Origin and Development of the Adipose Tissue, a Key Organ in Physiology and Disease

Parra-Peralbo, Esmeralda; Talamillo, Ana; Barrio, Rosa

doi:10.3389/fcell.2021.786129

Cited by 39 publications

(27 citation statements)

References 243 publications

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“…As LSCs displayed lower proliferation and adipogenic differentiation than ASCs, we hypothesized that these cell features would not account to the development of lipoma neoplasia. Because adipose tissue is a large endocrine organ, and especially mature adipocytes secrete around 600 different soluble factors to act in paracrine and/or endocrine manner to orchestrate tissue development and maintenance, 18 we expanded our study on the secretory activity of mature adipocytes and lipomacytes to determine a possible role of these cells on the local microenvironment and lipoma pathogenesis. This could shift the focus to a dysfunction of mature lipoma cells that, by going to affect the local microenvironment and consequently the activity of surrounding cells, could be the real protagonists in creating the situations necessary for the pathogenesis of the lipoma itself in vivo.…”

Section: Discussionmentioning

confidence: 99%

Adipose and lipoma stem cells: A donor‐matched comparison

Conte

Beier

Ruhl

2022

Cell Biochemistry & Function

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Lipomas are slow growing benign fat tumors that develop in soft tissues of the mesoderm. Thus, the specific (dys-)function of mesenchymal stem cells (MSCs) has been suggested in the development of lipomas, but details of the tumor pathogenesis remain unclear. Existing studies comparing stem cells from native adipose (adipose stem cells [ASCs]) and lipomatous tissues (LSCs) have reported contradicting findings.However, harvesting ASCs and LSCs from different individuals might have influenced proper comparison. Therefore, we aimed to characterize donor-matched ASCs and LSCs to investigate metabolic activity, proliferation, capability for tri-linear differentiation (chondrogenesis, adipogenesis, osteogenesis), and the secretome of mature adipocytes and lipomacytes. Both stem cell types did not differ in metabolic activity, but ASCs demonstrated stronger proliferation than LSCs. While there was no difference in proteoglycan accumulation during chondrogenic differentiation, adipogenesis was higher in ASCs, with more lipid vacuole formation. Conversely, LSCs showed increased osteogenesis by higher calcium deposition. Lipomacytes showed stronger secretory activity and released higher levels of certain adipokines. Our findings indicated that LSCs possessed important characteristics of MSCs, including ASCs. However, LSCs' low proliferation and adipogenic differentiation behavior did not appear to account for enhanced tissue proliferation, but the secretome of lipomacytes could contribute to lipomatous neoplasm.

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Section: Discussionmentioning

confidence: 99%

Adipose and lipoma stem cells: A donor‐matched comparison

Conte

Beier

Ruhl

2022

Cell Biochemistry & Function

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“…BAT generates heat by burning calories, whereas WAT storages excess energy (Chait and den Hartigh, 2020). The mass and metabolic activity of BAT decrease with age and weight (Alcalá et al, 2019;Parra-Peralbo et al, 2021). With obesity, lipid accumulation and mitochondrial dysfunction shift the function of BAT from thermogenesis to lipid storage (Shimizu and Walsh, 2015).…”

Section: Open Accessmentioning

confidence: 99%

Parental obesity-induced changes in developmental programming

Cechinel

Batabyal²,

Freishtat³

et al. 2022

Front. Cell Dev. Biol.

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Many studies support the link between parental obesity and the predisposition to develop adult-onset metabolic syndromes that include obesity, high blood pressure, dyslipidemia, insulin resistance, and diabetes in the offspring. As the prevalence of obesity increases in persons of childbearing age, so does metabolic syndrome in their descendants. Understanding how parental obesity alters metabolic programs in the progeny, predisposing them to adult-onset metabolic syndrome, is key to breaking this cycle. This review explores the basis for altered metabolism of offspring exposed to overnutrition by focusing on critical developmental processes influenced by parental obesity. We draw from human and animal model studies, highlighting the adaptations in metabolism that occur during normal pregnancy that become maladaptive with obesity. We describe essential phases of development impacted by parental obesity that contribute to long-term alterations in metabolism in the offspring. These encompass gamete formation, placentation, adipogenesis, pancreas development, and development of brain appetite control circuits. Parental obesity alters the developmental programming of these organs in part by inducing epigenetic changes with long-term consequences on metabolism. While exposure to parental obesity during any of these phases is sufficient to alter long-term metabolism, offspring often experience multiple exposures throughout their development. These insults accumulate to increase further the susceptibility of the offspring to the obesogenic environments of modern society.

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“…However, in addition to the disappearing larval adipocytes, the eclosed adult displays segmental plates of adult fat body lining the abdomen (Fig 1A ), with lesser amounts found in the head, thorax, and female gonads. In contrast to the well-known development of the larval fat body, adult fat body adipogenesis has remained mysterious to this date [16][17][18]. Clonal analysis shows that the adult fat body, like the larval fat body, is mesodermal in origin [19].…”

Section: Introductionmentioning

confidence: 99%

FGF signaling promotes spreading of fat body precursors necessary for adult adipogenesis in Drosophila

et al. 2023

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Knowledge of adipogenetic mechanisms is essential to understand and treat conditions affecting organismal metabolism and adipose tissue health. In Drosophila, mature adipose tissue (fat body) exists in larvae and adults. In contrast to the well-known development of the larval fat body from the embryonic mesoderm, adult adipogenesis has remained mysterious. Furthermore, conclusive proof of its physiological significance is lacking. Here, we show that the adult fat body originates from a pool of undifferentiated mesodermal precursors that migrate from the thorax into the abdomen during metamorphosis. Through in vivo imaging, we found that these precursors spread from the ventral midline and cover the inner surface of the abdomen in a process strikingly reminiscent of embryonic mesoderm migration, requiring fibroblast growth factor (FGF) signaling as well. FGF signaling guides migration dorsally and regulates adhesion to the substrate. After spreading is complete, precursor differentiation involves fat accumulation and cell fusion that produces mature binucleate and tetranucleate adipocytes. Finally, we show that flies where adult adipogenesis is impaired by knock down of FGF receptor Heartless or transcription factor Serpent display ectopic fat accumulation in oenocytes and decreased resistance to starvation. Our results reveal that adult adipogenesis occurs de novo during metamorphosis and demonstrate its crucial physiological role.

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Origin and Development of the Adipose Tissue, a Key Organ in Physiology and Disease

Cited by 39 publications

References 243 publications

Adipose and lipoma stem cells: A donor‐matched comparison

Adipose and lipoma stem cells: A donor‐matched comparison

Parental obesity-induced changes in developmental programming

FGF signaling promotes spreading of fat body precursors necessary for adult adipogenesis in Drosophila

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