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Review Article
Obesity and Metabolism
Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease
Chrysoula Boutari, Nikolaos Perakakis, Christos Socrates Mantzoros
Endocrinol Metab. 2018;33(1):33-43.   Published online March 21, 2018
DOI: https://doi.org/10.3803/EnM.2018.33.1.33
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  • 112 Web of Science
  • 106 Crossref
AbstractAbstract PDFPubReader   ePub   

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting 30% of the general population and 40% to 70% of obese individuals. Adipose tissue plays a crucial role in its pathogenesis, as it produces and secretes pro- and anti-inflammatory cytokines called adipokines. Adiponectin and leptin have well-determined actions in terms of NAFLD pathophysiology. Adiponectin deficiency is associated with a pro-inflammatory condition, as it is observed in obesity and other metabolic disorders. On the other hand, increased leptin levels, above the normal levels, act as a pro-inflammatory stimulus. Regarding other adipokines (resistin, visfatin, chemerin, retinol-binding protein 4, irisin), data about their contribution to NAFLD pathogenesis and progression are inconclusive. In addition, pharmacological agents like thiazolidinediones (pioglitazone and rosiglitazone), that are used in the management of NAFLD exert favourable effects on adipokine levels, which in turn may contribute to the improvement of liver function. This review summarizes the current knowledge and developments in the association between adipokines and NAFLD and discusses possible therapeutic implications targeting the modulation of adipokine levels as a potential tool for the treatment of NAFLD.

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Close layer
Original Article
Obesity and Metabolism
Serum Concentrations of Ghrelin and Leptin according to Thyroid Hormone Condition, and Their Correlations with Insulin Resistance
Kyu-Jin Kim, Bo-Yeon Kim, Ji-Oh Mok, Chul-Hee Kim, Sung-Koo Kang, Chan-Hee Jung
Endocrinol Metab. 2015;30(3):318-325.   Published online May 18, 2015
DOI: https://doi.org/10.3803/EnM.2015.30.3.318
  • 3,880 View
  • 45 Download
  • 9 Web of Science
  • 11 Crossref
AbstractAbstract PDFPubReader   
Background

Thyroid hormones can influence energy metabolism and insulin sensitivity via their interaction with adipocytokines and gut hormones. The aims of this study were to evaluate differences in serum ghrelin and leptin concentrations according to thyroid hormone levels, and to investigate the correlation of insulin resistance.

Methods

A total of 154 patients (57 hyperthyroid patients, 61 euthyroid patients, and 36 hypothyroid patients; mean age, 47.9 years) were enrolled. Serum leptin, ghrelin, and insulin levels were measured and insulin resistance was calculated using the formula of the homeostasis model assessment of insulin resistance (HOMA-IR).

Results

There were no differences in mean concentrations of ghrelin or leptin among the three groups. There were no significant differences in insulin levels between the groups (P=0.06), although hyperthyroid patients had borderline statistically significantly higher levels of insulin than did euthyroid subjects by post hoc test (26.4 µIU/mL vs. 16.1 µIU/mL, P=0.057). Regarding HOMA-IR index, the mean levels were highest in the hyperthyroid group among those of the three groups (hyperthyroid vs. euthyroid vs. hypothyroid, 6.7 vs. 3.8 vs. 4.4, P=0.068). Plasma levels of ghrelin were significantly negatively correlated with age, insulin, glucose, body mass index (BMI), and HOMA-IR. Plasma levels of leptin showed significant positive correlation with BMI and triglyceride. There were no significant correlations among thyroid hormone, thyrotropin, ghrelin, leptin, or insulin.

Conclusion

The present study found that serum ghrelin, leptin, and insulin levels didn't differ according to thyroid function conditions. Further studies with larger numbers of patients are required to establish a direct relationship between plasma ghrelin, leptin, and thyroid hormone.

