• Asian-Australasian Journal of Animal Sciences
• /
• v.14 no.9
• /
• pp.1209-1215
• /
• 2001

We conducted this study to investigate 24 h leptin profiles and to ascertain whether leptin secretion occurs in a pulsatile manner in cattle. Plasma leptin concentrations were measured every 10 min for 24 h in five Holstein steers aged 10 months. Simultaneously, feeding behavior was recorded every 5 min during this experiment. In two of the five cattle, leptin showed diurnal rhythmicity, which could be described by a cosine, with peaks between 15:00 and 16:00 and nadirs at around midnight. Pulsatile leptin release was quantified by model-free Cluster analysis. Plasma leptin showed a pulsatile pattern in all cattle, with an average number of pulses at 15 peaks/24 h. The daily number of pulses was not related to total time spent eating, ruminating or chewing. However, when divided into six 4 h time intervals, time spent ruminating was positively related with pulse number (p=0.05) in cattle showing no diurnal plasma leptin variation. These results suggest that cattle may have unique diurnal variation and pulsatile patterns of plasma leptin, differing from those of monogastric animals.

• BMB Reports
• /
• v.52 no.6
• /
• pp.385-390
• /
• 2019

Leptin, an adipokine regulating energy metabolism, appears to be associated with breast cancer progression. Insulin-like growth factor-1 (IGF-1) mediates the pathogenesis of breast cancer. The regulation of IGF-1 expression by leptin in breast cancer cells is unclear. Here, we found that leptin upregulates IGF-1 expression at the transcriptional level in breast cancer cells. Activating protein-1 (AP-1)-binding element within the proximal region of IGF-1 was necessary for leptin-induced IGF-1 promoter activation. Forced expression of AP-1 components, c-FOS or c-JUN, enhanced leptin-induced IGF-1 expression, while knockdown of c-FOS or c-JUN abrogated leptin responsiveness. All three MAPKs (ERK1/2, JNK1/2, and p38 MAPK) mediated leptin-induced IGF-1 expression. These results suggest that leptin contributes to breast cancer progression through the transcriptional upregulation of leptin via the MAPK pathway.

• The Journal of Korean Medicine
• /
• v.26 no.2 s.62
• /
• pp.241-251
• /
• 2005

Objectives: This experimental study was designed to investig:ue the effects of Oryungsan-gagampang on leptin and leptin receptor levels and differentiation of 3T3-L1 adipocyte. Methods: After 3T3-L1 adipocytes were incubated with various concentrations of Oryungsan-gagampang and Reductil(r) for 7 days, leptin and leptin receptor levels in 3T3-Ll adipocytes were measured by ELISA. To elucidate the mechanism of inhibitory effects of Oryungsan-gagampang on obesity, the 3T3-L1 adipocytes after oil red 0 staining were taken by digital photo system. Results: 1. Oryungsan-gagampang $1,000{\mu}g/ml$ significantly increased leptin levels in 3T3-L1 adipocytes in comparison with the control group (p<0.05), and Oryungsan-gagampang 0.1 10, $1,000{\mu}g/ml$ significantly increased leptin receptor levels in 3T3-L1 adipocytes in comparison with the control group (p<0.05). 2. Oryungsan-gagampang inhibited of differentiation of 3T3-L1 adipocytes. Conclusions: Oryungsan-gagampang showed significant effects on inhibiting differentiation of 3T3-Ll adipocytes, and increasing leptin levels and leptin receptor levels in 3T3-L1 adipocytes. Therefore, Oryungsan-gagampang could be used to treat obesity, but further studies are required.

• Clinical and Experimental Pediatrics
• /
• v.46 no.8
• /
• pp.795-802
• /
• 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
• /
• v.15 no.5
• /
• pp.725-731
• /
• 2002

