No abstract available.
Eating* ; Glucose* ; Leptin* ; Metabolism* ; Resistin*

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

Adult ; Fatty Liver ; etiology ; metabolism ; pathology ; Humans ; Liver ; metabolism ; Middle Aged ; Resistin ; metabolism

Adiponectin ; Ghrelin ; physiology ; Growth Hormone-Releasing Hormone ; Humans ; Leptin ; Receptors, Ghrelin ; Resistin

Resistin is a new adipokine found in vivo in recent years. Recent studies have indicated that resistin contributes to the development of insulin resistance and type 2 diabetes mellitus (T2DM) and mediates inflammatory reaction via different signal pathways. As a signal factor between inflammation and metabolism, resistin is expected to provide new insights for the treatment of insulin resistance and T2DM. However, because specific receptor of resistin has not been identified in the body so far, the molecular mechanism of resistin actions is still unclear. In this article, we review the latest progresses of resistin study, especially the role of resistin in insulin resistance and its signaling mechanism.
Diabetes Mellitus, Type 2 ; Humans ; Inflammation ; Insulin Resistance ; Resistin ; Signal Transduction

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

OBJECTIVETo investigate the alteration of serum resistin levels in normal pregnancy and preeclampsia.

METHODSBlood samples were take from 28 normal non-pregnant women, 27 women in the 1st, 26 in the 2nd and 26 in the 3rd trimester of normal pregnancy and 25 women with preeclampsia. Serum resistin concentration was determined using ELISA method.

RESULTSerum levels of resistin were not significantly different among non-pregnancy, the 1st and the 2nd trimester of pregnancy (P>0.05 for all). Serum resistin level was significantly elevated in the 3rd trimester of pregnancy as compared with non-pregnancy (P<0.01), the 1st (P<0.001) and the 2nd trimester of pregnancy (P<0.001). Serum resistin level was significantly lower in preeclampsia than in the 3rd trimester of normal pregnancy (P<0.001), but was comparable to that of non-pregnancy, the 1st and the 2nd trimester of pregnancy (P>0.05 for all).

CONCLUSIONThe decrease of serum resistin level in the preeclampsia may provide insight into the pathogenesis of the disease.

Adult ; Female ; Glucose Tolerance Test ; Humans ; Pre-Eclampsia ; blood ; Pregnancy ; Pregnancy Trimester, Third ; blood ; Resistin ; blood

Although the effect of mouse resistin on insulin-resistance has been well defined, but the biological function of human resistin is still unknown. This study was aimed to explore the possible physiological and pathological effects of human resistin, as well as the tissue distribution of human resistin and correlation of resistin gene expression with leukemia incidence. 152 leukemia patients without inflammatory complication and 100 healthy persons were selected as experimental and control groups respectively. The blood samples were collected, the total RNA was extracted, the expression distribution of resistin in different tissues was detected by semi-quantitative RT-PCR and then the statistical analysis was carried out. The results indicated that the expression of the human resistin gene was detected in normal fetus liver, adult bone marrow and umbilical cord blood and peripheral blood cells, while the resistin gene could not be amplified in fat, umbilical cord, placenta and adult liver. The resistin expression was detected in 21% leukemia patients and 27% healthy persons. The difference of the resistin gene expression between the two groups was not statistically significant (p>0.05). It is concluded that the higher expression of resistin exists in normal human fetus liver, adult bone marrow, umbilical cord blood and peripheral blood cells, which indicates that the distribution of human resistin correlates with normal hematopoiesis in certain extent, but its expression level and rate may not correlate with the incidence of leukemia.
Case-Control Studies ; Gene Expression ; Humans ; Leukemia ; genetics ; RNA, Messenger ; Resistin ; genetics

Adult ; Aged ; Anthracosis ; blood ; Humans ; Leptin ; blood ; Male ; Middle Aged ; Resistin ; blood

OBJECTIVE: The present study aims to analyze the levels of resistin, tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, IL-18, and C-reactive protein (CRP) in patients with Alzheimer's disease (AD) and also investigate a potential relationship between resistin levels and TNF-α, IL-1β, IL-6, IL-18, and CRP levels in patients with AD. METHODS: The study included fifty patients with AD and 30 healthy controls with normal cognitive functions. The serum resistin, TNF-α, IL-1β, IL-6, IL-18, and CRP levels were assessed. We performed a Mini-Mental State Examination (MMSE) to evaluate the general cognitive performance. RESULTS: The mean serum resistin, IL-1β, IL-18, and TNF-α levels were significantly higher in patients with AD compared with the controls (p=0.026, p=0.002, p=0.003, and p=0.038, respectively). The IL-6 and CRP levels did not differ between the groups (p=0.874 and p=0.941). The resistin levels were positively correlated with the levels of CRP and IL-18 (r=0.526, p<0.001; r=0.402, p=0.004, respectively). MMSE scores and inflammatory markers were not correlated (p>0.05 for all). CONCLUSION: Serum resistin levels were significantly increased and correlated with some inflammatory markers in AD patients, suggesting that resistin might play a role in the inflammatory process of AD.
Alzheimer Disease* ; C-Reactive Protein ; Cognition ; Cytokines* ; Humans ; Inflammation ; Interleukin-18 ; Interleukin-6 ; Interleukins ; Resistin* ; Tumor Necrosis Factor-alpha