Citations

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    Doaa El Amrousy, Dalia El-Afify, Shaimaa Salah
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    Avinash Patil, Suresh Vaikkakara, Mani Deepthi Dasari, Sandeep Ganta, Alok Sachan, Kiranmayi S. Vinapamula
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    Peeyush Yadav, G. G. Kaushik
    INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH.2021; : 52.     CrossRef
  • Acylated Ghrelin Attenuates l-Thyroxin–induced Cardiac Damage in Rats by Antioxidant and Anti-inflammatory Effects and Downregulating Components of the Cardiac Renin–angiotensin System
    Rehab Badi
    Journal of Cardiovascular Pharmacology.2021; 78(3): 422.     CrossRef
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    Chan-Hee Jung
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Close layer
Review Articles
Adrenal gland
Role of Reactive Oxygen Species in Hypothalamic Regulation of Energy Metabolism
Sabrina Diano
Endocrinol Metab. 2013;28(1):3-5.   Published online March 25, 2013
DOI: https://doi.org/10.3803/EnM.2013.28.1.3
  • 3,948 View
  • 43 Download
  • 21 Crossref
AbstractAbstract PDFPubReader   

To understand the etiology of metabolic disorders, including obesity and type II diabetes, it is essential to gain better insight into how stored and available energy sources are monitored by the central nervous system. In particular, a comprehension of the fine cellular interplay and intracellular mechanisms that enable appropriate hypothalamic and consequent endocrine and behavioral responses to both circulating hormonal and nutrient signals remains elusive. Recent data, including those from our laboratories, raised the notion that reactive oxygen species (ROS) generation is not merely a by-product of substrate oxidation, but it plays a crucial role in modulating cellular responses involved in the regulation of energy metabolism. These review summarizes the published recent data on the effect of ROS levels in the regulation of neuronal function, including that of hypothalamic melanocortin neurons, pro-opiomelanocortin and neuropeptide Y-/agouti related peptide-neurons, in the modulation of food intake.

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Close layer
Neuroendocrine Regulation of Energy Metabolism.
Marcelo O Dietrich, Tamas L Horvath
Endocrinol Metab. 2012;27(4):268-273.   Published online December 20, 2012
DOI: https://doi.org/10.3803/EnM.2012.27.4.268
  • 2,318 View
  • 25 Download
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AbstractAbstract PDF
Significant advancements have been made in the past century regarding the neuronal control of feeding behavior and energy expenditure. The effects and mechanisms of action of various peripheral metabolic signals on the brain have become clearer. Molecular and genetic tools for visualizing and manipulating individual components of brain homeostatic systems in combination with neuroanatomical, electrophysiological, behavioral, and pharmacological techniques have begun to elucidate the molecular and neuronal mechanisms of complex feeding behavior and energy expenditure. This review article highlights some of these advancements that have led to the current understanding of the brain's involvement in the acute and chronic regulation of energy homeostasis.

Citations

Citations to this article as recorded by  
  • Neuronal HSF-1 coordinates the propagation of fat desaturation across tissues to enable adaptation to high temperatures in C. elegans
    Laetitia Chauve, Francesca Hodge, Sharlene Murdoch, Fatemeh Masoudzadeh, Harry-Jack Mann, Andrea F. Lopez-Clavijo, Hanneke Okkenhaug, Greg West, Bebiana C. Sousa, Anne Segonds-Pichon, Cheryl Li, Steven W. Wingett, Hermine Kienberger, Karin Kleigrewe, Mari
    PLOS Biology.2021; 19(11): e3001431.     CrossRef
Close layer
Original Articles
The Effect of Leptin Level Fluctuations by a Repeated Fasting/Refeeding on the Leptin Sensitivity in OLETF Rats.
Sung Chul Park, Yong Hoon Park, So Young Park, Jong Yeon Kim, Yoon Ki Park, Tae Hyung Lee, Kyu Chang Won, Yong Woon Kim
J Korean Endocr Soc. 2008;23(5):310-318.   Published online October 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.5.310
  • 1,941 View
  • 30 Download
  • 4 Crossref
AbstractAbstract PDF
BACKGROUND
Leptin resistance is a common feature in obese subjects and animals, and this is commonly accompanied with hyperleptinemia. We speculated that one of the causes of leptin resistance is a persistently elevated leptin concentration and then we hypothesized that fluctuations of serum leptin would increase leptin sensitivity in the leptin-resistant state. METHODS: We used a repeated fasting and refeeding (RFR) protocol to produce fluctuation in leptin levels in 7 month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats and Long-Evans Tokushima Otsuka (LETO) rats, We then measured the leptin sensitivity following an intracerebroventricular (i.c.v.) infusion of leptin. RESULTS: The OLETF rats exhibited severe visceral fat deposition, hyperleptinemia and leptin resistance. However, in the OLETF-RFR rats, the anorexic effect following i.c.v. leptin infusion was restored. Moreover, the visceral fat mass and serum leptin levels decreased, while the serum adiponectin levels were elevated in the OLETF-RFR rats compared to the OLETF-Control rats. The leptin receptor content in the hypothalamus increased in the OLETF-RFR rats compared to the OLETF-Control rats, and the leptin receptor content in the OLETF-RFR rats decreased compared to that in the the LETO-Control rats. CONCLUSION: These results suggest that the intermittent suppression of the serum leptin level reversed the leptin resistance in OLEFT rats, and this may have occurred due to an increased number of leptin receptors in the hypothalamus.

