• Asian-Australasian Journal of Animal Sciences
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• v.21 no.2
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• pp.161-166
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• 2008

To determine if body weight change is directly related to altered leptin and neuropeptide Y (NPY) gene expression, we assessed adipose tissue weight, percent body fat, leptin and NPY mRNA levels and serum leptin concentration in pigs at weights of 1, 20, 40, 60, and 90 kg. The results indicated that the weight of adipose tissues and the percent body fat of pigs significantly increased and correlated with body weight (BW) from 1 to 90 kg (p<0.01). Serum leptin concentrations and leptin mRNA levels in omental adipose tissue (OAT) increased from 1 to 60 kg, and then decreased from 60 to 90 kg. At 60 kg, the serum leptin concentration and leptin mRNA level significantly increased by 33.5% (p<0.01) and 98.2% (p<0.01), respectively, as compared with the levels at 1 kg. At 60 kg, the amount of leptin mRNA in subcutaneous adipose tissue (SAT) was significantly higher than that of 1 and 40 kg animals (p<0.05). NPY gene expression in the hypothalamus also changed with BW and at 60 kg the NPY mRNA level significantly decreased by 54.0% (p< 0.05) as compared with that in 1 kg. Leptin mRNA in OAT was correlated with serum leptin concentrations (r = 0.98, p<0.01), body weight (r = 0.82, p<0.05) and percent body fat (r = 0.81, p<0.05). This is the first report of the developmental expression of leptin in porcine OAT, peritoneal adipose tissue (PAT) and SAT, and proves that the expression of leptin in OAT could reflect the levels of circulating leptin. These results provide some information for nutritional manipulation of leptin secretion which could lead to practical methods of controlling appetite and growth in farm animals, thereby regulating and improving efficiency of lean meat production and meat production quality.

• Journal of Animal Science and Technology
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• v.46 no.3
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• pp.295-300
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• 2004

The identification of the leptin gene in 1994 and it's adipocytes specific protein leptin hal provided the first physiological links to the regulatory system controlling body weight and fat deposits. The meat tastes is mainly determined by quantifY and quality of triglyceride stored in adipose tissue. This study was conducted to analyze genetic cbaracteristics of Hanwoo leptin gene and also to investigate the association of DNA marlcer with some economic meat traits for Hanwoo. The leptin hormone gene polymorphisms were identified by digestion with Kpn2 I and Msp I. Slaughter weight(SWI), slaughter peroentage(SP), longissimus muscle area(LMA), beef marbling score(MS) and back fat thickness(BF) were compared among three genotypes by P(R..RFlJ> and showed significant differences among genotypes. PCR-RFLP(Kpn2 I) were detected significant for SP, MS and BF. The allele was essociated with fatter carcasses and C allele with leaner carcasses.

• Nutritional Sciences
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• v.5 no.4
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• pp.190-196
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• 2002

Zinc deficiency has been shown to result in poor appetite, causing anorexia. However, the role of zinc in the regulation of food intake is not well understood. In the present study, we hypothesized that zinc deficiency dysregulates circulating leptin level and leptin mRNA gene expression, and that whether these changes were occuring as a direct result of, or as a compensatory effect of zinc deficiency in rats. After an adaptation period of 4 weeks, Sprague Dawley rats were provided with three different level of zinc, as one week of a Zn-adequate (30 mg/kg) diet, then two weeks of a Zn-depletion (1 mg/kg ), and finally by two weeks of a Zn-repletion (50 mg/kg) diet. At the end of each dietary experimental period, one third of the 26 rats were killed. Zinc levels of blood subfractions (plasma, yee blood cells and mononuclear cells) and in the liver were substantially decreased, despite the fact that food intake was not substantially decreased during the Zn-depletion period. Serum leptin concentration was significantly increased during the zinc depletion period. Leptin mRNA in adipose tissue was also shown to be highly expressed during the Zn-depletion period. Presumably, increased leptin level and leptin mRNA induction during Zn-depletion conditions may be the cause of lowered appetite which is the common symptom of Zn-deficiency. In conclusion, These increases in circulating leptin levels and in leptin gene expression would be the direct result of, rather than the compensatory effect of, zinc deficiency.

