Existing epidemiologic and clinical studies have demonstrated that obesity is associated with the risk of a variety of cancers. In recent years, an increasing number of experimental and clinical studies have unraveled the complex relationship between obesity and cancer risk and the underlying mechanisms. Obesity-induced abnormalities in immunity and biochemical metabolism, including chronic inflammation, hormonal disorders, dysregulation of adipokines, and microbial dysbiosis, may be important contributors to cancer development and progression. These contributors play different roles in cancer development and progression at different sites. Lifestyle changes, weight loss medications, and bariatric surgery are key approaches for weight-centered, obesity-related cancer prevention. Treatment of obesity-related inflammation and hormonal or metabolic dysregulation with medications has also shown promise in preventing obesity-related cancers. In this review, we summarize the mechanisms through which obesity affects the risk of cancer at different sites and explore intervention strategies for the prevention of obesity-associated cancers, concluding with unresolved questions and future directions regarding the link between obesity and cancer. The aim is to provide valuable theoretical foundations and insights for the in-depth exploration of the complex relationship between obesity and cancer risk and its clinical applications.
Humans ; Adipokines/metabolism* ; Bariatric Surgery ; Inflammation/therapy* ; Neoplasms/prevention & control* ; Obesity/therapy* ; Risk Factors

Objective To explore the clinical features and risk factors of poor prognosis in neonatal necrotizing enterocolitis(NEC).Methods A retrospective study was carried out in the infants with NEC admitted to 6 cooperative hospitals in Guangdong Province between January 2005 and December 2014.The clinical features and risk factors of poor prognosis in preterm and full-term infants diagnosed NEC,early onset and late onset NEC were analyzed.Results A total of 449 cases who met the criteria were admitted during the study time.The mortality was 23.6％ (106/449 cases),of which the preterm group was 24.6％ (58/238 cases) while the full-term group was 22.7％ (48/211 cases),the early onset group was 22.1％ (45/204 cases) while the late onset group was 24.3％ (57/235 cases).The median number of NEC onset in preterm group was 11 d after birth while the number of the full-term group was 6 d.Full-term infants who diagnosed NEC were more likely to manifest themselves as abdominal distension (52.1％ vs.42.0％,x2 =4.597,P =0.032),vomiting(36.5％ vs.17.2％,x2 =21.428,P =0.000) and bloody stool(30.3％ vs.21.4％,x2 =4.653,P =0.031);but in the onset of NEC,preterm infants more likely to have feeding intolerance (21.0％ vs.12.8％,x2=5.309,P =0.021).The early onset group of full-term NEC was much common in twins or multiplets(9.4％ vs.1.1％,x2 =6.226,P =0.013),which rate of surgical therapy was much higher (41.0％ vs.27.0％,P =0.036) and the breast-feeding rate before NEC was lower than the late onset group(14.5％ vs.32.6％,x2 =9.500,P =0.002),the differences were statistically significant.The gestational age and birth weight were bigger in the early onset group of preterm NEC[(33.8 ±2.5) weeks vs.(32.2 ±2.8) weeks,t =4.261,P =0.000;(2.1 ±0.5) kg vs.(1.7 ± 0.5) kg,t =4.735,P =0.000)],but length of stay was shorter than the late onset group (18.0 d vs.26.5 d,P =0.000).Logistic regression analysis showed that the risk factors of poor prognosis of full-term NEC were shock,peritonitis and sepsis;while risk factors of poor prognosis of preterm NEC were small for gestational age infant,pulmonary hemorrhage,shock,intestinal perforation and sepsis;the risk factors of poor prognosis of the early onset group of full-term NEC was shock;while those of the late onset group were shock and peritonitis;the risk factors of poor prognosis in the early onset group of preterm NEC were shock and sepsis,while those in the late onset group were pulmonary hemorrhage,shock,intestinal perforation and sepsis.Conclusions Compared to the preterm NEC,the onset time of full-term NEC was earlier and the clinical manifestations were more typical.Early identification and management of shock,peritonitis,intestinal perforation,sepsis and pulmonary hemorrhage can reduce the risk of poor prognosis of neonate NEC.