This experiment was performed to understand the changes in plasma leptin in association with plasma IGF-1, body weight and ADG from early growing to late finishing stages of Holstein steers. Blood collection was performed by arterial vein puncture at selected monthly ages of 1 (54 kg), 2.6 (103 kg), 7.2 (205 kg), 13.5 (314 kg), 16.9 (414 kg), 22.2 (550 kg), 24.9 (626 kg) and 27.4 months (695 kg). The blood was analyzed for leptin using the multi-species leptin RIA with recombinant bovine leptin (rbleptin) as standard, plasma IGF-1 was also measured using RIA. Against the standard rbleptin, the multi-species Leptin RIA system's sensitivity, cross reactivity, slope and recovery of 41.0 ng/ml rbleptin in plasma were 4.9 ng/ml, 11.22%, -1.396 and 97.8%, respectively. Plasma leptin measured were more than 5.0 ng/ml, which enable multi-species RIA system to investigate plasma leptin in normal growing steers. Body weight resulted to a highly significant second-degree polynomial relationship with plasma leptin (q=0.54, p<0.0001) and plasma IGF-1 (q=0.44, p<0.0001) from 1 to 27.4 monthly ages. However, the second-degree polynomial curve of plasma leptin and IGF-1 differs showing a concave and convex curvilinear relationship, respectively. ADG was not significantly associated to plasma leptin (r=0.06, p>0.05) and plasma IGF=1 (r=0.06, p>0.05) from 1 to 27.4 monthly ages. Low coefficient, but significant associated increase of plasma leptin and IGF-1 (r=0.12, p<0.008) from 1 to 27.4 months was observed. The uncoordinated increases of plasma IGF-1 at growing and plasma leptin at fattening period, may indicate (1) indirect involvement of endogenous IGF-1 on leptin secretion, and (2) IGF-1 level may signify lean and bone accretion while plasma leptin may mirror body fatness across the monthly ages of Holstein steers.

• Asian-Australasian Journal of Animal Sciences
• /
• v.20 no.1
• /
• pp.41-44
• /
• 2007

The callipyge mutation in sheep is a polar overdominant mutation that results in post-natal muscle hypertrophy in the loin and hindquarters of paternal heterozygotes (+/CLPG). Sheep that are homozygous for the callipyge allele (CLPG/CLPG) do not express the muscle hypertrophy phenotype, but serve as carriers for the mutation. Callipyge sheep are characterized by improved feed efficiencies and leaner carcasses. Leptin is a protein hormone secreted from adipose tissue and has been found to affect appetite and serve as an indicator of body fat mass. To date, very little knowledge is available as to the effect of the callipyge mutation on circulating leptin levels. Due to the interaction of leptin with feed intake and energy availability, and the fact that the majority of fetal growth occurs in late gestation, it is important to understand if the callipyge mutation interacts with leptin production in late gestational ewes. Therefore, our objective was to characterize serum concentrations of leptin in late gestational callipyge ewes vs. non-callipyge ewes. We evaluated genetically verified callipyge (n=6), homozygous (n=8) and normal (n=8) ewes weekly during the last eight wks of gestation through one wk post-partum. Weights were taken and body condition scores were assigned by trained personnel weekly. Blood was collected via jugular venipuncture on each sampling date and subjected to an ovine-specific leptin RIA. Genotype influences on peripheral concentrations of leptin were found to be highly significant (p=0.0005). Total leptin means for +/CLPG were 5.41${\pm}$0.40 ng/ml, CLPG/CLPG 8.11${\pm}$0.70 ng/ml, and +/+ 9.13${\pm}$0.93 ng/ml. Sampling date was also significant (p=0.0098) with all ewes showing a decrease in leptin levels throughout gestation and parturition. Using repeated measures, we were able to detect lower levels of plasma leptin in callipyge ewes, which may be indicative of their lower overall body fat content. These results indicate that the callipyge phenotype decreases the levels of adipose tissue and leptin production in gestating ewes.

• The Korean Journal of Physiology and Pharmacology
• /
• v.8 no.4
• /
• pp.227-235
• /
• 2004

The aim of the present study was to examine the effect of leptin on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. Leptin $(1{\sim}100\;ng/ml)$, when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced a dose-dependently the secretory responses of CA evoked by ACh $(5.32{\times}10^{-3}\;M)$, DMPP $(10^{-4}\;M)$ and McN-A-343 $(10^{-4}\;M)$, although it alone has weak effect on CA secretion. However, it did not affect the CA secretion evoked by excess $K^+\;(5.6{\times}10^{-2}\;M)$. Leptin alone produced a weak secretory response of the CA. Moreover, leptin (10 ng/ml) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$ ATPase. However, in the presence of U0126 $(1\;{\mu}M)$, an inhibitor of mitogen-activated protein kinase (MAPK), leptin no longer enhanced the CA secretion evoked by ACh and DMPP. Furthermore, in the presence of anti-leptin (10 ng/ml), an antagonist of Ob receptor, leptin (10 ng/ml) also no longer potentiated the CA secretory responses evoked by DMPP and Bay-K-8644. Collectively, these experimental results suggest that leptin enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors), but does not that by membrane depolarization. It seems that this enhanced effect of leptin may be mediated by activation of U0126-sensitive MAPK through the leptin receptors, which is probably relevant to the activation of the dihydropyridine L-type $Ca^{2+}$ channels located on the rat adrenomedullary chromaffin cells.

