Leptin expression in placental and fetal tissues: does leptin have a functional role?

Hoggard, Nigel; Haggarty, Paul; Thomas, L; Lea, Richard G.

doi:10.1042/0300-5127:0290057

Cited by 60 publications

(46 citation statements)

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“…Leptin and LR mRNAs are expressed in bone and cartilage of the femur and hind-limb digits of 13.5-day postcoitus fetal mouse (13,32). Also, leptin injections enhanced limb bone mass and density in juvenile leptin-deficient ob͞ob mice (33), although others found that leptin had negative effects on bone growth that are mediated by the hypothalamus (34).…”

Section: Tissue Distribution Of Leptin and Lr Mrnasmentioning

confidence: 99%

Leptin ( ob gene) of the South African clawed frog Xenopus laevis

Crespi

Denver

2006

Proc. Natl. Acad. Sci. U.S.A.

148

133

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Leptin, the protein product of the obese (ob) gene, is a type-I cytokine hormone secreted by fat that is integral to food intake regulation and influences almost every physiological system in juvenile and adult mammals. Since the identification of leptin in the mouse in 1994, biologists have searched for orthologous genes in other species with limited success. In this article, we report the identification and functional characterization of leptin and leptin receptor (LR) in Xenopus. Despite low amino acid sequence similarity to mammalian leptins (Ϸ35%) the frog protein has a nearly identical predicted tertiary structure and can activate the frog and mouse LRs in vitro. We showed that recombinant frog leptin (rxLeptin) is a potent anorexigen in frogs, as it is in mammals, but this response does not develop until midprometamorphosis. However, during early prometamorphosis, exogenous rxLeptin induced growth and development of the hind limb, where LR mRNA is expressed. The rxLeptin also stimulated cell proliferation in cultured hind limbs from early prometamorphic tadpoles, as measured by [ 3 H]thymidine uptake. These findings are evidence that leptin can influence limb growth and differentiation during early development. Furthermore, the isolation and characterization of leptin and its receptor in a nonamniote provides an essential foundation for elucidating the structural and functional evolution of this important hormone.evolution ͉ metamorphosis ͉ obesity T he protein hormone leptin is a type-I cytokine secreted by adipocytes that acts on the CNS to regulate food intake and metabolism (1, 2). In addition to the regulation of body weight, leptin influences reproduction, growth, stress responses, and thyroid function (3, 4). Actions of leptin are both acute and chronic. For example, postprandial increases in plasma leptin inhibit food intake, whereas daily mean plasma leptin concentrations communicate long-term energy status to the brain (5). These actions are mediated by membrane leptin receptors (LRs), of which six isoforms have been identified in mammals (6). Leptin binding to the long form of the LR (LRb) activates the Janus kinase 2͞signal transducer and activator of transcription 3 (STAT-3) signaling pathway (7), which mediates leptin effects on food intake, glucose metabolism, and weight gain but does not affect fertility (8).The rising prevalence of human obesity and metabolic disorders (9) has focused research on the physiological role of leptin in energy balance and food intake in adult mammals. Recently, links between birth weight and adult-onset metabolic disorders (10) has turned attention to possible relationships among leptin, growth, and development during fetal stages. Circulating leptin is elevated in the human fetus during late gestation and correlates with fat mass and birth weight (11,12). In the fetal mouse, leptin and LR are expressed in liver, heart, hair follicles, and primordial bone before the formation of adipose tissue (13,14), and leptin is found in the circulation of fetal sheep (15)...

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Section: Tissue Distribution Of Leptin and Lr Mrnasmentioning

confidence: 99%

Leptin ( ob gene) of the South African clawed frog Xenopus laevis

Crespi

Denver

2006

Proc. Natl. Acad. Sci. U.S.A.

148

133

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“…In addition to its effects on satiety, leptin has been suggested to be involved in reproduction (Smith et al 2002), hematopoiesis (Bennett et al 1996), lactation (Mounzih et al 1998), inflamation of some tissues (Yavuz et al 2004) and homeostasis of fatty acid (Unger 2003). Initially, leptin was thought to be exclusively produced by adipocytes, however, it is now evident that leptin is present, in lesser amounts, in many fetal and adult tissues, including placenta (Hoggard et al 2001), stomach (Bado et al 1998), skeletal muscle (Wang et al 1998), pancreas (Emilsson et al 2001), bone (Reseland et al 2001) and pituitary cell types in rodents (Jin et al 2000). It has been demonstrated that leptin receptors are widely expressed throughout the brain of mouse (Huang et al 1996;Li and Kane 2003), rat (Shioda et al 1998) and human (Couce et al 1997).…”

confidence: 99%

Exogenous Leptin Increases Lipid Peroxidation in the Mouse Brain

Kutlu

Canpolat

Aydın

et al. 2005

Tohoku J. Exp. Med.

