scholarly journals Consequences of Paternal Nutrition on Offspring Health and Disease

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2818
Author(s):  
Pauline Dimofski ◽  
David Meyre ◽  
Natacha Dreumont ◽  
Brigitte Leininger-Muller

It is well established that the maternal diet during the periconceptional period affects the progeny’s health. A growing body of evidence suggests that the paternal diet also influences disease onset in offspring. For many years, sperm was considered only to contribute half of the progeny’s genome. It now appears that it also plays a crucial role in health and disease in offspring’s adult life. The nutritional status and environmental exposure of fathers during their childhood and/or the periconceptional period have significant transgenerational consequences. This review aims to describe the effects of various human and rodent paternal feeding patterns on progeny’s metabolism and health, including fasting or intermittent fasting, low-protein and folic acid deficient food, and overnutrition in high-fat and high-sugar diets. The impact on pregnancy outcome, metabolic pathways, and chronic disease onset will be described. The biological and epigenetic mechanisms underlying the transmission from fathers to their progeny will be discussed. All these data provide evidence of the impact of paternal nutrition on progeny health which could lead to preventive diet recommendations for future fathers.

Dose-Response ◽  
2014 ◽  
Vol 12 (4) ◽  
pp. dose-response.1 ◽  
Author(s):  
Mark P. Mattson

Humans and their predecessors evolved in environments where they were challenged intermittently with: 1) food scarcity; 2) the need for aerobic fitness to catch/kill prey and avoid or repel attackers; and 3) exposure to biological toxins present in foodstuffs. Accordingly, cells and organ systems acquired and retained molecular signaling and metabolic pathways through which the environmental challenges enhanced the functionality and resilience of the cells and organisms. Within the past 60 years there has been a precipitous diminution of such challenges in modern societies because of the development of technologies that provide a continuous supply of energy-dense processed foods and that largely eliminate the need for physical exertion. As a consequence of the modern ‘couch potato’ lifestyle, signaling pathways that mediate beneficial effects of environmental challenges on health and disease resistance are disengaged, thereby rendering people vulnerable to obesity, diabetes, cardiovascular disease, cancers and neurodegenerative disorders. Reversal of the epidemic of diseases caused by unchallenging lifestyles will require a society-wide effort to re-introduce intermittent fasting, exercise and consumption of plants containing hormetic phytochemicals into daily and weekly routines.


Author(s):  
Samuel Furse ◽  
Adam J. Watkins ◽  
Davide Chiarugi ◽  
Nima Hojat ◽  
James Smith ◽  
...  

AbstractWhile the consequences of poor maternal diet on the offspring’s cardio-metabolic health have been studied in detail, the role of the father’s diet on the health of his offspring is poorly understood. We used a known mouse model to establish the impact of an isocaloric paternal low-protein high-carbohydrate diet on the offspring’s lipid metabolism. Detailed lipid profiles were acquired from F1 neonate (3 weeks), F1 adult (16 weeks) and F2 neonate male and female offspring, in serum, liver, brain, heart and abdominal adipose tissues by Mass Spectrometry and Nuclear Magnetic Resonance. Using a purpose-built computational tool for analysing lipid metabolism as a network, we characterised the number, type and abundance of lipid variables in and between tissues (Lipid Traffic Analysis), finding a variety of alterations associated with paternal diet. These elucidate a mechanism for the defective physiological behaviour of systems at risk of cardio-metabolic disease.


2021 ◽  
Vol 8 (10) ◽  
pp. 233
Author(s):  
Kikianne Kroeske ◽  
Ester Arévalo Sureda ◽  
Julie Uerlings ◽  
Dieter Deforce ◽  
Filip Van Nieuwerburgh ◽  
...  

Maternal diet during early gestation affects offspring phenotype, but it is unclear whether maternal diet during late gestation influences piglet metabolism. We evaluated the impact of two dietary protein levels in sow late gestation diet and piglet nursery diet on piglet metabolism. Diets met or exceeded the crude protein and amino acid requirements. Sows received either 12% (Lower, L) or 17% (Higher, H) crude protein (CP) during the last five weeks of gestation, and piglets received 16.5% (L) or 21% (H) CP from weaning at age 3.5 weeks. This resulted in a 2 × 2 factorial design with four sow/piglet diet treatment groups: HH and LL (match), HL and LH (mismatch). Piglet hepatic tissues were sampled and differentially expressed genes (DEGs) were determined by RNA sequencing. At age 4.5 weeks, 25 genes were downregulated and 22 genes were upregulated in the mismatch compared to match groups. Several genes involved in catabolic pathways were upregulated in the mismatch compared to match groups, as were genes involved in lipid metabolism and inflammation. The results show a distinct interaction effect between maternal and nursery diets, implying that sow late gestation diet could be used to optimize piglet metabolism.