• Clinical and Experimental Reproductive Medicine
• /
• v.27 no.1
• /
• pp.15-22
• /
• 2000

Objective: To elucidate the location of leptin and receptors of ovary specimens obtained from patients undergoing hysterectomy by immunohistochemical staining and to determine the effect of leptin on the steroidogenesis of cultured granulosa cells. Method: In the culturing process of the granulosa cells, FSH (1 IU/ml)and leptin (50 ng/ml), IGF-I (50 ng/ml) was administered to each study group (Group I: FSH; Group II: FSH, leptin; Group III: FSH, IGF-I; Group IV: FSH, IGF-I, leptin), and the levels of estradiol, progesterone, androstenedione in the culture media was measured by radioimmunoassay. Statistical analysis was conducted by one-way ANOVA with Scheffe test. Results: The results showed that leptin and leptin receptors were both found to be strongly stained in granulosa and theca cells, and also in some interstitial cells. Leptin receptors were also observed in cultured granulosa cells. While there was no statistically significant difference in the androstnedione concentrations between the groups, estradiol concentrations was significantly decreased in Group IV ($2202.0{\pm}151.14$ pg/ml) compared to Group III ($2859.0{\pm}122.6$ pg/ml), and progesterone concentrations were also significantly decreased in Group II($4696.3{\pm}190.6$ ng/ml) and Group IV ($4517{\pm}206.78$ ng/ml) compared to Group III($5546.0{\pm}179.5$ ng/ml). Conclustion: The study result of this study suggest that leptin is directly involved in the regulation of ovarian functions, in particular steroidogenesis.

• Journal of Community Nutrition
• /
• v.8 no.2
• /
• pp.69-75
• /
• 2006

Adipose tissue has now been recognized as a rich source of metabolically active molecules that include leptin and angiotensinogen (AGT), the precursor of angiotensin II (Ang II). Both of which have been implicated in the pathogenesis of metabolic alteration and hypertension associated with obesity. In this study, we examined the relationship between body mass index (BMI), adipocyte size, leptin, Ang II secretion and mRNA expression in human adipose tissue obtained from female subjects. Leptin and Ang II were analyzed using specific radioimmunoassay kits following a 48hour tissue culture. Leptin and Ang II secretion varied from 1.4 - 72.1ng/g and 0.8 - 57.3pg/g of tissue respectively. These large individual variations limit significant correlation between BMI, leptin and Ang II secretion. Ang II secretion was significantly higher in the obese than the non-obese (p < 0.05) and positively correlated with BMI. However, no difference in leptin secretion between the obese and the non-obese was observed and leptin secretion showed negative correlation with BMI. No difference in leptin and AGT mRNA expression in adipose tissue between the obese and the non-obese was observed. Although several limitations of this study, we found increased Ang II secretion in obese patients compared with non-obese patients, and positive correlation between AGT and BMI. Observed difference in AGT expression between the obese and the non-obese in this study might be of importance in relation with obesity related hypertension. (J Community Nutrition 8(2): 69-75, 2006)

• Biomolecules & Therapeutics
• /
• v.29 no.1
• /
• pp.11-21
• /
• 2021

Adipose tissue secretes many adipokines which contribute to various metabolic processes, such as blood pressure, glucose homeostasis, inflammation and angiogenesis. The biology of adipose tissue in an obese individual is abnormally altered in a manner that increases the body's vulnerability to immune diseases, such as psoriasis. Psoriasis is considered a chronic inflammatory skin disease which is closely associated with being overweight and obese. Additionally, secretion of leptin, a type of adipokine, increases dependently on adipose cell size and adipose accumulation. Likewise, high leptin levels also aggravate obesity via development of leptin resistance, suggesting that leptin and obesity are closely related. Leptin induction in psoriatic patients is mainly driven by the interleukin (IL)-23/helper T (Th) 17 axis pathway. Furthermore, leptin can have an effect on various types of immune cells such as T cells and dendritic cells. Here, we discuss the relationship between obesity and leptin expression as well as the linkage between effect of leptin on immune cells and psoriasis progression.