• Food Science of Animal Resources
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• v.25 no.1
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• pp.26-31
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• 2005

Leptin, the product of the obesity (ob) gene, is synthesized in adipocytes or fat cells and has been implicated in the regulation of food intake, energy balance and body composition in mammals. Therefore, the leptin gene could be a candidate gene controlling fat deposition, meat quality and carcass traits in cattle. In this study the microsatellite genotypes for leptin gene were determined and their effects on carcass traits and meat quality were estimated in Korean cattle. Six different microsatellite alleles within leptin gene were identified and gene frequencies of 173, 177, 184, 186, 190 and 192 bp alleles were 0.012, 0.308, 0.067, 0.260, 0.342 and 0.016, respectively. The microsatellite marker of the leptin gene showed a significant association with the carcass percentage (CP) and marbling score (MS). Animals with genotypes 192/192 and 177/184 had higher CP than animals with other genotypes. Animals with genotypes 184/192 and 177/184 had higher MS compared with animals with other genotypes. Thus, the results suggest that the 177, 184 and 192 bp alleles may be associated with increased carcass percentage and intramuscular fat levels. No associations were found between the microsatellite genotypes of the leptin gene and other carcass traits such as carcass weight (CW), backfat thickness (BF) and M. longissimus dorsi area (LDA). In conclusion, the microsatellite markers of the leptin gene may be useful for marker-assisted selection of carcass traits and meat quality in Korean cattle.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.24 no.3
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• pp.306-315
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• 2021

Purpose: Obesity is defined as the abnormal or excessive accumulation of fat over acceptable limits. Leptin is a metabolic hormone present in the circulation in amounts proportional to fat mass. Leptin reduces food intake and increases energy expenditure, thus regulating body weight and homeostasis. Various polymorphisms are present in the leptin gene and its receptor. These polymorphisms may be associated with obesity. This study aimed to show the association of leptin (+19) AG, leptin (2548) GA, and Gln223Arg leptin receptor polymorphisms with obesity and metabolic syndrome in Turkish children aged 6-17 years, and to conduct further investigations regarding the genetic etiology of obesity. Methods: A total of 174 patients diagnosed with obesity and 150 healthy children who were treated at Tokat Gaziosmanpasa Medical School Hospital between September 2014 and March 2015 were included in this study. The ages of the children were between 6 and 17 years, and anthropometric and laboratory results were recorded. Genotyping of leptin (+19) AG, leptin (2548) GA, and leptin receptor Gln223Arg polymorphisms was performed by polymerase chain reaction. Results: An association between leptin receptor Gln223Arg gene polymorphism and obesity was detected. Conclusion: Further studies are needed to determine the role of genetic etiologies and to indicate the role of leptin signal transmission impairment in the pathogenesis of obesity. We hope that gene therapy can soon provide a solution for obesity.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.1
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• pp.1-6
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• 2007

Leptin is the hormone product of the obese gene and is synthesized and secreted predominantly by white adipocytes and relates to the feedback system that regulates long-term body fat weight and composition. Therefore, the leptin gene could be an excellent candidate gene controlling fat deposition, carcass traits and meat quality in beef cattle. The objective of this study was to evaluate the association of 3 SNPs (A1127T and C1180T in exon 2 and C3100T in exon 3) in the bovine leptin gene with carcass and meat quality traits in Korean cattle. The C1180T SNP was associated with backfat thickness (BF) and marbling score (MS) (p<0.05). Animals with the genotype CC had higher BF than animals with TT genotype and higher MS compared with CT and TT genotypes. No significant associations were observed between the C3100T SNP and any carcass and meat quality traits analyzed. The effect of the A1127T SNP was not analyzed because the TT genotype was not detected and the AT genotype showed only 1.0% frequency. These results suggest that the C1180T SNP of the leptin gene may be useful as a genetic marker for carcass and meat quality traits in Korean cattle.