2021 ◽  
Author(s):  
Alaa Alkhalefah ◽  
Heather J Eyre ◽  
Rezwana Hussain ◽  
Jocelyn D Glazier ◽  
Nick Ashton

Pregnant Muslim women are exempt from fasting during Ramadan; however a majority are reported to fast. The impact of this form of maternal intermittent fasting (IF) on fetal development and offspring health is not well defined. Using a rat model, we have shown previously that maternal IF results in fetal growth restriction accompanied by changes in placental nutrient transport function. The aim of this study was to assess cardiovascular, metabolic and renal function in adult offspring of IF-exposed dams. Food was withheld from Wistar rats from 17:00 to 09:00 daily throughout pregnancy; controls had ad libitum access to food. Birth weight was unaffected; however male IF pups grew more slowly up to 10 weeks of age ( P < 0.01) whereas IF females matched their control counterparts. Systolic blood pressure (SBP), glucose tolerance and basal renal function at 14 weeks were not affected by IF exposure. When offered saline solutions (0.9-2.1%) to drink, females showed a greater salt preference than males ( P < 0.01); however there were no differences between dietary groups.  A separate group of pups was weaned onto a 4% NaCl diet. SBP increased in IF pups sooner, at 7 weeks ( P < 0.01), than controls which became hypertensive from 10 weeks. Renal function did not appear to differ; however markers of renal injury were elevated in IF males ( P < 0.05). Maternal IF does not affect resting cardiovascular, metabolic and renal function; but when challenged by dietary salt load male IF offspring are more prone to renal injury.


2007 ◽  
Vol 19 (1) ◽  
pp. 194
Author(s):  
N. A. Smith ◽  
P. Lonergan ◽  
P. Duffy ◽  
T. F. Crosby ◽  
P. Quinn ◽  
...  

Evidence from epidemiological and experimental studies has shown that maternal undernutrition during pregnancy can alter fetal growth and development and is associated with increased risk of hypertension and cardiovascular disease in the offspring. However, there is a paucity of data examining the effect of undernutrition during the periconceptual period on offspring health. Therefore, we investigated the impact of ewe undernutrition during the periconceptional period on lamb birth weight and blood pressure. Crossbred ewes (n = 166) were individually penned and randomly allocated to 1 of 2 treatments and fed either 0.7 (restricted) or 1.1 (control) maintenance energy requirements from 28 days prior until 7 days post-mating. After Day 7, ewes in both treatments were managed similarly until parturition. Following parturition, lamb gender, birth weight, and blood pressure were recorded. Lamb weight and blood pressure were subsequently measured at 4 and 10 weeks of age. Restricted ewes lost 2.6 � 0.2 kg over the treatment period compared with control ewes which gained 1.7 � 0.58 kg (P &lt; 0.01). There was no treatment effect on lamb birth weight in either singleton or twin gestations. However, at 4 and 10 weeks of age singleton lambs born to nutritionally restricted ewes were heavier than those born to control ewes (males, n = 17: 19.4 � 0.1 vs. 16.4 � 0.1 kg; females, n = 16: 34.9 � 1.0 vs. 30.9 � 1.6 kg, P &lt; 0.05). Blood pressure, measured within the first 24 h of life, was higher (P &lt; 0.05) in singleton lambs born to nutritionally restricted mothers compared to controls (males: systolic 126 � 11 vs. 94 � 5; diastolic 99 � 12 vs. 58 � 5; mean 112 � 11 vs. 77 � 5 mmHg; P &lt; 0.05; females: systolic 126 � 11 vs. 94 � 5; diastolic 99 � 12 vs. 58 � 5; mean 112 � 11 vs. 77 � 5 mmHg; P &lt; 0.05). This difference was no longer apparent at 4 or 10 weeks of age. Mean blood pressures of twin lambs at birth and 4 weeks of age were numerically greater in the restricted than in the control treatment but were significantly different only among male twin groups at 4 weeks of age (diastolic 77 � 4 vs. 94 � 4; mean 96 � 4 vs. 110 � 3 mmHg; P &lt; 0.01). Maternal undernutrition during the periconceptional period was associated with increased offspring weight at 4 and 10 weeks of age in singletons, as well as alterations in offspring cardiovascular function in both singletons and twins. These findings suggest that maternal nutrition at the time of conception influences offspring health. Exact mechanisms remain to be elucidated but may involve genetic modification. This research was funded by IRCSET and University College Dublin.


