Coronary Heart Disease: A Disorder of Growth

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Abstract

A new ‘developmental’ model for the origins of coronary heart disease and the related disorders of type 2 diabetes, hypertension and stroke is emerging. The finding that people who develop these disorders have altered growth in utero, during infancy and childhood provides a new starting point for research. The immediate prospect for prevention is through protecting infant growth and preventing accelerated weight gain in children made vulnerable to later disease by small size at birth and during infancy. Ultimately we need to optimize maternal diet and composition before and during pregnancy. Despite current levels of nutrition in Western countries the nutrition of many fetuses and infants remains suboptimal because the nutrients available are unbalanced or because their delivery is constrained by the long and vulnerable fetal supply line.

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Role of fetal and infant growth in programming metabolism in later life.

C. Hales, Tanay Desai (1997)

Fetal growth and development is dependent upon the nutritional, hormonal and metabolic environment provided by the mother. Any disturbance in this environment can modify early fetal development with possible long-term outcomes as demonstrated by extensive work on 'programming'. Growth restriction resulting from a deficit in tissue/organ cell number (as measured by tissue DNA content) is irrecoverable. However, when the cell size (or cell protein content) is reduced, the effects on growth may not be permanent. Recent epidemiological studies using archival records of anthropometric measurements related to early growth in humans have shown strong statistical associations between these indices of early development and diseases in later life. It has been hypothesised that the processes explaining these associations involve adaptive changes in fetal organ development in response to maternal and fetal malnutrition. These adaptations may permanently alter adult metabolism in a way which is beneficial to survival under continued conditions of malnutrition but detrimental when nutrition is abundant. This hypothesis is being tested in a rat model which involves studying the growth and metabolism in the offspring of rat dams fed a low-protein diet during pregnancy and/or lactation. Using this rat model, it has been demonstrated that there is: (i) Permanent growth retardation in offspring nursed by dams fed a low-protein diet. (ii) Permanent and selective changes in organ growth. Essential organs like the brain and lungs are relatively protected from reduction in growth at the expense of visceral organs such as the liver, pancreas, muscle and spleen. (iii) Programming of liver metabolism as reflected by permanent changes in activities of key hepatic enzymes of glycolysis and gluconeogenesis (glucokinase and phosphoenolpyruvate carboxykinase) in a direction which would potentially bias the liver towards a 'starved' setting. We have speculated that these changes could be a result of altered periportal and perivenous regions of the liver which may also affect other aspects of hepatic function. (iv) Deterioration in glucose tolerance with age. (v) An increase in the life span of offspring exposed to maternal protein restriction only during the lactation period, and a decrease in life span when exposed to maternal protein restriction only during gestation. These studies show that hepatic metabolism and even longevity can be programmed by events during early life.

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Metabolic zonation of the liver: Regulation and implications for liver function

Rolf Gebhardt (1992)

Liver parenchyma shows a remarkable heterogeneity of the hepatocytes along the porto-central axis with respect to ultrastructure and enzyme activities resulting in different cellular functions within different zones of the liver lobuli. According to the concept of metabolic zonation, the spatial organization of the various metabolic pathways and functions forms the basis for the efficient adaptation of liver metabolism to the different nutritional requirements of the whole organism in different metabolic states. The present review summarizes current knowledge about this heterogeneity, its development and determination, as well as about its significance for the understanding of all aspects of liver function and pathology, especially of intermediary metabolism, biotransformation of drugs and zonal toxicity of hepatotoxins.

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Fetal growth and coronary heart disease in South India

CE Stein, CHD Fall, K. Kumaran … (1996)

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Author and article information

Journal

Journal ID (publisher-id): HRE

Journal ID (nlm-ta): Horm Res Paediatr

Journal ID (doi): 10.1159/issn.1663-2818

Title: Hormone Research in Paediatrics

Publisher: S. Karger AG

ISBN: 978-3-8055-7539-3

ISBN: 978-3-318-00942-2

ISSN (Print): 1663-2818

ISSN (Electronic): 1663-2826

Publication date Subscription-year: 2003

Publication date (Print): January 2003

Publication date (Electronic): 17 November 2004

Volume: 59

Issue: Suppl 1

Pages: 35-41

Affiliations

MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK

Article

Publisher ID: 67843 Other ID: Horm Res 2003;59(suppl 1):35–41

DOI: 10.1159/000067843

PubMed ID: 12566719

SO-VID: 37b1ae95-d727-4bf3-9dc3-c6f6a76e8ea7

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Coronary Heart Disease: A Disorder of Growth

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Karger: Endocrinology

Most cited references 4

Role of fetal and infant growth in programming metabolism in later life.

Metabolic zonation of the liver: Regulation and implications for liver function

Fetal growth and coronary heart disease in South India

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