• Clinical and Experimental Pediatrics
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• v.46 no.8
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• pp.795-802
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• 2003

Purpose : We investigated the hormonal control of OB gene expression and leptin secretion in cultured human visceral adipose tissue. Methods : Visceral adipose tissues were cultured for up to 48 hrs in modified Eagle's medium with varying concentration of hormones : Control(no hormone), bovine insulin(100 nM), Dexamethasone(DEX, 100 nM), growth hormone(GH, 40 ng/mL), insulin+DEX(100 nM each), insulin+DEX+GH(100 nM insulin and DEX, 40 ng/mL GH). Quantitative analysis of leptin mRNA was performed by competitive reverse transcription polymerase chain reaction, and leptin secretion in culture medium was measured by IRMA using a commercial kit. Results : The addition of dexamethasone to the medium significantly increased OB gene expression and leptin secretion(P<0.05). Unlike dexamethasone, insulin did not affect OB gene expression and leptin secretion. Both insulin and dexamethasone, at high concentration, significantly stimulated leptin secretion compared with basal values(P<0.05). Leptin gene expression was not significantly increased by GH treatment alone, however GH, in combination with high concentrations of insulin and dexamethasone, attenuated the stimulatory effects of high concentrations of insulin and dexamethasone. Conclusion : Insulin cannot increase leptin secretion without the presence of dexamethasone. The mechanism suggested is that insulin may increase leptin secretion in cytoplasm only after dexamethasone increases the expression of OB gene. Further studies are necessary to elucidate the mechanism of the action of insulin on leptin secretion after increasing OB gene expression by dexamethasone.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.6
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• pp.850-855
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• 2007

Leptin is the adipocyte-specific product of the obese gene and plays a major role in food intake and energy metabolism. Leptin research was mainly focused on mammalian species, but understanding of leptin and its function in poultry is very poor. In this study, the duck leptin gene was amplified using the reverse transcription-polymerase chain reaction (RT-PCR) from duck liver RNA. The cDNA fragment was inserted into the pET-28a expression vector, and the resulting plasmid was expressed in Escherichia coli BL21 (DE3). Experimental mice were given an intraperitoneal injection of 10 mg/kg leptin dissolved in phosphate buffered saline (PBS), while the control mice were injected with PBS. The effect of leptin on food intake, body weight and fatty deposition in mice was detected. Sequence analysis revealed that duck leptin had a length of 438 nucleotides which encoded a peptide with 146 amino acid residues. The sequence shares highly homology to other animals. The coding sequence of duck leptin was 84 and 86% identical to human and pig leptin nucleotides sequence. Highest identity was with the rat coding sequence (95%). The identity of the amino acid sequence was 84, 82 and 96% respectively compared to that of the human, pig and rat. Results of SDS-PAGE analysis indicated that a fusion protein was specifically expressed in E. coli BL21 (DE3). The purified product was found to be biologically active during tests. Continuous administration of recombinant duck leptin inhibited food intake. Despite the decrease of food intake, leptin significantly induced body weight and fatty deposition. These changes were accompanied by a significant down-secretion of plasma glucose, cholesterol, triglyceride and insulin levels in mice. The observations provide evidence for an inhibitory effect of leptin in the regulation of food intake and for a potential role of duck leptin in the regulation of lipogenesis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6595-6599
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• 2013

Leptin and its receptor are involved in breast carcinogenesis as mitogenic factors. Therefore, they could be considered as targets for breast cancer therapy. Expression of the leptin receptor gene could be modulated by leptin secretion. Silibinin and curcumin are herbal compounds with anti-cancer activity against breast cancer. The aim of this study was to assess their potential to inhibit of expression of the leptin gene and its receptor and leptin secretion. Cytotoxic effects of the two agents on combination on T47D breast cancer cells was investigated by MTT assay test after 24h treatment. With different concentrations the levels of leptin, leptin receptor genes expression were measured by reverse-transcription real-time PCR. Amount of secreted leptin in the culture medium was determined by ELISA. Data were statistically analyzed by one-way ANOVA test. The silibinin and curcumin combination inhibited growth of T47D cells in a dose dependent manner. There were also significant difference between control and treated cells in leptin expression and the quantity of secreted leptin with a relative decrease in leptin receptor expression. In conclusion, these herbal compounds inhibit the expression and secretion of leptin and it could probably be used as drug candidates for breast cancer therapy through leptin targeting in the future.

