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 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.
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.
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.
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.
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.
Objective To investigate the effect and mechanism of leptin (LEP) on the osteoblastic differentiation of hBMSCs in vitro. Methods Whole bone marrow culture method was appl ied to culture hMBSCs and hBMSCs at passage 3 were divided into groups A, B, C, D, E and F, and when cell attachment was evident, 400, 200, 100 and 50 ng/mL LEP, 100 ng/mLBMP and common nutrient medium were added into each group, respectively. ALP staining and mineral ized nodules staining were conducted at 7 and 21 days after culture, respectively. And inverted phase contrast microscope observation was performed. ALP activity and osteocalcin (OCN) level of hBMSCs in each group was detected at 7, 14 and 21 days after culture to select the best induced concentration of LEP on osteoblastic differentiation. For groups of B, E and F at 7 days after culture, RT-PCR was adopted to detect the expression of such osteogenesis-related genes as core-binding factor α 1 (Cbfα1), ALP, Col I and OCN mRNA. Results At 7 days after induced culture, the ALP staining result showed that the endochylema in groups A, B, C, D and E were stained blue and the endochylema in the group F was sl ightly positive. At 21 days after induced culture, the mineralized nodules staining showed that cells in groups A, B, C, D and E were stained positively and cells in group F were negative. At 7, 14 and 21 days after culture, ALP and OCN activities in group B were less than that of group E (P lt; 0.05), but significant higher than that of groups A, C, D and F (P lt; 0.05), the optimal concentration of LEP was 200 ng/mL. At 7 days after culture, group F witnessed no expression of Cbfα1, ALP, Col I and OCN mRNA, while groups B and E witnessed expressions of all those indexes, but the expressions in group B were less than those of group E. Conclusion LEP can stimulate osteoblastic differentiation of hBMSCs in vitro, and the possible mechanism is its role of promoting the expression of osteoblastic related genes.
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.