Citations

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  • Reduced Striatal Dopamine Transporter Availability and Heightened Response to Natural and Pharmacological Stimulation in CCK-1R-Deficient Obese Rats
    Sevag Hamamah, Andras Hajnal, Mihai Covasa
    International Journal of Molecular Sciences.2023; 24(11): 9773.     CrossRef
  • Improvement of Leptin Resistance
    Yong Woon Kim
    Yeungnam University Journal of Medicine.2013; 30(1): 4.     CrossRef
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    Ki Hoon Kim, Hyun Kook Kim
    Korean Journal of Nutrition.2012; 45(1): 5.     CrossRef
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    Min Seon Kim
    Journal of Korean Endocrine Society.2008; 23(5): 298.     CrossRef
Close layer
Naloxone Increases the Anorexic Effect of MTII in OLETF Rats.
Jang Ho Bae, Yong Hoon Park, Sung Ho Kim, So Young Park, Jong Yeon Kim, Jo Young Son, Jung Yoon Huh, Kyu Chang Won, Yong Woon Kim
J Korean Endocr Soc. 2008;23(1):18-26.   Published online February 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.1.18
  • 1,954 View
  • 17 Download
  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Leptin, an adipocyte-derived hormone, inhibits obesity in lean subjects, but is not widely used because of leptin resistance. Thus, circumventing the arcuate nucleus of the hypothalamus, the site responsible for leptin resistance, has been evaluated for treatment of obesity. However, chronic treatment of melanotan II (MTII), a synthetic agonist of the melanocortin 3/4 receptor, induces tachyphylaxis. Here, we evaluated whether naloxone, a non-specific agouti-related peptide (AgRP) antagonist, increases the anorexic effect of MTII in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: We measured food intake following intracerebroventricular (i.c.v.) infusion of MTII and/or naloxone in OLETF rats. Sprague-Dawley rats were used as a normal control group. RESULTS: The anorexic effect of i.c.v. MTII infusion decreased with time in OLETF rats, indicating the development of tachyphylaxis. In normal control rats, naloxone alone decreased AgRP expression in the hypothalamus but failed to induce anorexia. Moreover, there was no additional anorexic effect with co-treatment of naloxone and MTII. In OLETF rats, naloxone alone did not show an anorexic effect despite increased POMC expression in the hypothalamus. However, naloxone sensitized the anorexic effect of MTII when treated together. CONCLUSION: These results suggest that naloxone augmented the anorexic effect of MTII when treated together in OLETF rats, but had no effect alone. These results suggest that a combination therapy of naloxone and a melanocortin receptor activator would be an effective modality for treatment of obesity.

