Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To investigate the effect of leptin on fibroblast proliferation and collagen synthesis as to elucidate that fibroblasts play a role in leptin’s effect on wound healing. Methods Purified dermal fibroblasts were derived from sucking wistar rat skin and exposedto leptin at concentration of 0, 10, 50, 100, 200, and 400 ng/ml. The survived fibroblasts were assessed by the colorimetric thiazolyl blue (MTT) assay. Replication of fibroblast was quantified by the incorporation of 3H-thymidine. Collagen synthesis of fibroblast cell was measured by the incorporation of 3H-proline into collagenasesensitive protein. Results The absorption of fibroblast exposed to leptin at concentration of 200 and 400 ng/ml 0.082±0.013, 0.091±0.018 was higher than that of control group 0.063±0.010, P＜0.05. The incorporations of 3H-thymidine of fibroblast exposed to leptin at concentration of 200 and 400 ng/ml 379±101 cpm,326±33 cpm were significantly higher than those of control group 219±56 cpm, P＜0.05. The incorporations of 3H-proline of fibroblast exposed to leptin at concentration of 200 and 400 ng/ml 911±55 cpm, 1 072±259 cpm were significantly higher than that of control group 679±176 cpm, P＜0.05. Conclusion Leptin can promote rat cutaneous fibroblast proliferation and collagen synthesis in vitro. This suggests that cutaneous fibroblast plays a role in leptin’s promoting skin wound healing and it may be one of the main mechanisms by which leptin enhances skin wound healing.
Obesity is closely related to thyroid function. The concentration of thyroid stimulating hormone (TSH) in obese patients is higher than that in the general population, and TSH will decrease accordingly after weight loss. Leptin is a bridge linking obesity and thyroid hormones, which can affect the release of TSH. There are many kinds of weight-reducing drugs that target the thyroid gland. Among them, thyroid hormone receptor-specific agonists may be potential drugs for future obesity treatment, but further studies are still needed.
ObjectiveTo investigate the effects of leptin on the oxidative damage in human retinal pigment epithelial (RPE) cells. MethodsHuman RPE cells (ARPE-19) were cultured in vitro, and randomly divided into control group and insulin resistance group. RPE cells were treated with 0, 10, 100 ng/mL leptin for 24, 48, 72 hours respectively. Then the levels of reactive oxygen species (ROS) expression in RPE cells were detected by 2', 7'-dichlorofluorescin-diacetate (DCFH-DA), and the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) expression in RPE cells were observed by immunocytochemistry (ICC), and the levels of human 8-oxoguanine DNA glycosylase l (hOGG1) expression in lysate were measured by Western blot. ResultsAfter 24, 48, 72 hours, the level of ROS (Control group:F=37.136, 37.178, 49.634; P < 0.05. Insulin resistance group:F=9.822, 28.881, 71.150;P < 0.05), 8-OHdG (Control group:F=88.643, 390.920, 1039.276;P < 0.05.Insulin resistance group:F=273.311, 299.155, 82.237;P < 0.05) and hOGGl (Control group:F=470.062, 1073.113, 295.456;P < 0.05. Insulin resistance group:F=240.032, 592.389, 527.760;P < 0.05) expression increased significantly with the increase of leptin concentration in control group and insulin resistance group. Under the same leptin concentration, the level of 8-OHdG has a trend that it was higher in the insulin resistance group than the control group. After 24 hours, the difference of hOGGl expression between control group and insulin resistance group was not significant (F=23.392, P > 0.05). After 72 hours, the level of hOGGl expression was significantly higher in the insulin resistance group than the control group (F=129.394, P < 0.05). The level of hOGGl expression was significantly higher at 48 hours than that at 24 hours and 72 hours (P < 0.05). ConclusionLeptin could induce the oxidative damage of RPE cells in normal and insulin resistance status. With the increase of leptin concentration and time extended, the degree of oxidative damage and its repair were both increased. The degree of oxidative repair increased with the increase of leptin concentration, but decreased with time extended.
Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.
