Influence of the presence of OB-Re on leptin radioimmunoassay

Murakami, Takashi; Otani, Shizuka; Honjoh, Tsutomu; Doi, Takashi; Shima, Keisuke

doi:10.1677/joe.0.1680079

Cited by 14 publications

(12 citation statements)

References 24 publications

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“…As expected, ob/ob mice on the KD and the SD had comparable low levels of serum leptin immunoreactivity (Fig. 4D), which probably reflects cross-immunoreactivity with the secretory form of the leptin receptor (21). Likewise, db/db mice on the KD had 430% higher serum ␤HB levels and tended to have higher serum leptin levels than db/db mice on the SD (Fig.…”

Section: Resultssupporting

confidence: 73%

Leptin Contributes to Slower Weight Gain in Juvenile Rodents on a Ketogenic Diet

et al. 2006

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ABSTRACT:The ketogenic diet (KD) is an efficacious therapy for medically refractory childhood epilepsy that also slows weight gain. We tested the hypothesis that the KD slows weight gain via neurohormones involved in energy homeostasis. We found that juvenile rodents fed a KD had slower weight gain than those fed a standard diet (SD). Rats fed a KD had higher serum leptin levels and lower insulin levels compared with those fed an SD. We investigated the increase in leptin further because this change was the only one consistent with slower weight gain. Although rats fed the SD experienced slower weight gain when calorie restricted, they had serum leptin levels similar to those fed the SD ad libitum. Furthermore, leptin deficient (ob/ob) and leptin receptor deficient (db/db) mice did not show slower weight gain on the KD. All animals on the KD had elevated serum ␤-hydroxybutyrate (␤HB) levels. Thus, ketosis is insufficient and a functioning leptin signaling system appears necessary for the KD to slow weight gain. The increase in leptin may contribute to the anticonvulsant effects of the KD. F ew treatment options exist for the 20 -30% of epileptic children whose seizures are refractory to medication. One option is the KD, a high-fat, low-carbohydrate, and adequate protein diet. The KD is remarkably effective in children with medically refractory epilepsy as 5-10% become seizure free and 30% have a Ͼ90% reduction in seizure frequency (1). Yet, its adverse effects and the parental effort involved in implementing and maintaining the diet limit its use. Thus, all epileptic children would benefit from a simpler method of attaining the diet's anticonvulsant effects, which requires elucidating its mechanism of action.Here we focus on what the impaired weight gain associated with the KD might reveal about the diet's anticonvulsant mechanism. Several studies report that children on the KD drop about 10 percentiles in weight, although appropriate weight gain is the goal (2,3). Recognizing that lowcarbohydrate diets, such as the Atkins diet, are ketogenic makes this impaired weight gain less surprising. Indeed, the Atkins diet and other low-carbohydrate KDs result in a 5% to 10% weight loss over 6 mo (4,5). Furthermore, rodents placed on a KD show slower weight gain (6,7).We hypothesized that the anticonvulsant and weight effects of the KD share a common mechanism involving a change in the serum levels of leptin, insulin, ghrelin, or cortisol. These peripherally released hormones help determine body weight because they regulate energy homeostasis (8). Importantly, leptin and insulin also modulate neuronal excitability (9,10). METHODSDietary protocols. Experimental protocols were approved by the Washington University Animal Studies Committee. Sprague-Dawley rats (Charles River Laboratories, Wilmington, MA), male ob/ob mice (Stock 000632, The Jackson Laboratory, Bar Harbor, ME), male C57BL/6J mice (Stock 000664, The Jackson Laboratory), male db/db mice (Stock 000642, The Jackson Laboratory), and male C57BLKS/J mice (Stock 0006...

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Section: Resultssupporting

confidence: 73%

Leptin Contributes to Slower Weight Gain in Juvenile Rodents on a Ketogenic Diet

et al. 2006

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“…25,31 The latter therefore often displayed artificially increased leptin levels due to the competitive interference of endogenous sOB-R with the binding sites of the antibody.…”

Section: Discussionmentioning

confidence: 99%

The soluble leptin receptor is crucial for leptin action: evidence from clinical and experimental data

Zastrow

Seidel

Kieß³

et al. 2003

Int J Obes

110

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OBJECTIVE:The soluble leptin receptor (sOB-R) was recently identified as the main leptin-binding protein in human blood. The aim of our study was to elucidate the effects of physiologically relevant amounts of sOB-R on leptin-induced proliferation in a cell model. SUBJECTS AND MEASUREMENTS:To determine molar ratios between sOB-R and leptin in vivo, we measured both parameters in the serum of 529 healthy children and adolescents. For our in vitro cell model, mouse pre-B cells, transfected with the long form of the murine leptin receptor (BAF3/L46), were incubated with recombinant human leptin at two different basal levels (0.5 and 0.1 nM) and with the sOB-R at varying levels. The proliferative response of the cells was quantified by a 3 H-thymidine uptake assay. RESULTS: Significantly higher molar sOB-R/leptin ratios were observed during the first years of life, up to a 7.67-fold excess of sOB-R (quartiles: 4.43/10.27) in boys, compared to the states of prepuberty and puberty. An up to 10-fold molar excess of the sOB-R, reflecting the in vivo situation, resulted in a significant suppression of leptin action in the cell model. In contrast, gradually decreasing ratios of lower than two, as calculated during the progression of childhood and in early puberty, corresponded to proliferative rates in vitro as determined at basal leptin concentrations.