Citations

Citations to this article as recorded by  
  • Naloxone Increases the Anorexic Effect of Melanocortin II
    Seungjoon Park
    Journal of Korean Endocrine Society.2008; 23(1): 15.     CrossRef
Close layer
The Effect of Fenofibrate and Exercise on Metabolic Syndrome and Hepatic Steatosis in OLETF Rats.
Kyung II Lee, Ji Min Kim, Ja Young Park, Ja Won Kim, Ji Young Mok, Mi Kyoung Park, Hye Jeong Lee, Sook Hee Hong, Wenjun Li, Duk Kyu Kim
J Korean Endocr Soc. 2007;22(3):192-202.   Published online June 1, 2007
DOI: https://doi.org/10.3803/jkes.2007.22.3.192
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AbstractAbstract PDF
BACKGROUND
The aim of this study is to verify the effects of fenofibrate monotherapy and fenofibrate combined with exercise for improving metabolic syndrome and hepatic steatosis. METHODS: Thirty-four weeks old OLETF rats (Otsuka Long-Evans Tokushima Fatty Rats, n = 20) were divided four groups: the regular diet group (n = 5, DD group), the exercise group (n = 5, DE group), the fenofibrate (100 mg/kg) treated group (n = 5, DF group) and the combination treatment group {fenofibrate and exercise (n = 5, EF group)}. After 5 weeks of treatment, blood was drawn for measuring the blood glucose, insulin, lipid and leptin levels. All the subjects were sacrificed for assessment of their body adiposity and hepatic steatosis. RESULTS: The total amount of food intake, body weight and total body weight of the rat were significantly decreased in the EF and DF groups compared to the DD group. The plasma triglyceride and glucose levels were significantly decreased in the EF and DF groups compared to the DD group. The HOMA-IR of EF, DF and DE groups were significantly decreased compared with that of the DD group. The plasma leptin levels of the EF and DF groups were significantly decreased compared with those of the DD and DE groups. The hepatic steatosis index was significantly decreased in the EF and DF groups compared to the DD and DE groups. CONCLUSION: Fenofibrate monotherapy was effective to control three major components (obesity, hypertriglyceridemia and hyperglycemia) of metabolic syndrome and hepatic steatosis in OLETF rats. Exercise combined with fenofibrate treatment showed an additional effect compared to that of fenofibrate monotherapy.

Citations

Citations to this article as recorded by  
  • Effect of Fenofibrate and Exercise on Metabolic Syndrome and Hepatic Steatosis
    Bong Soo Cha, Jae Hyuk Lee
    Journal of Korean Endocrine Society.2007; 22(3): 188.     CrossRef
Close layer
The Relationship between the Leptin Concentration and the Small Dense Low Density Lipoprotein Cholesterol Concentration in Korean Type 2 Diabetic Patients.
Wan Sub Shim, Hae Jin Kim, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Hyun Chul Lee, Bong Soo Cha
J Korean Endocr Soc. 2006;21(4):319-327.   Published online August 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.4.319
  • 1,842 View
  • 20 Download
  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Leptin has been suggested as a possible cause of atherosclerotic disease. The small dense low-density lipoprotein cholesterol (LDL-C) has also been regarded as a new surrogate marker in atherosclerotic disease. The aim of this study was to evaluate the relationship between the leptin concentration and the small dense LDL-C concentration in Korean type 2 diabetic patients. METHODS: One hundred-ninety one type 2 diabetic patients, who did not use any medication that could affect the concentration of lipid such as statin, fibrate, thiazolidinediones and corticosteroid, were enrolled in this study. We analyzed the relationship between leptin, the small dense LDL-C and the other metabolic parameters. RESULTS: The small dense LDL-C concentrations were higher in the group with the highest tertile of the leptin value, both in males and females than those patients in the group with the lowest tertile of the leptin value. The small dense LDL-C concentrations were also higher in the group with the highest tertile of leptin divided by the BMI value both in males and females than those patients in the group with the lowest tertile of the leptin value. The leptin concentration was positively correlated with the small dense LDL-C, total cholesterol, triglyceride, LDL-C, insulin and HOMAIR values after adjusting for age, gender and BMI. CONCLUSION: The association between leptin and small dense LDL-C could be a factor that explains the association between leptin and cardiovascular disease.

