BACKGROUND: Adipokines are associated with various metabolic disorders including insulin resistance, obesity and dyslipidemia. Metabolic disorders have also been reported to be associated with nonalcoholic fatty liver disease (NAFLD). We aimed to estimate changes in serum adipokines levels according to the degrees of steatosis and to determine independent factors influencing serum adipokines levels in Korean male patients with NAFLD. METHODS: 65 Korean male patients were subjected. The degrees of steatosis were stratified into the three groups, Group I: normal liver (27 subjects), Group II: mild fatty liver (24 subjects) and Group III: moderate to severe fatty liver (14 subjects), according to ultrasonographic liver findings. The anthropometric parameters, fasting serum adipokine levels including leptin, adiponectin and resistin were measured in all subjects. The level of insulin resistance was estimated using the HOMA-IR. RESULTS: Serum leptin levels were significantly different among the three groups (mean+/-SD: Group I (2.052+/-1.071), Group II (2.879+/-1.016), Group III (4.457+/-1.965 ng/mL), p<0.001). Serum adiponectin and resistin levels were not significantly different among the three groups (p=0.184, p=0.649, respectively). BMI and HOMA-IR were independent factors of changes in serum leptin levels (p=0.026, p=0.001, respectively), but independent factors of changes in serum adiponectin and resistin levels were not observed. CONCLUSIONS: Our study support a indirect role to induce metabolic disorder for leptin in the pathogenesis of NAFLD, but do not support roles for adiponectin and resistin in the pathogenesis of NAFLD. BMI and HOMA-IR were only independent factors of changes in serum leptin levels.
Adipokines* ; Adiponectin ; Dyslipidemias ; Fasting ; Fatty Liver* ; Humans ; Insulin Resistance ; Leptin ; Liver ; Male* ; Obesity ; Resistin

Fat accumulation has been shown to play important roles in the development of obesity-related disorders such as atherosclerosis, diabetes mellitus and hypertension. Recent studies have shown that fat tissue is not a simple energy storage organ, but exerts important endocrine functions. These are achieved predominantly through release of adipocytokines, which include several novel molecules released by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells, like TNF-alpha and IL-6. Adipocytokines may affect cardiovascular, hepatic, muscular and metabolic function. In this review, the recent research work of adipocytokines will be discussed.
Adipokines ; physiology ; Adiponectin ; physiology ; Adipose Tissue ; chemistry ; physiology ; Humans ; Leptin ; physiology ; Resistin ; physiology

PURPOSE: Adipocytokines, such as leptin, resistin, and adiponectin, are associated with obesity and breast cancer. Several studies have indicated that adipocytokines may influence tumor growth or differentiation. The aims of this study were to determine the expression of leptin, leptin receptor (ObR), adiponectin and adiponectin receptor (AdipoR) in human breast cancer, to evaluate their prognostic significance in the breast cancer. METHODS: Specimens from 198 patients with primary breast cancer were enrolled, and representative paraffin tumor blocks were selected for constructing tissue microarrarys (TMA). Immunohistochemical staining for leptin, ObR, adiponectin, and AdipoR was performed using TMA, and the clinicopathologic characteristics were evaluated from the patient's medical records. RESULTS: Stage 0 breast cancer accounted for 41 cases, and 157 cases were invasive cancer. Positive rates of leptin and ObR expression in the ductal carcinoma in situ (DCIS) group were significantly higher than those of the invasive cancer group (97.4% vs. 34.0%, p<0.001; 74.4% vs. 29.8%, p<0.001). However, positive rates of adiponectin and AdipoR expression in the invasive cancer group were significantly higher than those in the DCIS group (53.7% vs. 33.3%, p=0.024; 59.9% vs. 26.3%, p<0.001). High leptin expression was significantly associated with high Ki-67 expression (p=0.016). High adiponectin expression was significantly correlated with smaller tumor size (p=0.001). CONCLUSION: We suggest that losses of leptin and ObR expression could be associated with invasive cancer, whereas high adiponectin and AdipoR expression may be associated with breast cancer invasiveness.
Adipokines ; Adiponectin ; Breast ; Breast Neoplasms ; Carcinoma, Ductal ; Carcinoma, Intraductal, Noninfiltrating ; Humans ; Leptin ; Obesity ; Paraffin ; Receptors, Adiponectin ; Receptors, Leptin ; Resistin

