Prenatal and Childhood Growth, Chemerin Concentrations, and Metabolic Health in Adult Life

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Abstract

Several noncommunicable diseases have their origins in early developmental phases. One factor possibly explaining the association between early growth and later health could be adipocyte function. The objective of this study was to assess the association between the adipocytokine chemerin and early growth and later health. 1074 participants from Helsinki Birth Cohort Study born 1934–1944 with information on prenatal and childhood growth participated. Metabolic outcomes include glucose tolerance, adiposity, and chemerin concentration. Mean chemerin concentrations were 5.0 ng/mL higher in women than in men (95% CI 2.7 to 7.2, p < 0.001). The strongest correlate of chemerin concentration was adult waist circumference and body fat percentage ( r = 0.22, p < 0.001 and r = 0.21, p < 0.001, resp.). After adjustment for body fat percentage, chemerin concentration was 5.4 ng/mL lower in subjects with type 2 diabetes than in those with normal glucose tolerance (−0.2 to 10.9, p = 0.06). It was 3.0 ng/mL higher in those with metabolic syndrome than in those without (0.6 to 5.3, p = 0.01). No measure of early growth was associated with chemerin concentration. Our findings do not support a role for chemerin in linking early growth with later metabolic health.

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Most cited references 34

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Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease.

Keith M. Godfrey, Karen A. Lillycrop, Graham Burdge … (2007)

There is now considerable evidence that elements of the heritable or familial component of disease susceptibility are transmitted by nongenomic means, and that environmental influences acting during early development shape disease risk in later life. The underlying mechanisms are thought to involve epigenetic modifications in nonimprinted genes induced by aspects of the developmental environment, which modify gene expression without altering DNA sequences. These changes result in life-long alterations in gene expression. Such nongenomic tuning of phenotype through developmental plasticity has adaptive value because it attempts to match an individual's responses to the environment predicted to be experienced. When the responses are mismatched, disease risk increases. An example of such mismatch is that arising either from inaccurate nutritional cues from the mother or placenta before birth, or from rapid environmental change through improved socioeconomic conditions, which contribute substantially to the increasing prevalence of type-2 diabetes, obesity, and cardiovascular disease. Recent evidence suggests that the effects can be transmitted to more than the immediately succeeding generation, through female and perhaps male lines. Future research into epigenetic processes may permit us to develop intervention strategies.

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Chemerin activation by serine proteases of the coagulation, fibrinolytic, and inflammatory cascades.

Brian Zabel, Samantha J. Allen, Paulina Kulig … (2005)

Proteases function at every level in host defense, from regulating vascular hemostasis and inflammation to mobilizing the "rapid responder" leukocytes of the immune system by regulating the activities of various chemoattractants. Recent studies implicate proteolysis in the activation of a ubiquitous plasma chemoattractant, chemerin, a ligand for the G-protein-coupled receptor CMKLR1 present on plasmacytoid dendritic cells and macrophages. To define the pathophysiologic triggers of chemerin activity, we evaluated the ability of serum- and inflammation-associated proteases to cleave chemerin and stimulate CMKLR1-mediated chemotaxis. We showed that serine proteases factor XIIa and plasmin of the coagulation and fibrinolytic cascades, elastase and cathepsin G released from activated neutrophil granules and mast cell tryptase are all potent activators of chemerin. Activation results from cleavage of the labile carboxyl terminus of the chemoattractant at any of several different sites. Activation of chemerin by the serine protease cascades that trigger rapid defenses in the body may direct CMKLR1-positive plasmacytoid dendritic cell and tissue macrophage recruitment to sterile sites of tissue damage, as well as trafficking to sites of infectious and allergic inflammation.

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Early adiposity rebound in childhood and risk of Type 2 diabetes in adult life.

C Osmond, T. Forsen, J Tuomilehto … (2003)

Type 2 diabetes is associated with a small body size at birth and a high BMI in adult life. The aim of our study was to assess the associations between Type 2 diabetes and birth size, infant growth and age at adiposity rebound. We carried out a longitudinal study of 8760 subjects born in Helsinki during 1934 to 1944. On average, they had 18 measurements of height and weight between birth and 12 years of age. In western countries BMI usually decreases after the age of 2 years and rises again at around 6 years--the so-called adiposity rebound. We defined age at adiposity rebound by the age of lowest BMI between one and 12 years. We identified people with Type 2 diabetes using a national register. A total of 290 individuals developed Type 2 diabetes in adult life. The cumulative incidence of Type 2 diabetes decreased progressively from 8.6% in persons whose adiposity rebound occurred before the age of 5 years to 1.8% in those in whom it occurred after 7 years ( p<0.001). Early adiposity rebound was preceded by low weight gain between birth and 1 year ( p<0.001). Large differences in the incidence of Type 2 diabetes are associated with growth rates in utero, weight gain in infancy and age at adiposity rebound.

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Author and article information

Journal

Journal ID (nlm-ta): Int J Endocrinol

Journal ID (iso-abbrev): Int J Endocrinol

Journal ID (publisher-id): IJE

Title: International Journal of Endocrinology

Publisher: Hindawi Publishing Corporation

ISSN (Print): 1687-8337

ISSN (Electronic): 1687-8345

Publication date (Print): 2016

Publication date (Electronic): 24 January 2016

Volume: 2016

Electronic Location Identifier: 3838646

Affiliations

¹National Institute for Health and Welfare, Department of Chronic Disease Prevention, 00271 Helsinki, Finland

²Department of General Practice and Primary Health Care, University of Helsinki and Helsinki University Hospital, 00014 Helsinki, Finland

³Folkhälsan Research Centre, 00250 Helsinki, Finland

⁴Institute of Biomedicine, Exercise Medicine, University of Eastern Finland, 70211 Kuopio, Finland

⁵MRC Lifecourse Epidemiology Unit (University of Southampton), Southampton General Hospital, Southampton SO16 6YD, UK

Author notes

*Johan G. Eriksson: johan.eriksson@ 123456helsinki.fi

Academic Editor: Kristin Eckardt

Article

DOI: 10.1155/2016/3838646

PMC ID: 4745322

PubMed ID: 26904119

SO-VID: b1c42222-7397-424b-ab65-e9ef8760ec57

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.