Chromosomal and Other Genetic Influences on Birth Weight Variation

Polanl, P. E.

doi:10.1002/9780470720097.ch8

Cited by 29 publications

(3 citation statements)

References 116 publications

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“…If this condition continued, they might continue to falter and become short-statured adults. Growth faltering is a significant public health concern because attained height has important implications for adult work performance [23] and reproductive outcomes [24,25].…”

Section: Discussionmentioning

confidence: 99%

Zinc Deficiency among Adolescence in Stunting Locus Area, Lombok, Indonesia

Irawati¹,

Nurbaiti²,

Ekawanti³

2021

Advances in Health Sciences Research

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Adolescence is at risk for zinc deficiency due to their high acceleration of growth, with bone mineral deposition reaching 80-90% by the adolescent phase. In zinc deficiency, adjustments in zinc pools were made, including the release of zinc retention in bones. Severe zinc deficiency could lead to growth retardation. This study aimed to determine the occurrence of zinc deficiency in the early adolescent stage (10 -12 years) in the stunting locus area, Lombok. In the first stage, a cross-sectional design was conducted among children aged 10 -12 years in Mataram City and East Lombok. In the second stage, subjects were assigned to the stunting and non-stunting group with a case-control design. Zinc intake assessment of 3-day 24 hours recall and concentration of zinc serum were used to determine zinc status. Approximately 34% of the subjects were stunting (n=774). Further analysis showed that 100% of the subjects (n=207) had a low zinc intake, with the average zinc intake below 45% of the recommended dietary allowance for zinc. The occurrence of zinc deficiency according to zinc serum concentration was only 2% of subjects. No significant difference in zinc intake and zinc serum was found between the stunted and non-stunted groups. Low zinc intake was observed among children in stunting locus districts. However, the proportion of zinc deficiency based on zinc serum concentration was very small. Zinc serum concentration may not capture zinc deficiency in the population, especially the mild or moderate ones.

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Section: Discussionmentioning

confidence: 99%

Zinc Deficiency among Adolescence in Stunting Locus Area, Lombok, Indonesia

Irawati¹,

Nurbaiti²,

Ekawanti³

2021

Advances in Health Sciences Research

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“…A esse respeito, vale citar estudo clinico que mostra um coeficiente de correlação de pesos de nascimento de meio-irmãos maternos de 0,581, para apenas 0,102 para meio-irmãos paternos (como termo de comparação, irmãos sucessivos tinham coeficiente de correlação igual a 0,523). Polani (1974), trabalhando com dados de Karn, Penrose e outros, acha que o peso do feto recebe as seguintes influências relativas: 38% genéticas e 62% do ambiente; incluindo o organismo materno.…”

Section: Influências Diversas No Retardo Do Crescimento Do Fetounclassified

Considerações sobre neonatos de baixo peso ao nascer

Araújo¹,

Bezerra²,

Maranhão³

2014

IDonline

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“…During early pre-natal development, the pattern of growth is largely dictated by the foetal genome, but as the body size increases, the foetus becomes constrained by maternal and environmental influences such as uterine blood flow, maternal size and maternal disease (see review by Gluckman and Liggins 1984). The influence of foetal and maternal genotypes has been analysed for their relative contribution towards the ultimate foetal Polani 1974). The interaction between the two genomes determines the successful growth and development of the embryo/foetus.…”

Section: Regulation Of Foetal Growth and Developmentmentioning

confidence: 99%

Pathophysiology, cellular and molecular mechanisms of foetal growth retardation

Han

1993

Equine Veterinary Journal

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Summary In mammals, size at birth is the outcome of length of gestation and rate of foetal growth. In the absence of premature delivery, foetal size within species is determined principally by foetal growth rate which is dependent on both genetic and epigenetic factors. Failure of either of these mechanisms leads to foetal growth retardation. In mammals, including human infants, foetal growth retardation can occur naturally or pathologically. One major cause for natural foetal growth retardation or runting is the increase in litter size. In many cases, however, the cause of runting is unknown. Parental genotype or antigenic differences between the mother and the developing conceptus may be potential causes. Pathological foetal growth retardation or intrauterine growth retardation (IUGR) is due to genetic causes (chromosomal abnormalities or inherited syndromes) or epigenetic causes (intrauterine infections, toxins and chemicals, maternal diseases of pregnancy affecting the placenta). The underlying pathophysiological processes that occur at the cellular and molecular level in IUGR are still unknown. Reduction in the supply of substrates that are necessary for normal cellular function, and alteration in mediator molecules that regulate cellular growth and differentiation, are important mechanisms. A decrease in growth promoting factors or an increase in growth inhibitory factors may lead to growth failure. Growth factors and their receptors are expressed in the developing embryo (as early as the 1–2‐cell stage), placenta and maternal uterine tissues, suggesting that these molecules may play a role in regulating normal growth and differentiation of the conceptus as well as maternal reproductive tissues. The local expression within developing tissues indicates that these factors act in either autocrine or paracrine mechanism. Recent studies using gene targeting to knock out one allele of insulin‐like growth factor II (IGF II) gene in mice which resulted in growth retarded pups at birth, strongly support the importance of local IGF II in regulating tissue growth. Foetal growth retardation has also been induced experimentally in several species using one of the following methods: (i) maternal undernutrition, (ii) chronic hypoxia, (iii) prolonged reduction in uterine blood flow, (iv) reduction in placental size, and (v) endocrine alterations. These models provide useful information on the physiological mechanisms underlying a specific type of growth retardation. These in‐vivo models and in‐vivo tissue culture models can now be analysed by biochemical and molecular biological techniques to unravel the basic mechanisms that underlie foetal growth retardation.

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Chromosomal and Other Genetic Influences on Birth Weight Variation

Cited by 29 publications

References 116 publications

Zinc Deficiency among Adolescence in Stunting Locus Area, Lombok, Indonesia

Zinc Deficiency among Adolescence in Stunting Locus Area, Lombok, Indonesia

Considerações sobre neonatos de baixo peso ao nascer

Pathophysiology, cellular and molecular mechanisms of foetal growth retardation

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