Sarcopenia is an age-related disease that mainly involves decreases in muscle mass, muscle strength and muscle function. At the same time, the body fat content increases with aging, especially the visceral fat content. Adipose tissue is an endocrine organ that secretes biologically active factors called adipokines, which act on local and distant tissues. Studies have revealed that some adipokines exert regulatory effects on muscle, such as higher serum leptin levels causing a decrease in muscle function and adiponectin inhibits the transcriptional activity of Forkhead box O3 (FoxO3) by activating peroxisome proliferators-activated receptor-γ coactivator -1α (PGC-1α) and sensitizing cells to insulin, thereby repressing atrophy-related genes (atrogin-1 and muscle RING finger 1 [MuRF1]) to prevent the loss of muscle mass. Here, we describe the effects on muscle of adipokines produced by adipose tissue, such as leptin, adiponectin, resistin, mucin and lipocalin-2, and discuss the importance of these adipokines for understanding the development of sarcopenia.
Humans ; Adipokines ; Leptin ; Adiponectin ; Sarcopenia ; Muscles

BACKGROUND: The aims of this study were to compare adipokine concentrations of pregnant women in the 24th~28th weeks of gestation to those of non-pregnant women. We compared the concentrations of adipokines in women with gestational diabetes mellitus (GDM), gestational impaired glucose tolerance (GIGT) and normal glucose tolerance (NGT). We also investigated the role of adipokines in the development of gestational glucose intolerance. METHODS: We surveyed 129 pregnant women who underwent a 100 g oral glucose tolerance test (OGTT) during the 24th~28th weeks of gestation. Participants were classified into three groups: (1) NGT (n = 40), (2) GIGT (n = 45), and (3) GDM (n = 44). Pregnant subjects with NGT were matched to non-pregnant controls for BMI and age (n = 41). RESULTS: Pregnant women with NGT exhibited significantly decreased adiponectin levels and elevated leptin levels compared to non-pregnant controls. Mean plasma resistin levels were significantly higher in women with GDM and GIGT than in women with NGT. Resistin and fasting glucose were significant predictors for the development of gestational glucose intolerance. CONCLUSION: Plasma adiponectin levels were decreased and leptin levels were increased in pregnant subjects with NGT compared to BMI and age matched non-pregnant controls. Women with GDM and GIGT exhibit significantly elevated concentrations of resistin compared with women with NGT. Increased resistin levels were also associated with the development of gestational glucose intolerance. Resistin may play an important role on the development of gestational glucose intolerance in Korean women.
Adipokines ; Adiponectin ; Diabetes, Gestational ; Fasting ; Female ; Glucose ; Glucose Intolerance ; Glucose Tolerance Test ; Humans ; Leptin ; Plasma ; Pregnancy ; Pregnant Women ; Resistin

PURPOSE: The objective of this study was to compare the levels of adipocytokines in obesity group with those in control group and examine their correlation with insulin resistance. METHODS: We enrolled 36 obese children (male:female [M:F]=17:19; age, 9.3+/-1.9 yrs) with > or =95th percentile body mass indexes (BMIs) (obesity group) and 35 healthy children (M:F=16:19; age, 9.1+/-2.1 yrs) with 25th-75th percentile BMIs (control group). We measured the serum leptin, adiponectin, and resistin levels and insulin resistance in both the groups. RESULTS: The weights, heights, BMIs, fasting sugar levels, insulin levels, and homeostasis model assessment for insulin resistance (HOMA-IR) values were higher in the obesity group than in the control group. As compared to the control group, the obesity group showed significantly higher leptin levels and lower adiponectin levels; no significant difference was observed in the resistin levels. The leptin/adiponectin (L/A) ratio was higher in the obesity group than in the control group. In the obesity group, HOMA-IR showed significant positive correlations with weight, height, BMI, and leptin level. However, it was not correlated with age and adiponectin and resistin levels. In the obesity group, leptin level showed significant positive correlations with age, weight, height, and BMI, while adiponectin and resistin levels showed no such correlations with the other variables CONCLUSION: We suggest that adiponectin plays an important protective role against weight gain in obese children. Further, L/A ratio can be used as a parameter for predicting the prognosis of obese children.
Adipokines ; Adiponectin ; Body Mass Index ; Child ; Fasting ; Homeostasis ; Humans ; Insulin ; Insulin Resistance ; Leptin ; Obesity ; Prognosis ; Resistin ; Weight Gain ; Weights and Measures