• Journal of Life Science
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• v.9 no.3
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• pp.253-261
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• 1999

Leptin gene, an obesity gene, has been known to involve in the regulation of food intake and body weight. It is also thought to be related to the glucose metabolism, insulin secretion and type II diabetes mellitus. Recently, the production of recombinant leptin protein has been attempted for the application in the treatment of obesity and the correction of hereditary obesity and type II diabetes. In the present study, leptin cDNA was cloned from mouse fat cells by RT-PCR and prokaryotic expression of leptin was attempted in order ot prepare a leptin-specific antigen. Immunization of a rabbit with the leptin-specific antigen into a rabbit resulted in the generation of leptin-specific antiserum that could be useful in the detection of leption expressed in various tissues. The sequence of leptin cDNA prepared in the present study wa identical to the previously reported one. Transformation of E. coli(DH5a) cells with the leptin cDNA-inserted translation vector, pGEX-4T-3-leptin followed by treatment with IPTG (0.1mM) resulted in the expression of a large amount of GST-leptin fusion protein with a molecular weight of 44 KDa as an inclusion body. Denaturation of the insoluble fusion protein by 8M urea, 6M guanidium-HCI or 0.1% 2-mercaptoethanol followed by a slow oxidation could not solubilize the inclusion body. The cell extract was subjected to SDS-PAGE and GST-leptin protein electroeluted from the gel was then injected into a rabbit subcutaneously for the immunization. Anti-GST-leptin rabbit antiserum which had a cross reactivity to the GST-leptin protein was generated. Leptin protein expressed in mouse brain and fat tissues was detected by Western blot immunodetection system using the antiserum generated in the present study.

• Nutritional Sciences
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• v.6 no.2
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• pp.73-77
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• 2003

PAI-1 (plasminogen activator inhibitor-1), leptin, and resistin are synthesized and secreted by Int cells of rodents and have recently been postulated to be an important link to obesity. This study was conducted to identify the nutritional regulation of PAI-1, leptin, and resistin gene expression in 0b/ob mice. The mice were divided into four groups according to nutritional status: control, 48 hour fasting, 48 hour-fasting/12 hour-refeeding, and 48 hour-fasting/24 hour-refeeding. The mRNA levels of each peptide were measured by semi-quantitative RT-PCR. In visceral fat tissue, the level of PAI-1 mRNA increased markedly when 48h-fasted animals were refed with a high carbohydrate-low fat diet. However, lasting/refeeding did not appreciably change PAI-1 mRNA levels in subcutaneous fat tissue. Similar results were obtained for resistin mRNA levels in both types of fat tissues. These findings suggest that visceral adipose tissue might be more sensitively involved in the nutritional regulation of PAI-1 and resistin gene expression compared to subcutaneous fat tissue. The level of leptin mRNA decreased markedly in the 48h-fasted animals, and increased markedly when 48h-fasted animals were refed with a high carbohydrate-low fat diet. The nutritional regulation of leptin mRNA showed similar patterns in both types of fat tissues. In conclusion, the nutritional regulation of gene expression encoding PAI-1, resistin, and leptin from adipocytes may vary according to the type of adipose tissue.

• Clinical and Experimental Pediatrics
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• v.55 no.9
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• pp.337-343
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• 2012

Purpose: Leptin has been considered a link between metabolic state and reproductive activity. Defective reproductive function can occur in leptin-deficient and leptin-excessive conditions. The aim of this study was to examine the effects of centrally injected leptin on the hypothalamic KiSS-1 system in relation to gonadotropin-releasing hormone (GnRH) action in the initial stage of puberty. Methods: Leptin (1 ${\mu}g$) was injected directly into the ventricle of pubertal female mice. The resultant gene expressions of hypothalamic GnRH and KiSS-1 and pituitary LH, 2 and 4 hours after injection, were compared with those of saline-injected control mice. The changes in the gene expressions after blocking the GnRH action were also analyzed. Results: The basal expression levels of KiSS-1, GnRH, and LH were significantly higher in the pubertal mice than in the prepubertal mice. The 1-${\mu}g$ leptin dose significantly decreased the mRNA expression levels of KiSS-1, GnRH, and LH in the pubertal mice. A GnRH antagonist significantly increased the KiSS-1 and GnRH mRNA expression levels, and the additional leptin injection decreased the gene expression levels compared with those in the control group. Conclusion: The excess leptin might have suppressed the central reproductive axis in the pubertal mice by inhibiting the KiSS-1 expression, and this mechanism is independent of the GnRH-LH-estradiol feedback loop.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.11
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• pp.1548-1551
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• 2005

The leptin, an anti-obesity protein, is a hormone protein expressed and secreted mainly from adipocyte tissue, and involved in regulation of body weight, food intake and energy metabolism. In an effort to discover polymorphism(s) in genes whose variant(s) might be implicated in phenotypic traits of growth, we have sequenced exons and their boundaries of leptin gene including 1,000 bp upstream of promoter region with twenty-four unrelated Korean cattle. Fifty-seven sequence variants were identified: fourteen in 5' flanking region, twenty-seven in introns, eight in exons, and eight in 3' flanking region. By pair-wise linkage analysis among polymorphisms, ten sets of SNPs were in absolute linkage disequilibrium (LD) (|D'| = 1 and $r^2$ = 1). Among variants identified, thirty-six SNPs were newly identified, and twenty-one SNPs, which were reported in other breeds, were also confirmed in Korean cattle. The allele frequencies of variants were quite different among breeds. The information from SNPs of bovine leptin gene could be useful for further genetic studies of this gene.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.433-438
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• 1999