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“…It was reported that secretions of soluble Ob-R, which is a leptin binding protein, into the maternal circulation may lower the rate of leptin clearance and increase plasma leptin concentrations. [6][7][8][9] Thus, we measured maternal parametrial visceral fat leptin mRNA and placental soluble Ob-R mRNA expression. Interestingly, in non-pregnant mice, leptin mRNA expression in visceral fat was not influenced by maternal dietary Zn deficiency and supplementation.…”

Section: Discussionmentioning

confidence: 99%

Section: )mentioning

confidence: 99%

“…It was reported that secretions of soluble Ob-R, which is a leptin binding protein, into the maternal circulation may lower the rate of leptin clearance and increase plasma leptin concentrations. [6][7][8][9] Dramatic changes in energy homeostasis are well recognized in pregnant women, with major features including increased food intake, decreased insulin sensitivity, and hyperlipidemia. Placental leptin may regulate conceptus growth and placental function by regulating glucose metabolism and insulin sensitivity.…”

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confidence: 99%

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Effects of Zinc Deficiency and Supplementation on Leptin and Leptin Receptor Expression in Pregnant Mice

Ueda

Nakai

Konishi

et al. 2014

Biological & Pharmaceutical Bulletin

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Leptin is an adipose-derived hormone that primarily regulates energy balance in response to nutrition. Human placental cells produce leptin, whereas murine placental cells produce soluble leptin receptors (Ob-R). However, the roles of these proteins during pregnancy have not been elucidated completely. As an essential metal, zinc (Zn) is central to insulin biosynthesis and energy metabolism. In the present study, the effects of Zn deficiency and supplementation on maternal plasma leptin and soluble Ob-R regulation in pregnant mice placentas were examined using enzyme-linked immunosorbent assay, reverse transcriptionpolymerase chain reaction, and Western blotting. Nutritional Zn deficiency significantly reduced plasma insulin concentrations and fetal and placental weights in pregnant mice. Plasma leptin concentrations in pregnant mice also increased 20-to 40-fold compared with those in non-pregnant mice. Although dietary Zn deficiency and supplementation did not affect plasma leptin concentrations in non-pregnant mice, Zndeficient pregnant mice had significantly reduced plasma leptin concentrations and adipose leptin mRNA expression. In contrast, Zn-supplemented pregnant mice had increased plasma leptin concentrations without increased adipose leptin mRNA expression. Placental soluble Ob-R mRNA expression also decreased in Zndeficient mice and tended to increase in Zn-supplemented mice. These results indicate that Zn influences plasma leptin concentrations by modulating mRNA expression of soluble Ob-R in the placenta, and leptin in visceral fat during pregnancy. These data suggest that both adipose and placenta-derived leptin system are involved in the regulation of energy metabolism during fetal growth. Key words leptin; leptin receptor; dietary zinc; pregnancy; placentaLeptin is a 16-kDa protein hormone encoded by lep and is mainly produced in adipose tissues. Initial studies indicated that it regulates body weight by suppressing appetite and stimulating energy consumption via the hypothalamic leptin receptor (Ob-R).1,2) In addition to its known role in energy metabolism, pleiotropic effects of leptin have been identified, involving modulation of thermogenesis, homeostasis, hematopoiesis, angiogenesis, neuroendocrine, and immune functions. Moreover, leptin regulates ovarian function, oocyte maturation, and implantation.3,4) Recently, significantly elevated plasma leptin concentrations were found in pregnant women, with considerable leptin secretion from the placenta in comparison with that observed in non-pregnant women. 5)In the second and third trimesters, plasma leptin concentrations further increased in comparison with that observed in the first trimester and returned to normal after expulsion of placenta, suggesting that the placenta is the major source of leptin during pregnancy. 5) Leptin is not produced in mouse placentas, although plasma leptin concentrations are also elevated during pregnancy, and high placental production of soluble Ob-R has been demonstrated in mice. It was reported that secretions ...

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Influence of the presence of OB-Re on leptin radioimmunoassay

Cited by 14 publications

References 24 publications

Leptin Contributes to Slower Weight Gain in Juvenile Rodents on a Ketogenic Diet

Leptin Contributes to Slower Weight Gain in Juvenile Rodents on a Ketogenic Diet

The soluble leptin receptor is crucial for leptin action: evidence from clinical and experimental data

Effects of Zinc Deficiency and Supplementation on Leptin and Leptin Receptor Expression in Pregnant Mice

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