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  • Relationships among Serum Adiponectin, Leptin and Vitamin D Concentrations and the Metabolic Syndrome in Farmers
    Seo-Eun Yeon, Hee-Ryoung Son, Jung-Sook Choi, Eun-Kyung Kim
    Korean Journal of Community Nutrition.2014; 19(1): 12.     CrossRef
  • The Effect of Visceral Fat Area and Adipocytokines on Acute Myocardial Infarction: A Case-Control Study in Adult Korean Population
    Kang-Kon Lee, Young-Sung Suh, Keun-Sang Yum
    The Korean Journal of Obesity.2012; 21(1): 57.     CrossRef
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The Relationship of Ghrelin and Leptin with the Biochemical Markers for Adult Growth Hormone Deficiency.
Chan Hee Jung, Eun Jung Rhee, Se Yeon Kim, Ki Won Oh, Won Young Lee, Sun Woo Kim
J Korean Endocr Soc. 2006;21(3):213-221.   Published online June 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.3.213
  • 2,665 View
  • 18 Download
AbstractAbstract PDF
BACKGROUND
In spite of the increasing information that has recently been accumulated on the involvement of ghrelin and leptin in energy balance control, the relationship between ghrelin or leptin and the growth hormone (GH)-Insulin like growth factor-1 (IGF-1) axis in the pathological condition characterized by growth hormone deficiency (GHD) has been poorly clarified. Therefore, we performed this study to evaluate the correlation of the plasma levels of ghrelin and leptin with the anthropometric and biochemical markers in GHD adults and also in healthy adults. METHODS: For the 60 male adults (GHD, n = 12; healthy control, n = 48; average age, 54 years), we investigated the correlations between the serum leptin and ghrelin levels with the anthropometric and biochemical factors in the two groups, as divided by their GH status. The diagnosis of GHD was made on the basis of a peak response for serum GH of less than 5 micro/L to a GH provocative test (L-dopa test). All the subjects underwent assessment of waist circumference, BMI and percentage body fat for their body composition. The plasma ghrelin, leptin, insulin, GH and IGF-1 were measured. RESULTS: The groups were well-matched for their age, BMI, waist circumference and percentage of body fat. The ghrelin and leptin levels were not significantly different between the two groups. There was no correlation between the peak GH level or the area under the curve of growth hormone (GHAUC) and the ghrelin concentrations in the GHD subjects. Plasma leptin correlated positively with the percentage of body fat, the total cholesterol and the LDL-cholesterol, but it had no correlation with the peak GH or GHAUC in the GHD subjects. CONCLUSIONS: It is possible that the ghrelin concentrations appeared normal in the GHD subjects. Further studies are needed to clarify these controversies about the relation of ghrelin and leptin with the GH and IGF-1 levels.
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Relationship between Adiponectin, Leptin and Body Fat in Men with Hypogonadism Before and After Testosterone Treatment.
Sang Wan Kim, Joon Ku Kang, Do Joon Park, Chan Soo Shin, Kyung Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee
J Korean Endocr Soc. 2004;19(5):473-484.   Published online October 1, 2004
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BACKGROUND
Testosterone replacement therapy in men with hypogonadism improves sexual function, decreases body fat, and increases the mass and function of lean muscle. These beneficial effects of testosterone replacement therapy are accompanied by slight lowering of the high density lipoprotein (HDL) cholesterol levels, increase in the hematocrit/hemoglobin ratio and size of the prostate gland. It is presently unknown whether the effect of testosterone on body fat could also reduce the risk of atherosclerotic disease associated with obesity. We investigated the relationship between body fat and blood leptin and adiponectin levels to elucidate the effect of testosterone on body fat metabolism, as well as the effect of testosterone on lipid and bone metabolism. METHODS: We selected 28 men, who were hypogonadal (mean serum testosterone+/-SD, 22.3+/-35.3 ng/dL) due to an organic disease, and them with oral testosterone (testosterone undecanoate) for 12 months. We measured the body composition, serum leptin, plasma adiponectin, biochemical bone markers, bone mineral density, prostate-specific antigen, and serum lipids