2013 ◽  
Vol 72 (3) ◽  
pp. 317-325 ◽  
Author(s):  
Simon C. Langley-Evans

The developmental origins of health and disease hypothesis postulates that exposure to a less than optimal maternal environment during fetal development programmes physiological function, and determines risk of disease in adult life. Much evidence of such programming comes from retrospective epidemiological cohorts, which demonstrate associations between birth anthropometry and non-communicable diseases of adulthood. The assertion that variation in maternal nutrition drives these associations is supported by studies using animal models, which demonstrate that maternal under- or over-nutrition during pregnancy can programme offspring development. Typically, the offspring of animals that are undernourished in pregnancy exhibit a relatively narrow range of physiological phenotypes that includes higher blood pressure, glucose intolerance, renal insufficiency and increased adiposity. The observation that common phenotypes arise from very diverse maternal nutritional insults has led to the proposal that programming is driven by a small number of mechanistic processes. The remodelling of tissues during development as a consequence of maternal nutritional status being signalled by endocrine imbalance or key nutrients limiting processes in the fetus may lead to organs having irreversibly altered structures that may limit their function with ageing. It has been proposed that the maternal diet may impact upon epigenetic marks that determine gene expression in fetal tissues, and this may be an important mechanism connecting maternal nutrient intakes to long-term programming of offspring phenotype. The objective for this review is to provide an overview of the mechanistic basis of fetal programming, demonstrating the critical role of animal models as tools for the investigation of programming phenomena.


2009 ◽  
Vol 68 (4) ◽  
pp. 416-421 ◽  
Author(s):  
Michael E. Symonds ◽  
Sylvain P. Sebert ◽  
Helen Budge

Changes in maternal diet at different stages of reproduction can have pronounced influences on the health and well-being of the resulting offspring, especially following exposure to an obesogenic environment. The mechanisms mediating adaptations in development of the embryo, placenta, fetus and newborn include changes in the maternal metabolic environment. These changes include reductions in a range of maternal counter-regulatory hormones such as cortisol, leptin and insulin. In the sheep, for example, targeted maternal nutrient restriction coincident with the period of maximal placental growth has pronounced effects on the development of the kidney and adipose tissue. As a consequence, the response of these tissues varies greatly following adolescent-onset obesity and ultimately results in these offspring exhibiting all the symptoms of the metabolic syndrome earlier in young adult life. Leptin administration to the offspring after birth can have some long-term differential effects, although much higher amounts are required to cause a response in small compared with large animal models. At the same time, the responsiveness of the offspring is gender dependent, which may relate to the differences in leptin sensitivity around the time of birth. Increasing maternal food intake during pregnancy, either globally or of individual nutrients, has little positive impact on birth weight but does impact on liver development. The challenge now is to establish which components of the maternal diet can be sustainably modified in order to optimise the maternal endocrine environment through pregnancy, thus ensuring feto–placental growth is appropriate in relation to an individual's gender and body composition.


Author(s):  
Sarah A. Luse

In the mid-nineteenth century Virchow revolutionized pathology by introduction of the concept of “cellular pathology”. Today, a century later, this term has increasing significance in health and disease. We now are in the beginning of a new era in pathology, one which might well be termed “organelle pathology” or “subcellular pathology”. The impact of lysosomal diseases on clinical medicine exemplifies this role of pathology of organelles in elucidation of disease today.Another aspect of cell organelles of prime importance is their pathologic alteration by drugs, toxins, hormones and malnutrition. The sensitivity of cell organelles to minute alterations in their environment offers an accurate evaluation of the site of action of drugs in the study of both function and toxicity. Examples of mitochondrial lesions include the effect of DDD on the adrenal cortex, riboflavin deficiency on liver cells, elevated blood ammonia on the neuron and some 8-aminoquinolines on myocardium.


2011 ◽  
Vol 21 (3) ◽  
pp. 112-117 ◽  
Author(s):  
Elizabeth Erickson-Levendoski ◽  
Mahalakshmi Sivasankar

The epithelium plays a critical role in the maintenance of laryngeal health. This is evident in that laryngeal disease may result when the integrity of the epithelium is compromised by insults such as laryngopharyngeal reflux. In this article, we will review the structure and function of the laryngeal epithelium and summarize the impact of laryngopharyngeal reflux on the epithelium. Research investigating the ramifications of reflux on the epithelium has improved our understanding of laryngeal disease associated with laryngopharyngeal reflux. It further highlights the need for continued research on the laryngeal epithelium in health and disease.


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