Synthesis of Leptin in Human Placenta

Señarı́s, Rosa; García‐Caballero, Tomás; Casabiell, Xesús; Gallego, Rosalı́a; Castro, Ramón; Considine, Robert V.; Diéguez, Carlos; Casanueva, Felipe F.

doi:10.1210/endo.138.10.5573

Cited by 265 publications

(123 citation statements)

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“…The OB gene, 9 expressed at least in adipose tissue, 32 placenta, 33 and the stomach, 34 encodes a secreted protein which acts as an adipocyte-derived satiety factor regulating body weight homeostasis and energy expenditure. 35,36 Our data show an association between WAT OB gene expression and plasma leptin levels (P 0.09), both being increased in cafeteria diet-induced obese rats as compared to lean animals fed a normal laboratory chow.…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Berraondo

Marti

Duncan³

et al. 2000

Int J Obes

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OBJECTIVE: The anti-obesity properties of a new b 3 -adrenergic agonist (Trecadrine) were examined in a diet-induced obesity model, including the effects on OB and uncoupling protein (UCP-1 and -2) gene expression. MEASUREMENTS: Control rats and cafeteria-fed rats were treated with placebo or Trecadrine for 35 days. Leptin and UCP (1 and 2) mRNA levels were determined by reverse transcription ± polymerase chain reaction (RT-PCR) methodology in adipose tissue and gastrocnemius muscle. RESULTS: Animals fed a cafeteria diet increased body weight, fat content, white adipose tissue (WAT), brown adipose tissue (BAT) weights and oxygen consumption in relation to lean controls. A rise in plasma leptin, WAT OB gene expression as well as circulating free fatty acids levels was found in obese rats as compared with lean controls. Trecadrine administration to cafeteria-fed animals decreased fat content, WAT weight, circulating leptin and fatty acids concentrations, and WAT OB gene expression, reaching comparable values to lean controls, while WAT O 2 consumption was increased in these animals. Also, an increase in BAT UCP1 mRNA levels was found through a twoway analysis of variance in control and obese animals after Trecadrine administration. Gastrocnemius muscle UCP2 gene expression was reduced in lean Trecadrine-treated and diet-induced obese animals as compared to controls, while an increase was found in cafeteria-fed animals after Trecadrine administration. A negative correlation between WAT O 2 consumption and UCP2 expression was found in control animals, but not in the cafeteria-fed groups, suggesting a differential response to the b 3 -adrenergic compound in lean and obese animals, which is in agreement with the reported statistical interactions between obesity and Trecadrine administration found for WAT O 2 consumption and muscle UCP2 expression, as well as for plasma leptin and WAT leptin expression. CONCLUSION: The new b 3 -adrenergic agonist, Trecadrine, decreases fat content and increases gastrocnemius muscle UCP2 gene expression in a diet-induced obesity model. This sheds additional light on the action mechanism of compounds with af®nity for b 3 -adrenoceptors and other potential anti-obesity agents.

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Section: Discussionmentioning

confidence: 99%

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Berraondo

Marti

Duncan³

et al. 2000

Int J Obes

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“…Human placental leptin is identical to that from adipose tissue on the basis of size, charge and immunoreactivity (Senaris et al, 1997). However, although it has the same promoter, the human placental leptin gene has an upstream enhancer that is used in the placental JEG-3 and JAR choriocarcinoma cell lines but not in adipocytes or non-placental HeLa cells.…”

Section: Functionmentioning

confidence: 99%

Placental leptin

Ashworth¹,

Hoggard²,

Thomas³

et al. 2000

Reviews of Reproduction

175

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“…Leptin is secreted predominantly from adipocytes, and the blood-cerebrospinal fluid barrier at the choroids plexus and the blood-brain barrier at the cerebral endothelium are two major controlling sites for the entry of circulating leptin into the brain (Zhang et al 1994;Zlokovic et al 2000). Nevertheless, recent works indicate that leptin gene is also expressed in placenta (Senaris et al 1997), stomach (Bado et al 1998), heart (Matsui et al 2007), skeletal muscle (Wang et al 1998), and mammary gland (Smith-Kirwin et al 1998). Morash et al (1999) also report that gene and protein of leptin are expressed in rat cortex, cerebellum, hypothalamus, and pituitary gland in the CNS (Morash et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Leptin induces migration and invasion of glioma cells through MMP‐13 production

Yeh

Lee

et al. 2008

Glia

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Leptin, the product of the obses gene, plays an important role in the regulation of body weight by coordinating metabolism, feeding behavior, energy balance and neuroendocrine responses. However, central regulation of leptin gene expression is different from that in the adipocytes. In addition, leptin has been found in many tumor cell lines and has been shown to have mitogenic and angiogenic activity in a number of cell types. Glioma is the most common primary adult brain tumor with poor prognosis due to the spreading of tumor cell to the other regions of brain easily. Here we found that malignant C6 glioma cells expressed more leptin and leptin receptors than non-malignant astrocytes. Furthermore, it was found that exogenous application of leptin enhanced the migration and invasion of C6 glioma cells. In addition, we found that the expression of matrix metalloproteinase-13 (MMP-13) but not of MMP-2 and MMP-9 was increased in response to leptin stimulation. The leptin-induced increase of cell migration and invasion was antagonized by MMP-13 neutralizing antibody or silencing MMP-13. The up-regulation of MMP-13 induced by leptin was mainly through p38 MAP kinase and NF-κB pathway. In addition, migration-prone sublines demonstrate that cells with increasing migration ability had more expression of MMP-13 and leptin. Taken together, these results indicate that leptin enhanced migration and invasion of C6 glioma cells through the increase of 2

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Synthesis of Leptin in Human Placenta

Abstract: leptin is synthesized as a single molecular variant identical to human recombinant leptin in human placentae at delivery.

Cited by 265 publications

References 0 publications

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Placental leptin

Leptin induces migration and invasion of glioma cells through MMP‐13 production

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