before and 3, 6 and 12 months after treatment. We analyzed the relationship between body fat and blood leptin and adiponectin levels. RESULTS: The mean serum testosterone concentration reached the subnormal range after 6 months of treatment, which remained for the duration of treatment. The fat mass decreased and muscle mass increased, not within the first 6 months, but principally within 12 months (p<0.05). Although the decrease in the serum leptin level was not statistically significant, there were positive correlations between the leptin level and fat mass before and after 6 months of treatment (p<0.05). The plasma adiponectin did not increase or correlate with body fat parameters. The bone mineral densities of the lumbar spine (L2-L4) and femoral neck did not increased, but the serum osteocalcin and urine N-telopeptide were significantly decreased (p<0.05 and <0.01, respectively). The HDL-cholesterol decreased, principally within the first 6 months (p<0.01), but the total and LDL cholesterols, and the triglycerides remained unchanged during the course of treatment. There was also no change in prostate-specific antigen. CONCLUSION: Twelve months of oral testosterone replacement in men with hypogonadism improved body composition and bone metabolism, but demonstrated subnormal serum testosterone levels, had no effect on the leptin and adiponectin levels and decrease in HDL-cholesterol levels. It will be necessary to examine the long-term effects of testosterone replacement on the incidence of cardiovascular events as well as cardiovascular risk factors in men with hypogonadism
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Relationship between Serum Leptin, Adiponectin, Resistin and Ghrelin Levels, and Bone Mineral Density in Men.
Ki Won Oh, Eun Joo Yun, Eun Jung Rhee, Won Young Lee, Ki Hyun Baek, Kun Ho Yoon, Moo Il Kang, Cheol Young Park, Sung Hee Ihm, Moon Gi Choi, Hyung Joon Yoo, Sung Woo Park
J Korean Endocr Soc. 2004;19(4):379-392.   Published online August 1, 2004
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BACKGROUND
Fat mass is an important determinant of bone mineral density (BMD), but the mechanism involved in this relationship is uncertain. Several lines of evidence have suggested the effects of fat mass on BMD may be mediated by hormonal factors, with the principal candidates being serum sex hormones, insulin, leptin and adiponectin. Thus, the aim of this study was to investigate the relationship between the serum adipocytokine and ghrelin levels, and BMD in men. METHODS: Eighty men, aged 42~70 (mean age, 54.5 yr), were selected as the study subjects. The serum concentrations of leptin and ghrelin were measured with RIA, the adiponectin with ELISA and the resistin with EIA. The serum concentrations of estradiol, total testosterone and the biochemical markers of bone turnover were measured by standard methods. The BMD at the lumbar spine and femoral neck were measured by dual energy x-ray absorptiometry. RESULTS: The serum leptin level was found to correlate to the BMI, waist to hip ratio (WHR), blood pressure, fasting blood sugar, serum fasting insulin, total cholesterol, triglyceride and calcium levels. Although the serum leptin level was not significantly correlated to the serum estradiol level, it did show a weak trend. The serum adiponectin level were correlated to the BMI, WHR and serum fasting insulin level; and the resistin to serum total cholesterol and low density lipoprotein cholesterol levels; ghrelin to age, WHR and serum triglyceride levels. A significant negative correlation was observed between the serum resistin level and lumbar spine BMD. Also, there was a significant negative correlation between the serum leptin level and lumbar spine BMD. The above correlations were observed only when the BMI and the serum estradiol and insulin levels were included as independent variables in the regression analysis model. The serum adiponectin level was not significantly correlated with the BMD, either in the presence or absence of the BMI and serum insulin level. CONCLUSION: The serum adipocytokine level was observed to be partly associated with the BMD in men. Therefore, these data suggest that leptin and resistin may play roles in the bone mineral metabolism in men. Further studies are needed to larify this relationship
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Association between Serum Leptin Concentration and Bone Mineral Density in Healthy Korean Women.
