydrogenase type 2 enzyme (HSD2). Maternal protein restriction during pregnancy has been shown to result in a decrease in placental HSD2 expression and fetal glucocorticoid overexposure, especially late in gestation, resulting in low birth weight and “fetal programming” of the offspring. This dietary intervention impairs fetal growth and cardiovascular function in adult C57BL/6 offspring, but the impact on placental HSD2 has not been defined. The goal of the current study was to examine the effects of a maternal low-protein diet (18% versus 9% protein) on placental HSD2 gene expression and enzyme activity in mice during late gestation. In contrast to previous studies in rats, a maternal low-protein diet did not affect HSD2 protein or enzyme activity levels in the placentas of C57BL/6 mice and this was irrespective of the gender of the offspring. These data suggest that the effects of maternal protein restriction on adult phenotypes in C57BL/6 mice depend upon a mechanism that may be independent of placental HSD2 or possibly occurs earlier in gestation.


2021 ◽  
Author(s):  
Ioannis Kanakis ◽  
Moussira Alameddine ◽  
Leighton Folkes ◽  
Simon Moxon ◽  
Ioanna Myrtziou ◽  
...  

ABSTRACTNutrition plays a key role in pre- and postnatal growth of the musculoskeletal system. Maternal diet during gestation and lactation affects the development of skeletal muscles in the offspring and determines muscle health in later life, however, the molecular mechanisms that govern these effects are largely unknown. In this study, we aim to describe the association between maternal low protein diet-induced changes in offspring skeletal muscle and the differential expression (DE) of small non-coding RNAs (sncRNAs). We used a mouse model of maternal protein restriction to characterise the impact of early-life undernutrition on skeletal muscle morphology in male offspring at weaning. Mouse dams were fed either a normal (N, 20%) or a low protein (L, 8%) diet during gestation and newborn pups were cross-fostered to N or L lactating dams, resulting in the generation of NN, NL and LN offspring groups. Total body and tibialis anterior (TA) weights were decreased in NL males but not different in the LN group, as compared to NN, although neonates from low protein fed dams were smaller at birth than those born to dams fed a normal protein. However, histological evaluation of TA muscle revealed reduced muscle fibre size in both groups at the end of lactation. Small RNA-seq analysis demonstrated DE of multiple classes of sncRNAs, including miRs, snoRNAs and snRNAs. Bioinformatic analyses of miRs-15a, −34a, −122 and −199a, in combination with known myomiRs, confirmed their implication in key muscle-specific biological processes and cellular functions and suggest a promising set of miRs in muscle physiology studies. To our knowledge, this is the first comprehensive report for the DE of sncRNAs in nutrition-associated programming of skeletal muscle development, highlighting the need for further research.


2005 ◽  
Vol 109 (4) ◽  
pp. 413-420 ◽  
Author(s):  
Leanne Bellinger ◽  
Simon C. Langley-Evans

Undernutrition in fetal life programmes risk of obesity and the metabolic syndrome in adult life. Rat studies indicate that exposure to a maternal low-protein diet throughout fetal life establishes a preference for high-fat foods. The present study aimed to assess the effect of low protein exposure during discrete 7-day periods of gestation upon feeding behaviour (full gestation 22 days). Pregnant rats were fed control or low-protein diet, with low-protein feeding targeted at day 0–7 (LPEarly), day 8–14 (LPMid) or day 15–22 (LPLate) of gestation. At 12 weeks of age, offspring were placed on a macronutrient self-selection regimen. Prenatal protein restriction programmed feeding behaviour in female, but not male, offspring. Among females, all low-protein exposed groups consumed less fat than the control group (P<0.05). Male offspring showed no changes in feeding behaviour. In males and females fed a low-fat chow diet, there were metabolic differences between the groups. LPEarly and LPLate males had greater hepatic glycogen stores than control animals. There were no differences in the size of abdominal fat depots in either male or female rats exposed to low-protein diet at any point in gestation. The data suggest that programming of feeding behaviour is likely to be gender-specific and dependent upon the timing of nutrient insult in fetal life. This work may have implications for the development of the metabolic syndrome.


Reproduction ◽  
2020 ◽  
Vol 159 (5) ◽  
pp. 627-641 ◽  
Author(s):  
Hannah L Morgan ◽  
Isaac Ampong ◽  
Nader Eid ◽  
Charlène Rouillon ◽  
Helen R Griffiths ◽  
...  

The link between male diet and sperm quality has received significant investigation. However, the impact diet and dietary supplements have on the testicular environment has been examined to a lesser extent. Here, we establish the impact of a sub-optimal low protein diet (LPD) on testicular morphology, apoptosis and serum fatty acid profiles. Furthermore, we define whether supplementing a LPD with specific methyl donors abrogates any detrimental effects of the LPD. Male C57BL6 mice were fed either a control normal protein diet (NPD; 18% protein; n = 8), an isocaloric LPD (LPD; 9% protein; n = 8) or an LPD supplemented with methyl donors (MD-LPD; choline chloride, betaine, methionine, folic acid, vitamin B12; n = 8) for a minimum of 7 weeks. Analysis of male serum fatty acid profiles by gas chromatography revealed elevated levels of saturated fatty acids and lower levels of mono- and polyunsaturated fatty acids in MD-LPD males when compared to NPD and/or LPD males. Testes of LPD males displayed larger seminiferous tubule cross section area when compared to NPD and MD-LPD males, while MD-LPD tubules displayed a larger luminal area. Furthermore, TUNNEL staining revealed LPD males possessed a reduced number of tubules positive for apoptosis, while gene expression analysis showed MD-LPD testes displayed decreased expression of the pro-apoptotic genes Bax, Csap1 and Fas when compared to NPD males. Finally, testes from MD-LPD males displayed a reduced telomere length but increased telomerase activity. These data reveal the significance of sub-optimal nutrition for paternal metabolic and reproductive physiology.


2000 ◽  
Vol 83 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Margaret O. Nwagwu ◽  
Anna Cook ◽  
Simon C. Langley-Evans

Intrauterine growth retardation associated with maternal undernutrition is proposed to play a significant role in the aetiology of hypertension and CHD. Animal experiments suggest that the kidney, which is extremely vulnerable to the adverse effects of growth-retarding factors, may play an important role in the prenatal programming of hypertension. Maintenance of renal haemodynamic functions following structural impairment in fetal life is proposed to require adaptations which raise systemic blood pressure and promote a more rapid progression to renal failure. Rats were fed on diets containing 180 g casein/kg (control) or 90 g casein/kg (low protein) during pregnancy. The offspring were studied in terms of blood pressure, creatinine clearance, blood urea N, plasma and urinary albumin, renal morphometry and metabolic activity at 4, 12 and 20 weeks of age. Blood pressure was elevated at all ages in the low-protein-exposed offspring, relative to control rats. Rats (4 weeks old) exposed to the low-protein diet had smaller kidneys which were shorter and wider than those of control animals. Creatinine clearance was significantly reduced in 4-week-old rats exposed to the low-protein diet. Renal morphometry and creatinine clearance at older ages were not influenced by prenatal diet. Blood urea N, urinary output and urinary albumin excretion were, however, significantly greater in low-protein-exposed rats than in control rats at 20 weeks of age. These findings are suggestive of a progressive deterioration of renal function in hypertensive rats exposed to mild maternal protein restriction during fetal life. This is consistent with the hypothesis that adaptations to maintain renal haemodynamic functions following impairment of fetal nephrogenesis result in an accelerated progression towards glomerulosclerosis and increased intrarenal pressures mediated by rising vascular resistance.


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