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.
Objective To discuss the correlation between the letpin level and the pathogenesis of avascular necrosis of the femoral head (ANFH) by measuring the leptin expression of the femoral head in patients with ANFH. Methods Between July 2009 and February 2011, 16 patients with ANFH (including 10 cases of steroid-induced ANFH and 6 cases of alcohol-induced ANFH, ANFH group) and 11 patients with proximal femur fracture (control group) were included in the experiment. There was no significant difference in age, weight, and body mass index between 2 groups (P gt; 0.05). The peripheral blood and bone marrow were extracted to measure the blood lipid level and the free fat (FF) content, respectively. ELISA was used to detect the levels of the leptin, soluble leptin receptor (sLR), osteoprotegerin (OPG), and soluble receptor activator of nuclear factor κB (sRANKL); the leptin biological activity and the activity of osteoclasts were calculated. The femoral head specimens were harvested to count leptin-positive cells by immunohistochemical staining. Results No significant difference in the blood lipid level was found between 2 groups (P gt; 0.05), but the FF content in ANFH group was significantly lower than that in control group (t= — 14.230, P=0.000). The intramedullary leptin expression was found in both groups; however, the intramedullary leptin level in ANFH group decreased significantly when compared with the level in control group (t=4.425, P=0.002). There were significant differences in the levels of leptin, OPG, and sRANKL between 2 groups (P lt; 0.05). The leptin biological activity of ANFH group was significantly lower than that of control group (P lt; 0.05), but the activity of osteoclasts of ANFH group was significantly higher than that of control group (P lt; 0.05). There was a positive correlation between the leptin level and leptin biological activity (r=0.922 7, P=0.000 0), and a negative correlation between the leptin level and OPG content (r= — 0.396 2, P=0.040 8), FF content (r= — 0.806 1, P=0.000 0), while it had no correlation between the leptin level and sLR and sRANKL content (P gt; 0.05). Conclusion Intramedullary expression and bioactivity of the leptin decrease significantly in ANFH patients, which may play an important role in the pathogenesis of ANFH.
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.
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.
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.
ObjectivesTo systematically review the association between serum leptin level and hepatitis C virus.MethodPubMed, EMbase, Web of Science, CNKI, CBM, VIP and WanFang Data databases were electronically searched to collect case-control studies on the association between serum leptin level and hepatitis C virus from 2007 to July, 2017. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then, meta-analysis was performed by using RevMan 5.3 software.ResultsA total of 11 studies including 1 115 patients were included. The results of meta-analysis showed the serum leptin level was higher in hepatitis C patients than in healthy people (SMD=0.68, 95%CI 0.44 to 0.91, P<0.000 01). The results of subgroup analysis showed that, in hepatitis C patients whose serum leptin levels detected by RIA and European population, serum leptin levels were higher. Women had higher serum leptin levels than men in hepatitis C virus patients (P<0.000 01).ConclusionThe serum leptin level is associated with hepatitis C virus and the serum leptin levels of women are higher than those in men. Due to limited quantity and quality of the included studies, more high quality studies are required to verify above conclusions.
Objective To study the leptin-mediated intracellular signal pathways and their effects on wound healing.Methods The literature was reviewed extensively, concerning the physical and chemical characters of leptin, the mechanism of its receptor action, the receptor-related intracellular signal pathways and their roles on wound healing. Results Leptin was a protein hormone expressed by ob gene with relative molecular mass 16×103, it could activate the main singal pathways such as Janus kinase/signal transducer and activator of transcription, mitogenactivated protein kinases and phosphoinositide-3-kinase pathways through binding with its specific receptor, to participate in the modulation of multiple functions including energy metabolism, weight balance and wound healing. Leptin receptors were widely distributed in various tissues, which suggest the multiple functions of leptin. Local leptin expression was increased after skin injured, and it could stimulate keratinocytes proliferation, epithelialization, fibroblast proliferation and collagen synthesis, resulting in accelarated wound repair. Leptin expression was significantly increased after mucosal injury or bacteria infections, leading to accelarated mucosal repair through modulation of mucosal glandular secretion, improvment of mucosal blood flow, and synergistic action with endothelin-1.Conclusion Leptin can promote wound healing through activating its receptor-related intracellular signal pathways.
Objective To assess the correlation between central sleep apnea (CSA) and serum leptin (LEP) levels in patients with chronic heart failure. Methods The level of serum LEP and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured by forward-looking method in patients with chronic heart failure who underwent polysomnography during hospitalization from December 2015 to April 2017 in Department of Cardiology and Respiratory Medicine, Renmin Hospital of Wuhan University. And its correlation with CSA was analyzed. Patients were divided into three groups according to the left ventricular ejection fraction (LVEF), and then according to the presence or absence of CSA into CSA group and without SDB group. Results Of the 71 patients with heart failure, 31 had LVEF≥45%, 19 were between 35% and 45% and 21 were≤35% ; 32 of whom were CSA and 39 had no SDB. The lEP concentrations in the LVEF subgroup of CSA groups were significantly lower than those in the control group without SDB, with significantly higher levels of NT-proBNP. Logistic regression showed that CSA was associated with logarithmic LEP (lnLEP) (OR=0.047, 0.030, 0.021, P<0.05). In severe heart failure (LVEF≤35%) group, high NT-proBNP was the risk of CSA (OR=5.942, P=0.045) and the incidence of CSA was as high as 71.4%, which was significantly higher than other groups. However, after adjustment for confounding factors such as age, sex and body mass index (BMI), the correlation no longer existed (OR=6.432, P=0.105). Moreover, CSA with severe cardiac insufficiency had lower LEP than those without SDB. After adjustment for confounding factors such as age, sex and BMI, CSA and lnLEP remained significantly correlated (OR=0.013, P=0.002). Meanwhile, linear correlation analysis also showed that NT-proBNP was negatively correlated with lnLEP (R=–0.751, P<0.001). After adjusting for age, sex, and BMI, this relationship still existed (R=–0.607, P=0.004). Conclusion Decreased levels of leptin and elevated NT-proBNP in patients with chronic heart failure may indicate the presence of CSA.
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.