ObjectiveTo explore the levels of serum leptin,TNF-α,IL-8 and hypersensitivity C-reactive protein (hs-CRP) in stable COPD patients with different body mass index (BMI). Methods30 healthy controls with BMI 18.5 to 23.9 kg/m2 and 105 patients with stable COPD were recruited in the study. The serum levels of leptin,TNF-α,and IL-8 were determined by radioimmunoassay and hs-CRP level was determined by versatile biochemical automatic analyzer. The COPD patients were divided into a low BMI group (BMI<18.5 kg/m2,n=32),a normal BMI group (BMI 18.5-23.9 kg/m2,n=48),and a high BMI group (BMI≥23.9 kg/m2,n=25). ResultsSerum leptin level in the COPD patients was significantly reduced compared with the control subjects (P<0.05). Serum leptin levels were reduced in the low BMI and the high BMI groups compare with the normal BMI group [(7.89±3.16)ng/L and (10.52±5.98)ng/L vs. (13.04±5.73) ng/L,P<0.01 or P<0.05]. Leptin level in the low BMI group was lower than that in the high BMI group (P<0.05). Serum TNF-α levels were significantly increased in the low BMI group compared with the normal BMI and high BMI groups [(229.39±89.57)μg/L vs. (180.06±74.24) μg/L and (189.46±82.41) μg/L,P<0.01]. Serum TNF-α level in the COPD patients was significantly increased compared with the control subjects [(192.37±83.65) μg/L vs. (178.59±60.38) μg/L,P<0.05]. The IL-8 levels were not significant different among three BMI groups with COPD. The hs-CRP level in the high BMI group was higher than that in the low BMI and normal BMI groups (P<0.05). ConclusionLeptin and TNF-α may be involved in weight-loss of COPD malnutritional patients.
Objective To investigate the relatingship between leptin receptor gene Gln223Arg polymorphism and obstructive sleep apnea hyponea syndrome (OSAHS) in Han population in Southwest China. Methods Two hundred and fifteen cases of subjects (including 116 cases in OSAHS group and 99 cases in control group) were selected in Han population in Southwest China. Polymerase chain reaction (PCR) was used to analyse Gln223Arg leptin receptor gene polymorphism. The levels of serum LEP and TI were determined by double antibody sandwich enzyme-linked immunosorbent assay (ELISA). Simultaneous determination of body mass index (BMI) and neck circumference (NC) and waist circumference (WC) were conducted. Results In the OSAHS group, the leptin receptor gene polymorphism Gln223Arg GG, AA and GA genotype frequency was 0.854, 0.017 and 0.129, respectively. G allele and A allele frequency frequency was 0.918 and 0.082, respectively. In the control group, leptin receptor gene polymorphisms Gln223Arg GG, AA and GA genotype frequency was 0.840, 0.020 and 0.14,respectively. G allele and A allele frequency was 0.90 and 0.10, respectively. Genotype frequencies of the two groups were not statistically significant (χ2=0.784, P>0.05). There were differences in BMI, WC and NC between the OSAHS patients with GG and the OSAHS patients with (GA+AA) genotype (P<0.05), but no difference was found in LEP and TI levels (allP>0.05). In control, mild, moderate and severe OSAHS group, the levels of serum LEP and TI were increased gradually, and the difference was statistically significant (allP<0.05). Conclusions Gln223Arg leptin receptor genotype polymorphisms may be involved in obesity, but they have no relationship with the incidence of OSAHS in Han population in Southwest China. In OSAHS patients, Gln223Arg polymorphism has no relationship with LEP or TI. Patients with OSAHS have hyperleptinemia and hyperinsulinemia.
ObjectiveTo systematically evaluate the relationship between the-2548G/A polymorphism in the leptin gene and antipsychotic-induced weight gain (AIWG). MethodsLiterature for the relationship between the-2548G/A polymorphism in the leptin gene and AIWG was retrieved in electronic databases including PubMed, EMbase, CNKI and WanFang Data from establishment dates to June, 2013. Two reviewers independently screened studies according to the inclusion and exclusion criteria, extracted data and evaluated the methodological quality of the included studies. Then meta-analysis was performed using RevMan 5.2 software. ResultsA total of 7 case-control studies were included, involving 404 AIWG cases and 508 controls (patients with no significant changes of weight after taking antipsychotic drugs). The results of meta-analysis showed that, regarding the total population, the-2548G/A polymorphism of the leptin gene was not associated with AIWG (OR=1.16, 95%CI 0.70 to 1.93, P=0.57). After stratification analysis, according to Chinese or non-Chinese origin, the results showed that significant association was found between the-2548G/A polymorphism of leptin gene and AIWG for Chinese (OR=2.15, 95%CI 1.41 to 3.26, P=0.000 4) but not for non-Chinese (OR=0.69, 95%CI 0.45 to 1.07, P=0.10). ConclusionThe current evidence suggests that the-2548G/A polymorphism in the leptin gene is associated with increased risk of AIWG for Chinese. Due to limited quantity of the included studies, the aforementioned conclusion needs to be further validate by more high-quality and large-scale studies.