Yumie Rhee, Dae Jung Kim, Se Hwa Kim, Chul Woo Ahn, Bong Soo Cha, Kyung Rae Kim, Hyun Chul Lee, Sung Kil Lim
J Korean Endocr Soc. 2003;18(2):177-183.   Published online April 1, 2003
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BACKGROUND
Leptin is known to affect bone metabolism both centrally and peripherally. This study was performed to investigate the relationship between leptin and bone mineral density(BMD) in healthy premenopausal and postmenopausal Korean women. METHODS: 140 women were recruited for a routine health check-up. Anthro-pometric and biochemical data were checked as usual. BMDs were measured by dual x-ray absorptiometry of the spine and femur in 67 premenopausal women and 73 postmenopausal women, in addition to their serum leptin levels. RESULTS: Serum leptin level showed no correlation with BMD in premenopausal women, but there was a positive correlation betwen serum leptin and spinal BMD in postmenopausal women(r=0.468, p<0.001). After the correcting for age, body mass index, and duration of menopause, the serum leptin level and BMD still showed a positive correlation(r=0.217, p=0.088) although weak. The women in the lowest quartile of serum leptin level showed significantly lower lumbar and femoral neck BMD. CONCLUSION: Leptin level seems to have a weak relationship with BMD showing different features in premenopausal and postmenopausal women.
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Fos Expression Induced by Combined Injection of Leptin and Cholecystokinin in the Rat Brain.
Young Uck Kim, Kyung Suk You, Ho Suck Kang, Choon Hee Chung, Tae Sun Hwang
J Korean Endocr Soc. 2002;17(4):486-500.   Published online August 1, 2002
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BACKGROUND
Several studies have reported that cholecystokinin (CCK), a short-term meal related satiety signal, and leptin, long-term signal for controlling feeding behaviour and body weight, act synergistically to inhibit food intake. However the mechanism and neuroanatomical basis for this response remain unclear. To clarify the neuronal mechanisms underlying the synergistic interaction between leptin and CCK, we examined the neuron activated by single or combined injection of leptin and CCK in fasted rats using immunohistochemistry for Fos. The expression of Fos can be used to trace neuronal activation pathways. METHODS: The rats were divided into 4 groups; Tris solution-saline, Tris solution-CCK, leptin-saline, leptin-CCK. Rats were received a single intracerebroventricular injection of either 3mul Tris solution or 3microgram leptin, and a single intraperitoneal injection of either 2mul saline or 2microgram/kg sulfated CCK-8. The changes of the Fos expression were investigated in the paraventricular nucleus (Pa), retrochiasmatic area (RCh), lateral hypothalamic nucleus (LH), central nucleus of amygdala(Ce), supraoptic nucleus (SO), arcuate nucleus (Arc), ventromedial hypothalamic nucleus(VMH),dorsomedial hypothalamic nucleus (DM), ventral premammillary nucleus (PMV), superior lateral subdivision of parabrachial nucleus (LPBS), external lateral subdivision of parabrachial nucleus (LPBE), supragenual nucleus (SGe), area postrema (AP), medial area (SolM) and commissural area (SolC) of nucleus of the solitary tract nuclei. RESULTS: CCK increased the Fos expression in the Pa, RCh, LH, Ce, SO, Arc, VMH, DM, PMV, LPBS, LPBE and SolM. Leptin increased the Fos expression in the Pa, RCh, LH, SO, Arc, VMH, DM, PMV, LPBS, LPBE, SGe, AP and SolM. Injections of leptin and CCK significantly enhanced the Fos expression in the Pa, RCh, VMH, DM, LPBS, and SolM compared with those induced by leptin or CCK alone. CONCLUSION: Our results suggest that the Pa, RCh, VMH, DM, LPBS and SolM may be essential sites mediating the synergistic effect of leptin and CCK to regulate food intake.
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Changes in Plasma Leptin Levels Relating to Short-Term Thyroid Manipulation in Rats.
Min Seon Kim, Cho Ya Yoon, Young Min Cho, Hye Seung Jung, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Stephen R Bloom
J Korean Endocr Soc. 2002;17(2):197-205.   Published online April 1, 2002
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BACKGROUND
