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 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.
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 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.
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 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.
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 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.