Two components of the neuroendocrine-hormonal response to long-term treatment of acarbose, adipose tissue-derived leptin and central neuropeptide Y (NPY), were investigated in the ICR mice on a high- carbohydrate diet. Acarbose, administered 5 or 50 mg per 100 g diet for four weeks, dose dependently suppressed body weight gain. The body weight gain was reduced along with the amount of daily food intake in 50 mg acarbose-treated group at $7^{th}\;and\;28^{th}$ day. 5 or 50 mg acarbose treatment administered for four weeks reduced leptin mRNA levels to 62% and 77% of the control group, demonstrating that the amount of leptin mRNA in adipocytes correlates with body weight. As dose of acarbose increased, leptin mRNA level also increased, suggesting that potent inhibition of ${\alpha}-glycosidase$ by a higher dose of acarbose furthers the enzyme activity and leptin gene consequently. On the other hand, central expression level of NPY gene was increased significantly compared with the control group at the same amount of acarbose administered, reflecting that leptin and NPY operate in a negative-feedback circuit to regulate body fat stores.

• YAKHAK HOEJI
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• v.44 no.5
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• pp.391-398
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• 2000

Leptin, the product of the ob gene, is a small peptide molecule synthesized by white adipocytes with an important role in the regulation of body fat and food intake. Based on the evidence that synthesis of leptin is regulated by female sex hormone, estrogen, this present study was investigated whether sex hormone precursor DHEA, can regulate obese gene expression in lean and genetically obese (ob/ob) mice. Antiobesity activity of DHEA was evaluated by determining body weight, food consumption, epididymal fat weight and serum levels of cholesterol and triglyceride in ICR, C57BL/6J, and ob/ob mice. The treatment of C57BL/6J lean and obese mice with a diet containing 0.3% and 0.6% DHEA resulted in lowered rates of weight gain in comparison to non-treated mice, although much greater response was found in the obese mice. All other concentrations of DHEA (0.015%, 0.06%, 0.15%, 0.3%) except the highest one(0.6%) showed no significant effects on weight gain in ICR mice. Food consumption was significantly decreased in all mice treated with 0.6% DHEA, whereas it was not decreased in ICR mice at lower concentrations than 0.6% DHEA. DHEA decreased significantly epididymal adipose tissue weight and serum triglyceride levels dose dependently in lean and obese mice. However serum cholesterol levels were decreased at lower concentrations than 0.15% DHEA and increased at concentrations of 0.3% and 0.6% DHEA in lean and obese mice. These increases in serum cholestrol levels at high concentrations of DHEA might result from the fact that DHEA has a cholesterol moiety thereby interfered the assay system. As an approach to elucidate the mechanism for antiobesity activity of DHEA, we examined mRNA levels of obese gene in the adipocyte and obese gene product (leptin) in the serum. The results showed that DHEA did not affect obese gene expression in ICR and C57BL/6J mice. Therefore, we concluded that antiobesity activity of DHEA was not modulated by obese gene expression.

• IMMUNE NETWORK
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• v.2 no.4
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• pp.202-207
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• 2002

Background: Kawasaki disease is an acute febrile illness with systemic vasculitis which primarily affects children, We examined the production of leptin in plasma and gene expressions of CXC chemokines in peripheral blood mononuclear cells from patients with Kawasaki disease. Methods: Consecutive 39 samples from 13 patients according to the different clinical stages (acute, subacute, convalescent) of Kawasaki disease were collected. The plasma leptin levels according to clinical stages of Kawasaki disease were examined by ELISA and the expression of IP-10, Mig and IL-8 mRNAs in 39 samples (13 samples of each stage) from 13 cases were examined by RT-PCR. Results: There were not significant changes of plasma leptin levels according to the clinical stages of Kawasaki disease. The mean values of plasma leptin concentrations during each of the stages (n=13, p>0.05, pg/ml) were $335.8{\pm}549.0$ in acute, $358{\pm}347.6$ in subacute, and $443.6{\pm}645.9$ in convalescent stage. The mRNAs of IP-10, Mig, and IL-8 were expressed in 13/13 (100%), 2/13 (15%), 9/13 (69%) during acute stage, 13/13 (100%), 6/13 (46%), 13/13 (100%) during subacute stage, and 13/13 (100%), 4/13 (31%), 10/13 (77%) during the convalescent stage, respectively. In three patients, the production of leptin and expression of IP-10 mRNA were dramatically decreased according to the process of the clinical stages. In five patients with prominent cervical lymphadenopathy, the expression of IL-8 mRNA during the subacute stage was more elevated than the acute and convalescent stages. Conclusion: This data suggests that the production of leptin and the gene expressions of IP-10, Mig and IL-8 seem to have no significant correlation to the clinical stages of Kawasaki disease. However, expression patterns of IP-10, Mig and IL-8 mRNA may be related to the specific clinical manifestations, and the expression of IP-10 may also be correlated to leptin levels with pericardial involvement.