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 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.
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.
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 explore the relationship between the -2548 G/A functional polymorphism in the 5′ promoter region of the leptin gene and gallstones. Methods The -2548 G/A polymorphisms of leptin gene were determined by polymerase chain reactionrestriction fragment length polymorphism technology (PCRRFLP) in 118 patients with cholesterol gallstones and 53 normal control subjects. Then the allele and genotype distribution were studied. Results The distribution of leptin2458 G/A in two groups was statistically significantly different: the genotype frequency of AA+GA of patients in gallstone group was higher than that in control group (χ2=4.251, P=0.039). AA+AG genotype had 2.813 times greater risk for gallstone disease compared with GG genotype (OR=2.813, 95% CI=1.020-7.757). Allele frequency distribution in the two groups was different: the allele frequency of A of patients in gallstone group was higher than that in control group (χ2=5.791, P=0.016). The risk of gallstone disease in the A alleles carriers was 1.777 times as higher as the carriers of G alleles (OR=1.777, 95% CI=1.110-2.844). ConclusionThe -2548 G/A polymorphism in the 5′ promoter region of leptin gene is significantly correlated with the gallstones. The A alleles of leptin may be a genetic factor which contributes to individual susceptibility for gallstone, while the G alleles of leptin may be a genetic factor that prevents people from gallstone.
ObjectiveTo investigate the role of leptin receptor gene Gln223Arg polymorphism in pathogenesis of asthma. MethodsOne hundred and eighty-five asthmatic outpatients and inpatients in the Qingdao Municipal Hospital between June 2009 and May 2012 were recruited in the study.Two hundred and seven healthy volunteers were recruited as control.Peripheral blood was sampled from all subjects for measuring serum leptin level by ELISA,and analyzing leptin receptor gene Gln223Arg genotypes by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) in white blood cells. ResultsThere was significant difference in frequency distribution of leptin receptor gene Gln223Arg genotype between the asthma group and the health group (χ2=6.173,P=0.013,OR=1.697,95%CI 1.115-2.585).The GG genotype was associated with a 1.895-fold increased risk for asthma than the GA+AA genotype (χ2=7.283,P=0.007,OR=1.895,95%CI 1.187-3.024).The serum leptin level of the GG genotype group was significantly higher than that in the GA+AA genotype group[(2.56±1.47) ng/mL vs.(2.16±1.66) ng/mL]. ConclusionLeptin receptor gene Gln223Arg polymorphism is correlated with asthma, and the G allele might be the genetic factor that contributes to individual susceptibility for asthma by causing high serum leptin level.
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 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 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 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.