Adipocytokines (adiponectin, leptin and resistin) are known to play a major role in development of cardiovascular disease (CVD) and intervention program is effective in reducing CVD risk factors. However, intervention program to improve the CVD risk factors including adipocytokines has been less studied. This study investigated the effects of 12-weeks worksite intervention program on cardiovascular risk factors, adipocytokines and nutrients intakes in industrial workers. 157 industrial male workers (32 metabolic syndrome (MS) subjects, 125 healthy subjects using age-matched stratified random sampling) received 5 face-to-face counseling based on their health profiles. Anthropometry, biochemical parameters and nutrients intakes were measured. The diagnosis of MS was adapted from modified NCEP-ATP III criteria (2001) and Asia-Pacific definition criteria (2000) for waist circumference (WC). After the intervention program, WC, BMI, SBP, insulin, leptin and intakes of total energy and fiber were significantly decreased (p < 0.05), while adiponectin was significantly increased (p < 0.05) in MS subjects. The WC, BMI, SBP, total cholesterol, LDL and HDL-cholesterol, HbA1c, leptin and intakes of total energy, protein and fat were significantly decreased (p < 0.05) and adiponectin was significantly increased (p < 0.05) in normal subjects. Multiple linear regression revealed that adiponectin was positively correlated with HDL-cholesterol (p < 0.01). Leptin was positively correlated with WC (p < 0.01), and resistin was positively correlated with HbA1c (p < 0.05) and intakes of total energy (p < 0.05), and negatively correlated with HDL-cholesterol (p < 0.05). The results of the 12 weeks intervention showed a positive impact on adipocytokines and nutrients intakes of industrial workers to reduce cardiovascular risk factors. Further research is needed to verify a tailored long-term worksite intervention program including adipocytokines as a protective factor for the CVD.
Adipokines ; Adiponectin ; Anthropometry ; Cardiovascular Diseases ; Cholesterol, LDL ; Counseling ; Humans ; Insulin ; Leptin ; Linear Models ; Male ; Resistin ; Risk Factors ; Waist Circumference ; Workplace

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.
Adipokines* ; Adiponectin ; Adipose Tissue ; Cytokines ; Hand ; Leptin ; Liver ; Liver Diseases ; Nicotinamide Phosphoribosyltransferase ; Non-alcoholic Fatty Liver Disease* ; Obesity ; Resistin ; Thiazolidinediones

No abstract available.
Adipokines*

New insights in the complex metabolic pathways and its control mechanism for energy homeostasis have refined our understanding of the pathophysiology of obesity. It is now recognized that there are several additional regulatory mechanism such as peripheral signals including leptin, ghrelin, GLP-1 and PYY and cellular signals including uncoupling proteins and beta Adrenergic receptors, which contribute to the regulation of food intake and energy expenditure, respectively. In addition, the function of adipocyte as an endocrine organ in energy homeostasis has been recently emphasized. Recent findings suggest that elevated levels of adipokines, such as leptin, adiponectin, resistin and TNF-alpha, in addition to increased free fatty acid level could be related to the pathophysiology of insulin resistance in obesity. For effective treatments and prevention of obesity, further studies on the circuits of neural and endocrine interactions in the regulation of energy homeostasis are needed.
Adipocytes ; Adipokines ; Adiponectin ; Eating ; Energy Metabolism ; Ghrelin ; Glucagon-Like Peptide 1 ; Homeostasis* ; Insulin Resistance ; Leptin ; Metabolic Networks and Pathways ; Obesity* ; Receptors, Adrenergic, beta ; Resistin ; Tumor Necrosis Factor-alpha