Growth and development of adipose tissue

Poissonnet, Claude M.; LaVelle, Marquisa; Burdi, Alphonse R.

doi:10.1016/s0022-3476(88)80520-1

Cited by 79 publications

(52 citation statements)

References 69 publications

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“…Little is known about the formation of WAT during human development, and most of the data concerning adipocyte differentiation have been obtained from in vitro studies (1,2). Interestingly, while in rodents WAT cannot be macroscopically detected during embryogenesis and develops mainly after birth, in human fetuses the formation of WAT starts well before birth (18). In accordance with the study of Poissonnet et al (19), we detected preadipocytes in periorbital tissue at 12 weeks of gestation using the preadipocyte marker Pref1, an epidermal growth factor-like domain-containing transmembrane protein expressed by adipocyte precursors and known to inhibit adipocyte differentiation (20,21).…”

Section: Discussionmentioning

confidence: 99%

PKA regulatory subunit R2B is required for murine and human adipocyte differentiation

Peverelli¹,

Ermetici²,

Corbetta³

et al. 2014

EJEA

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Adipogenesis is a complex process modulated by several factors, including cAMP signaling. The main cAMP target is protein kinase A (PKA), a tetrameric enzyme with four regulatory subunits showing tissue-specific expression and function: PRKAR2B is the main regulatory subunit in adipose tissue in mice and in adult humans. This study aimed to evaluate the expression of PKA regulatory subunits in human adipose tissue during fetal development and to investigate their role in the differentiation of 3T3-L1 and primary human preadipocytes. The expression of PKA regulatory subunits was evaluated in fetal adipose tissue (immunohistochemistry) and in cultured 3T3-L1 and primary human preadipocytes (western blot analysis). Cultured cells were transiently transfected with siRNA against PRKAR2B and induced to differentiate. Differentiation was evaluated by intracellular triglyceride staining (Oil Red O) and expression of molecular markers of adipocyte differentiation. In this study, we found that PRKAR2B is the main regulatory subunit in human adipose tissue during fetal development, from 12 weeks of gestation to the end of gestation, as well as in 3T3-L1 and primary human preadipocytes. The expression of PRKAR2B increases progressively during in vitro differentiation. The silencing of PRKAR2B abolishes the increase in the expression of peroxisome proliferator-activated receptor gamma (PPARg (PPARG)), fatty acid synthase, aP2 (FABP4), and lipoprotein lipase, as well as intracellular triglyceride accumulation, resulting in impaired adipocyte differentiation in both mouse and human cell systems. In conclusion, PRKAR2B is the key PKA regulatory subunit involved in mouse and human adipose tissue development. The physiological increase in the expression of PRKAR2B is an essential event in adipogenesis in both mice and humans, and it might represent a possible target for future strategies for obesity treatment.

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Section: Discussionmentioning

confidence: 99%

PKA regulatory subunit R2B is required for murine and human adipocyte differentiation

Peverelli¹,

Ermetici²,

Corbetta³

et al. 2014

EJEA

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“…Accumulation of body fat is initiated at about 25 weeks of gestation 16 and B40% of the variation in birth weight reflects differences in the magnitude of fat deposition. 17 Thus, infants born with a lower birth weight are likely to have a reduced fat mass.…”

Section: The Developmental Origins Of Human Metabolic Diseasementioning

confidence: 99%

Epigenetic changes in early life and future risk of obesity

2010

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The rapid increase in incidence of obesity over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing obesity in later life. Initially, human studies showed that low birth weight was associated with an increased risk of obesity but increasingly there is evidence that overnutrition in the early life can also increase susceptibility to future obesity. These findings have now been replicated in animal models, which have shown that both maternal under-and overnutrition can induce persistent changes in gene expression and metabolism. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of obesity opens the possibility that interventions, either through nutrition or specific drugs, may modify long-term obesity risk and combat this rapid rise in obesity.

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“…Most patients with suspected soft tissue neoplasms present with a painless mass, although pain is reported in one-third of cases [2]. Delay in diagnosis is common; the most common misdiagnoses include post-traumatic or spontaneous hematoma and "lipoma.…”

Section: Introductionmentioning

confidence: 99%