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Review
. 2023 Dec 8;11(12):3252.
doi: 10.3390/biomedicines11123252.

The Impact of Maternal Obesity on Adipose Progenitor Cells

Simon Lecoutre  1 , Salwan Maqdasy  2 , Mélanie Lambert  3   4 , Christophe Breton  5   6
Affiliations
Review

The Impact of Maternal Obesity on Adipose Progenitor Cells

Simon Lecoutre et al. Biomedicines. .

Abstract

The concept of Developmental Origin of Health and Disease (DOHaD) postulates that adult-onset metabolic disorders may originate from suboptimal conditions during critical embryonic and fetal programming windows. In particular, nutritional disturbance during key developmental stages may program the set point of adiposity and its associated metabolic diseases later in life. Numerous studies in mammals have reported that maternal obesity and the resulting accelerated growth in neonates may affect adipocyte development, resulting in persistent alterations in adipose tissue plasticity (i.e., adipocyte proliferation and storage) and adipocyte function (i.e., insulin resistance, impaired adipokine secretion, reduced thermogenesis, and higher inflammation) in a sex- and depot-specific manner. Over recent years, adipose progenitor cells (APCs) have been shown to play a crucial role in adipose tissue plasticity, essential for its development, maintenance, and expansion. In this review, we aim to provide insights into the developmental timeline of lineage commitment and differentiation of APCs and their role in predisposing individuals to obesity and metabolic diseases. We present data supporting the possible implication of dysregulated APCs and aberrant perinatal adipogenesis through epigenetic mechanisms as a primary mechanism responsible for long-lasting adipose tissue dysfunction in offspring born to obese mothers.

Keywords: adipose tissue; developmental origin of health and disease; epigenome; fat expansion; gene expression; maternal obesity; perinatal period.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Perinatal environment plays a crucial role in adipogenesis, shaping both early and adult adipose tissue plasticity. Early-life obesity encourages the formation of fat cells (i.e., higher adipose precursor cells (APCs) proliferation) and programs the expansion of adipose tissue. It may result in exacerbated adipogenesis (i.e., higher hypertrophy and/or hyperplasia) throughout life. On the one hand, these processes may raise the body’s adiposity level, contributing to the onset of childhood obesity that may persist in adulthood. On the other hand, the APCs may deplete prematurely, leading to impaired adipose tissue plasticity and its associated metabolic diseases later in life.
Figure 2
Figure 2
Epigenetic memory hypothesis: unraveling the mechanism connecting maternal obesity to adipose tissue dysfunction in offspring. Maternal obesity may create an unfavorable nutritional and hormonal milieu, influencing chromatin remodeling during perinatal adipogenesis. This intracellular remodeling may impact the gene-regulatory machinery and gene expression patterns, resulting in impaired adipocyte function. The epigenomic changes initiated in the perinatal period may persist into adulthood as an enduring epigenetic memory, contributing to a predisposition to obesity (i.e., higher adipocyte number and/or size, lower preadipocyte number, and impaired adipose tissue plasticity) and associated metabolic dysfunction later in life.
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