Physiological role of epidermal growth factor on adipose tissue development in vivo.

Serrero, Ginette; Mills, Dianne

doi:10.1073/pnas.88.9.3912

Cited by 73 publications

(42 citation statements)

References 30 publications

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“…Available data in rats are consistent with a role of EGF on adipose tissue development. In newborn rats, daily EGF injections decrease both body and fat pad weight gains with no effects on other organs (Serrero and Mills, 1991). The number of adipocyte precursors per fat pad is higher in fat pads from EGF-treated animals than in control rats, but triglyceride storage in these tissues is lower.…”

Section: Leptinmentioning

confidence: 90%

Growth and development of adipose tissue and gut and related endocrine status during early growth in the pig: impact of low birth weight

Morise

Louveau

Huërou‐Luron

2008

Animal

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With genetic selection, the increase in litter size has led to higher variation in within-litter birth weights in pigs. This has been associated with a reduction in mean birth weights and a rise in the proportion of piglets weighing less than 1 kg at birth. Low birth weight pigs exhibit lower postnatal growth rates and feed efficiency, which may be explained by an inadequate digestion and/or nutrient use as a consequence of prenatal undernutrition. It is now documented that there is a relationship between birth weight and subsequent pattern of growth and development of tissues and organs. During the neonatal period, the rapid somatic growth is accompanied by tremendous anatomical, physiological and chemical composition changes. The present review focuses primarily on the influence of low birth weight on adipose tissue and the gastrointestinal tract growth and development during the suckling period. The importance of the somatotropic axis, insulin, thyroid hormones, glucocorticoids, epidermal growth factor and leptin in the regulation of these developmental processes is also considered.

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Section: Leptinmentioning

confidence: 90%

Growth and development of adipose tissue and gut and related endocrine status during early growth in the pig: impact of low birth weight

Morise

Louveau

Huërou‐Luron

2008

Animal

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“…Moreover, primary rat adipogenic precursor cells are also inhibited from becoming adipocytes in the presence of EGF (14), and EGF-treated animals show retardation of the development of adipose tissue (16). Although the precise mechanism of this …”

Section: Discussionmentioning

confidence: 99%

Regulation of Peroxisome Proliferator-activated Receptor γ Activity by Mitogen-activated Protein Kinase

Camp¹,

Tafuri²

1997

Journal of Biological Chemistry

420

275

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Adipocyte differentiation is regulated both positively and negatively by external growth factors such as insulin, platelet-derived growth factor (PDGF), and epidermal growth factor (EGF). A key component of the adipocyte differentiation process is PPAR␥, peroxisomal proliferator-activated receptor ␥. To determine the relationship between PPAR␥ activation and growth factor stimulation in adipogenesis, we investigated the effects of PDGF and EGF on PPAR␥1 activity. PDGF treatment decreased ligand-activated PPAR␥1 transcriptional activity in a transient reporter assay. In vivo [ 32 P]orthophosphate labeling experiments demonstrated that PPAR␥1 is a phosphoprotein that undergoes EGF-stimulated MEK/mitogen-activated protein (MAP) kinase-dependent phosphorylation. Purified PPAR␥1 protein was phosphorylated in vitro by recombinant activated MAP kinase. Examination of the PPAR␥1 sequence revealed a single MAP kinase consensus recognition site at Ser 82 . Mutation of Ser 82 to Ala inhibited both in vitro and in vivo phosphorylation and growth factor-mediated transcriptional repression. Therefore, phosphorylation of PPAR␥1 by MAP kinase contributes to the reduction of PPAR␥1 transcriptional activity by growth factor treatment.Peroxisome proliferator-activated receptors (PPARs) 1 are members of the nuclear hormone receptor superfamily (1). These receptors heterodimerize with retinoic acid-like receptor, RXR, and become transcriptionally active when bound to ligand. The three PPAR isoforms (␣, ␦, and ␥) differ in their C-terminal ligand binding domains, and each appears to bind and respond to a specific subset of agents including hypolipidemic drugs, long chain fatty acids, aracadonic acid metabolites, and antidiabetic thiazolidinediones (2-4). PPAR␥ is expressed predominantly in mouse white and brown fat, with lower levels in liver, whereas PPAR␣ is present in heart, kidney, and liver (5, 6). PPAR␦ expression is ubiquitous (7,8).Ectopic expression of either PPAR␣ or PPAR␥ in NIH-3T3 cells is sufficient to induce adipocyte differentiation in the presence of PPAR␥ activators (9, 10). The rapid induction of PPAR␥ during adipocyte differentiation and its enriched expression in adipose tissues suggest that PPAR␥ is responsible for the initiation and maintenance of the adipocyte phenotype in vivo (9). Previously two isotypes of PPAR␥ (PPAR␥1 and PPAR␥2) have been identified in 3T3-L1 adipocytes (11). Zhu et al. (12) have demonstrated that these two isotypes are derived from a single PPAR␥ gene by alternative promoter usage and RNA splicing. However, thus far, no functional difference has been found between the two isotypes.Adipogenesis is a complex process; multiple hormones and factors regulate the conversion of progenitor cells to adipocytes. Insulin and/or insulin-like growth factor enhance the ability of PPAR ligand to induce differentiation of both 3T3-L1-and PPAR␥-overexpressing cell lines (9, 13). In contrast, growth factors such as epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and fibroblast gro...

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“…It has been reported that EGF has a dual effect on fat synthesis [42,43]. It decreases adipogenesis in undifferentiated preadipocytes but increases adipogenesis in differentiated adipocytes [44].…”

Section: Discussionmentioning

confidence: 99%

Protein kinase A suppresses the differentiation of 3T3-L1 preadipocytes

Wang

Zhou

et al. 2008

Cell Res

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cAMP and protein kinase A (PKA) are widely known as signaling molecules that are important for the induction of adipogenesis. Here we show that a strong increase in the amount of cAMP inhibits the adipogenesis of 3T3-L1 fibroblast cells. Stimulation of PKA activity suppresses adipogenesis and, in contrast, inhibition of PKA activity markedly accelerates the adipogenic process. As adipogenesis progresses, there is a significant increase in the expression level of PKA regulatory subunits and a corresponding decrease in PKA activity. Moreover, treatment of 3T3-L1 cells with epidermal growth factor (EGF) stimulates PKA activity and blocks adipogenesis. Inhibition of PKA activity abolishes this suppressive effect of EGF on adipogenesis. Moreover, activation of PKA induces serine/threonine phosphorylation, reduces tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) and the association between PKA and IRS-1. Taken together, our study demonstrates that PKA has a pivotal role in the suppression of adipogenesis. cAMP at high concentrations can suppress adipogenesis through PKA activation. These findings could be important and useful for understanding the mechanisms of adipogenesis and the relevant physiological events.

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Physiological role of epidermal growth factor on adipose tissue development in vivo.

Cited by 73 publications

References 30 publications

Growth and development of adipose tissue and gut and related endocrine status during early growth in the pig: impact of low birth weight

Growth and development of adipose tissue and gut and related endocrine status during early growth in the pig: impact of low birth weight

Regulation of Peroxisome Proliferator-activated Receptor γ Activity by Mitogen-activated Protein Kinase

Protein kinase A suppresses the differentiation of 3T3-L1 preadipocytes

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