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Cited by 130Adipokines, Inflammation, and Metabolic DiseasesBirth, Development, and HealthAdipose Tissue and Metabolism

Adipocytes and adipose tissue.

Kiess, Wieland, Petzold, Stephanie, Töpfer, Madlen, Garten, Antje, Blüher, Susann, Kapellen, Thomas, Körner, Antje, Kratzsch, Jürgen·2008·Best Practice & Research Clinical Endocrinology & Metabolism
DOI 10.1016/j.beem.2007.10.002
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Abstract

An epidemic of obesity is taking place in most societies around the world. Overall obesity substantially increases the risk of subsequent morbidity. In children and adolescents the degree of body fat mass depends upon ethnic background, gender, developmental stage and age. Obesity is characterized by increases in the number or size of fat cells, or a combination of both. It is generally believed that the number of fat cells depends on age of onset and degree of obesity. This chapter provides information on intrauterine growth of fetal adipose tissue, the earliest period of onset of proliferation, and some of the factors that interact to enhance or suppress development. Fetal adipose tissue development is regulated by the complex interaction of transcription factors, nutrients and adipocytokines. Maternal, endocrine, and paracrine factors also influence specific changes in angiogenesis, adipogenesis, and metabolism. During embryogenesis and in fetal life, leptin and adiponectin, two important adipocytokines, are present at high concentrations in the circulation and in tissues. Developmental stages and metabolic processes influenced by specific hormones and paracrine factors have been identified through examination of the offspring of obese and diabetic pregnancies, hormonal manipulation during late pregnancy in animal models, and the use of cell cultures. Collectively, the results of the studies cited herein delineate the basis for imprinting or conditioning of fetal pre-adipocytes at the paracrine/autocrine level, and of fetal adipose tissue development and metabolism.

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  • Obese subjects are hyperleptinemic compared with lean persons.

    “However, although obese subjects are hyperleptinemic compared with lean persons (11), they appear either to be tolerant or resistant to the central hypothalamic effects of leptin.”

    From Leptin in humans: lessons from translational research (2009) · cites this paper as [11]

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Authors
Kiess, W., Petzold, S., Töpfer, M., Garten, A., Blüher, S., Kapellen, T., Körner, A., & Kratzsch, J.
Affiliations
Leipzig University (DE)
Corresponding author
Kiess, Wieland
ORCID
Venue
Best Practice & Research Clinical Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2008-02
Volume
22
Issue
1
Pages
135-153
ISSN
1521-690X (ISSN-L)
DOI
10.1016/j.beem.2007.10.002
OpenAlex
W1985271863
Cited by
130
References
55
Citations by year
2026: 4 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 11 · 2020: 3 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 4 · 2015: 11 · 2014: 8 · 2013: 11 · 2012: 8
FWCI
1.28
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Best Practice & Research Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
adipocytes, adipose tissue, obesity, adipogenesis, angiogenesis, leptin, adiponectin, adipokines, fetal growth, maternal factors, paracrine factors, developmental programming, childhood obesity, adipocyte proliferation
MeSH terms
Adipose Tissue, Animals, Female, Humans, Infant, Male, Obesity, Pregnancy, Adipocytes, Gene Expression Regulation, Developmental, Adipogenesis, Adipokines, Mesenchymal Stem Cells

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