ObjectiveTo investigate the levels of nutritional status, serum leptin, TNF-α, IL-8 and C-reactive protein(CRP) in patients with two clinical phenotypes of COPD. MethodsNutritional parameters, including body mass index, percent ideal body weight, triceps skin-fold thickness, mid-upper arm circumference, albumin, lymphocytes count, serum leptin, TNF-α, IL-8 and CRP levels were determined in 40 healthy controls and 120 patients with COPD. The COPD patients were divided into a typical emphysema type(A group) and a bronchitis type(B group), both groups included COPD patients in acute exacerbation phase and in stable phase. ResultsThe nutritional parameters in B group were higher than those in A group(P < 0.05). Serum leptin level was lower in stable A group and stable B group than that in the control group[(7.76±2.93) ng/L and (10.04±5.11) ng/L vs. (14.93±8.47) ng/L, P < 0.05], higher in A group[(12.99±5.56) ng/L)] and B group in acute exacerbation phase[(13.52±5.82) ng/L] than that in stable phase(P < 0.05), and lower in stable A group than that in stable B group (P < 0.05). Serum TNF-αlevel was higher in A group with acute exacerbation than that in B group with acute exacerbation and the control group[(234.65±95.74)μg/L and(195.03±88.00)μg/L vs. (182.07±42.35)μg/L, P < 0.05], and higher in stable A group than that in stable B group[(225.31±84.14)μg/L vs. (188.17±72.62)μg/L, P < 0.05]. Serum IL-8 level in A and B groups in acute exacerbation phase and stable phase was higher than that in the control group(P < 0.05), and was not significantly different between A group and B group in acute exacerbation or stable phase(P > 0.05). The CRP level was higher in A group and B group with acute exacerbation than that in the control group[(46.87±35.89) mg/L and(70.11±65.50) mg/L vs. (5.05±4.49) mg/L, P < 0.01], and higher in B group with acute exacerbation than that in A group with acute exacerbation (P < 0.05). ConclusionsThere are differences in nutritional status, serum leptin, TNF-αand CRP levels between the emphysema type and bronchitis type of COPD, while the IL-8 level is not different between two phenotypes. Leptin and TNF-αmay be involved in weight-loss of malnutritional COPD patients.
Objective To evaluate the relationship between leptin level in serum and clinicopathologic features of colorectal cancer. Methods ABC-ELLSA was used to detect the leptin level in 30 cases of colorectal cancer without dystrophy (cancer group) and 24 normal controls (control group). The expressions of K-ras， p53， adenomatous polyposis coli （APC） gene and delete in colorectal carcinoma gene (DCC) mRNA of the tumor were examined by RT-PCR, the levels of serum CEA and CA19-9, and other clinicopathologic features were also recorded. Results The leptin level in cancer group 〔（3.53±1.72） μg/L〕 was higher than that in control group 〔（2.27±1.01） μg/L〕, P＜0.05, and the difference was independent on gender. There were no significant differences of leptin level in different tumor stages and different tumor location （Pgt;0.05）. Leptin level of poorly differentiated tumor was obviously lower than that of well differentiated and moderately differentiated tumor （P＜0.05）. There were no associations between leptin level and the levels of CEA and CA19-9, likewise there were no associations between leptin level and the expressions of K-ras, p53, APC and DCC in tumor （Pgt;0.05）. Conclusion The leptin level of colorectal cancer patient is higher than that of normal person, which is affected by the differentiation of tumor. But there are no significant correlations between the level of leptin in serum and TNM stage, tumor location, tumor markers of serum, K-ras, p53, APC or DCC in tumor.