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Leptin, a hormone produced by the adipose tissues, reduces appetite and food intake, and increases energy expenditures by sending signals to the brain cells. As human obesity is associated with hyperleptinemia and increased systemic oxidative stress, we investigated whether leptin affects lipid peroxidation and antioxidant status in the brain. Leptin was intraperitoneally administered to adult male BALB/c mice (n = 6) at a dose of 40 μ g/animal for 5 days, while control mice (n = 6) received phosphate buffered saline. All animals were decapitated one hour after the last injection, and the brain tissues were removed. Total brain tissues were homogenized with phosphate buffered saline. Lipid hydroperoxide and glutathione levels were measured by enzyme immunoassays. Data were statistically analysed by using Mann Whitney's U-test. Lipid hydroperoxide levels were significantly higher in the brain tissue of leptin-treated mice (3.44 ± 0.36 nmol/g tissue, mean ± S.E.M.) than those of the control mice (2.20 ± 0.38 nmol/g tissue, p < 0.01). In contrast, leptin-treated mice had significantly lower glutathione levels in the brain tissue compared to the control (12.97 ± 1.32 and 17.91 ± 0.82 nmol/g tissue, respectively, p < 0.05). These results indicate that exogenous leptin increases lipid peroxidation and inhibits antioxidant system in the mouse brain. We therefore suggest that leptin may augment oxidative stress in the brain. leptin; lipid peroxidation; brain and mouse

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“…During pregnancy, the placenta is an additional source of adipokines like leptin and resistin (17,58). The antidiabetic and antiatherogenic properties of adiponectin are well documented (6), and in contrast to other adipokines, plasma adiponectin levels are decreased in obesity, insulin-resistant diabetes, and coronary vascular disease (2,18,19,25,54,60).…”

mentioning

confidence: 99%

Increased plasma levels of adipokines in preeclampsia: relationship to placenta and adipose tissue gene expression

Haugen¹,

Ranheim²,

Harsem³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

163

171

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Adipokines are predominantly secretory protein hormones from adipose tissue but may also originate in placenta and other organs. Cross-sectionally, we monitored maternal plasma concentration of adiponectin, resistin, and leptin and their mRNA expression in abdominal subcutaneous adipose tissue and placenta from preeclamptic (PE; n ϭ 15) and healthy pregnant (HP; n ϭ 23) women undergoing caesarean section. The study groups were similar in age and BMI, whereas HOMA-IR tended to be higher in the PE group. In fasting plasma samples, the PE group had higher concentrations of adiponectin (18.3 Ϯ 2.2 vs. 12.2 Ϯ 1.1 g/ml, P ϭ 0.011), resistin (5.68 Ϯ 0.41 vs. 4.65 Ϯ 0.32 ng/ml, P ϭ 0.028), and leptin (34.4 Ϯ 3.2 vs. 22.7 Ϯ 2.1 ng/ml, P ϭ 0.003) compared with the HP group. Adiponectin and leptin concentrations were still different between PE and HP after controlling for BMI and HOMA-IR, whereas resistin concentrations differed only after controlling for BMI but not HOMA-IR. We found similar mean mRNA levels of adiponectin, resistin, and leptin in abdominal subcutaneous adipose tissue in PE and HP women. When data were pooled from PE and HP women, resistin mRNA levels in adipose tissue also correlated with HOMA-IR (r ϭ 0.470, P ϭ 0.012) after controlling for BMI and pregnancy duration. Resistin mRNA levels in placenta were not significantly different between PE and HP, whereas leptin mRNA levels were higher in PE placenta compared with HP. Thus increased plasma concentrations of adiponectin and resistin in preeclampsia may not relate to altered expression levels in adipose tissue and placenta, whereas both plasma and placenta mRNA levels of leptin are increased in preeclampsia.adiponectin; resistin; leptin; pregnancy PREECLAMPSIA IS CHARACTERIZED BY HYPERTENSION, increased vascular resistance, proteinuria, edema, and coagulopathy and has been linked to maternal systemic endothelial cell dysfunction (43). Delivery of the placenta results in clinical resolution, and placenta is viewed as the essential organ in the development of preeclampsia (42). Increased risk of preeclampsia has been reported with increased obesity (37). Development of insulin resistance in the third trimester of pregnancy (21), together with adipose tissue accumulation (11), is a possible adaptation of the maternal metabolism to optimize fetal nutrition. Insulin resistance has a potential role in pregnancy-induced hypertension, and extensive insulin resistance is often observed during preeclampsia (45). Furthermore, placenta secretes a variety of hormones that may play a role in both gestational insulin resistance and preeclampsia.Adipose tissue has an endocrine function, secreting several metabolically active proteins, such as leptin, resistin, adiponectin, TNF-␣, and IL-6, termed adipokines (50). During pregnancy, the placenta is an additional source of adipokines like leptin and resistin (17, 58). The antidiabetic and antiatherogenic properties of adiponectin are well documented (6), and in contrast to other adipokines, plasma adiponectin levels are ...

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Leptin expression in placental and fetal tissues: does leptin have a functional role?

Cited by 60 publications

References 2 publications

Leptin ( ob gene) of the South African clawed frog Xenopus laevis

Leptin ( ob gene) of the South African clawed frog Xenopus laevis

Exogenous Leptin Increases Lipid Peroxidation in the Mouse Brain

Increased plasma levels of adipokines in preeclampsia: relationship to placenta and adipose tissue gene expression

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