Leptin, an adipocyte derived hormone, and thyroid hormone have similar effects on energy homeostasis, such that a shortage of both hormones is associated with decreased energy expenditure and increased body weight. Therefore, for the maintenance of energy homeostasis may require a close interaction between leptin and thyroid hormone. This study was performed to investigate the change in plasma leptin levels relating to short-term thyroid manipulation causing no significant change in body weight. METHODS: Hypothyroidism was induced by surgical thyroidectomy and hyperthyroidism by subcutaneous injection of 50 g of L-T3/100 g body weight/day, for 5 days, in 6~8 weeks old male Wistar rats. Body weights and food intakes were monitored daily until sacrifice. Plasma samples were collected, and the thyroid stimulating hormone (TSH), free triiodothyronine (T3) and leptin levels measured. The plasma leptin levels in rats with hypothyroidism and hyperthyroidism were compared with those of body weights at death and food intakes during the study, atched controls. RESULTS: The rats treated with L-T3 consumed equal amount of food as freely fed, rats but their final body weights were significantly lower (L-T3 treated 220.0 +/- 1.8 vs. freely fed 226.0 +/- 2.0 g, p<0.05). There was no difference in food intake during study, and final body weight, between the thyroidectomised rats and their paired controls (thyroidectomised 220.4 +/- 1.7 vs. paired 223.9 +/- 4.7 g, P=NS). Plasma leptin levels in the L-T3 treated rats were significantly lower than those in freely fed rats (L-T3 treated 1.7 +/- 0.1 vs. freely fed 4.8 +/- 0.2 ng/ml, p<0.005). Conversely, the thyroidectomised rats had higher plasma leptin levels, compared to those of their paired controls (thyroidectomised 4.8 +/- 0.3 vs. paired 1.7 +/- 0.1 ng/ml, p<0.005). CONCLUSION: The Plasma leptin levels in the rats were decreased by short term hyperthyroidism, while they were increased by short term hypothyroidism. These findings suggest that thyroid hormones may affect the production or secretion of leptin
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Relationship between Plasma Leptin Levels and Carotid Intima-Medial Thickness in Korean Adults.
Hyejin Lee, Eunsoon Hong, Youngsun Hong, Yeon Ah Sung
J Korean Endocr Soc. 2002;17(1):87-94.   Published online February 1, 2002
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BACKGROUND
Many studies have recently shown that leptin can promote angiogenesis via endothelial leptin receptors and induce oxidative stress in endothelial cells; These findings suggest the relationship between cardiovascular risk and blood leptin concentration. In the present study, we investigated the relationship between leptin concentration and carotid intima-medial thickness (CIMT) as an indicator of early atherosclerosis in adults. METHEODS: The study subjects comprised 138 (45 men and 93 women; mean age 42.4+/-7.5 years; mean BMI 24.0+/-2.7 kg/m2) without history of diabetes, hypertension or cardiovascular disease. We measured CIMT by high resolution ultrasonography and plasma leptin levels by radioimmunoassay. RESULTS: 1) No significant differences in age, BMI or CIMT between male and female subjects were noted, but the leptin levels in female were significantly higher than those in males. (8.42+/-5.90 ng/mL vs. 3.08+/-1.00 ng/mL, p<0.001) 2) CIMT showed a significant positive correlation with age (r=0.31, p< 0.001), BMI (r=0.25, p<0.01) and level (r=0.42, p<0.05) in simple regression analysis. 3) When male and female subjects were each divided into 3 groups by leptin concentration, no significant difference in CIMT among female subjects was found. In male subjects, CIMT was significantly higher in the highest tertile of leptin level than in the other 2 groups (0.65+/-0.03 mm vs. 0.56+/-0.07 mm and 0.53+/-0.07 mm, p<0.01) after adjustment for BMI and age. However, this difference was not significant after adjustment for smoking. 4) CIMT (0.61+/-0.05 mm vs. 0.53+/-0.07 mm, p<0.01) and leptin concentrations (3.57+/-2.13 ng/mL vs. 2.20+/-1.39 ng/mL, p<0.05) were significantly higher in male smokers than in male non-smokers. CONCLUSION: Our results demonstrated significant correlation of CIMT to plasma leptin level before adjustment for smoking. A possible explanation is the permissive action of smoking on the atherogenic effect of leptin. However, further studies to elucidate the relationships and interactions among smoking, leptin level and the development of atherosclerosis will be needed.
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