• Preventive Nutrition and Food Science
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• v.9 no.4
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• pp.336-341
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• 2004

Leptin, resisitn and PAI-1 (plasminogen activator inhibitor-1) are synthesized and secreted by rodent fat cells and recently postulated to be an important link to obesity. This study was conducted to characterize the hormonal regulation of leptin, resistin, and PAI-1 gene expression in the 3T3-L1 adipocytes. The cells were treated with 0.5 $\mu$M insulin, 1 $\mu$M dexamethasone (Dex), or 0.05 $\mu$M triiodothyronine (T3) for 72 hours. The mRNA levels of each peptide were measured by semi-quantitative RT-PCR. The mRNA level of the leptin-producing ob gene was significantly increased by insulin, Dex, and T3 by 3.2-, 3.1- and 2.7-fold, respectively, compared to the control (p < 0.05). The level of resistin mRNA was increased by insulin, Dex, and T3 by 2.7-, 2.5- and 2-fold, respectively, compared to the control (p < 0.05). Likewise, the level of PAI-1 mRNA was significantly increased by insulin, Dex, and T3 compared to the control (p < 0.05). Taken together, our results suggest that insulin, Dex, and T3 may regulate the gene expression of leptin, resistin, and PAI-1 in 3T3-L1 adipocytes.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.5
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• pp.487-498
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• 2016

Leptin, an adipokine predominantly produced from adipose tissue, is well known to induce tumor growth. However, underlying molecular mechanisms are not established yet. While p53 has long been well recognized as a potent tumor suppressor gene, accumulating evidence has also indicated its potential role in growth and survival of cancer cells depending on experimental environments. In the present study, we examined if p53 signaling is implicated in leptin-induced growth of cancer cells. Herein, we demonstrated that leptin treatment significantly increased p53 protein expression in both hepatic (HepG2) and breast (MCF-7) cancer cells without significant effect on mRNA expression. Enhanced p53 expression by leptin was mediated via modulation of ubiquitination, in particular ubiquitin specific protease 2 (USP2)-dependent manner. Furthermore, gene silencing of p53 by small interfering RNA (siRNA) suppressed leptin-induced growth of hepatic and breast cancer cells, indicating the role of p53 signaling in tumor growth by leptin. In addition, we also showed that knockdown of p53 restored suppression of caspase-3 activity by leptin through modulating Bax expression and prevented leptin-induced cell cycle progression, implying the involvement of p53 signaling in the regulation of both apoptosis and cell cycle progression in cancer cells treated with leptin. Taken together, the results in the present study demonstrated the potential role of p53 signaling in leptin-induced tumor growth.

• 한국생물공학회:학술대회논문집
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• 2001.11a
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• pp.779-781
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• 2001

Human leptin is a 16kDa protein and is known to influence body weight control. It is composed of 146 amino acids. In this study, human leptin gene was obtained from homosapiens leptin mRNA using RT-PCR. And leptin gene was inserted into secretion vectors and Saccharomyces cerevisiae was transformed. In flask culture, Saccharomyces cerevisiae transformant showing high leptin expression titre was selected and with the best transformant, fed-batch fermentation and purification was optimized. As a result, about 2 g/L of leptin was expressed and the yield of purification was about 80%.

• Journal of Microbiology and Biotechnology
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• v.10 no.6
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• pp.753-758
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• 2000

Human leptin is identified as a 16kDa (146 amino acids) protein secreted from adipocytes which influences body weight homeostasis. In order to produce active leptin, the human obese gene coding for leptin was expressed in Bacillus subtilis WB600 strain which is deficient in six extracellular proteases. The recombinant leptin was produced in a culture supernatant, and in a culture supernatant, it was contained as high as 48% for total proteins. After simple purification steps, which consisted of ammonium sulfate precipitation and anion-exchange column chromatography, 2.3 mg of leptin with a purity greater than 95% was obtained from the 0.51 culture with the recovery yield of 38.3%. The purified leptin showed the correct folding structure with one disulfied bond.