Objective To study the composition of gut microbiome in neonates with severe bilinebinemia (serum total bilirubin ＞ 342 μmol/L),and to explore the relationship between gut microbiome and bilirubin brain injury.Methods A prospective study was conducted.The neonates with serum total bilirubin ＞ 342 μmol/L from September 2016 to March 2017 in Guangzhou Women and Children's Medical Center,Guangzhou Medical University,were enrolled in the study and 16S rDNA sequence analysis technology was used to detect the composition of gut microbiome in all subjects.According to the results of brain magnetic resonance imaging (MRI),brain stem auditory evoked potential (BAEP) and clinical manifestations,the subjects were divided into the brain injury group (26 cases) and no brain injury group (28 cases).The differences of the composition of gut microbiome between the 2 groups were compared,and the levels of unconjugated bilirubin in serum and cerebrospinal fluid were also compared.Results The level of unconjugated bilirubin in serum of the brain injury group was (463.51 ± 110.62) μmol/L,but in no brain injury group was(364.18 ±63.13) μmol/L,and there was significant difference between the 2 groups(t =4.090,P =0.000 1).The level of unconjugated bilirubin in the cerebrospinal fluid of the brain injury group was (9.53 ± 2.68) μmol/L,but in no brain injury group was (6.94 ± 2.31) μmol/L,and there was significant difference between the 2 groups (t =3.812,P =0.000 3).There was no correlation between the level of unconjugated bilirubin in the cerebrospinal fluid and serum between the 2 groups(r =0.137,0.081,all P ＞0.05).The abundance of gut microbiome in the brain injury group was lower than that in no brain injury group in genus level,among which Fusobacterium,Catabacter,Succinivibrio,Clostridium and Bacteroides were significantly different (all P ＜ 0.05).Conclusions The occurrence of bilirubin brain injury depends on the level of unconjugated bilirubin in serum cerebrospinal fluid,but it may be more directly dependent on the level of bilirubin in the cerebrospinal fluid.The diversity of gut microbiome in neonates with bilirubin brain injury was significantly lower than that in no brain injury group.The level of unconjugated bilirubin in cerebrospinal fluid may be related to the different blood-brain barrier permeability caused by different composition of gut microbiome.

Objective To elucidate the association of fibroblast growth factor 23 (FGF23)with coronary artery calcification in patients with moderate and advanced stage chronic kidney diseases (CKD). Methods Serum intact FGF23 levels in 150 patients with CKD stage 3 to 5 and 25 age- and sex-matched healthy controls were measured by ELISA.The association between FGF23 and coronary artery calcification was studied. Results Serum FGF23 levels in CKD patients were significantly higher than those in healthy controls [196.46 (83.09,355.02) ng/L vs 27.17 (21.63,51.20) ng/L,P＜0.01].The levels of FGF23 were significantly higher in dialyzed patients than those in non-dialyzed patients (P＜0.01),and hemodialysis patients had higher levels as compared to peritoneal dialysis ones [6048.29 (1129.08,34807.45) ng/L vs 1625.80 (602.83,7521.78) ng/L,P＜0.01].The incidence of coronary artery calcification was relatively high in patients with moderate and advanced stage CKD (74/130,56.9％ ).Serum FGF23 level was positively correlated with coronary artery calcification score (CaS) (r=0.177,P＜0.05).Logistic regression analysis showed that age (β=0.091,OR=1.095,P＜0.01),duration of dialysis (β=2.013,OR=7.483,P＜0.05) and FGF23 level (β=0.838,OR=2.311,P＜0.05) were independent risk factors for coronary artery calcification in patients with moderate and advanced stage CKD.ROC curve of coronary artery calcification revealed that area under curve (AUC) of FGF23 was 0.705 (P＜0.01).With the cut-off value of FGF23 as 786.73 ng/L,the diagnostic sensitivity and specificity in coronary artery calcification were 62.5％ and 75.9％.ROC curve of coronary artery calcification showed that AUC of alkaline phosphatase (AKP) was 0.626 (P=0.017).With the cutoff value of AKP as 79.75 U/L,the diagnostic sensitivity and specificity in coronary artery calcification were 84.5％ and 41.5％.There was no diagnostic value of serum phosphorus in coronary artery calcification. Conclusions Serum FGF23 level is correlated with coronary artery.calcification in patients with moderate and advanced stage CKD.The sensitivity of FGF23 is lower and the specificity is higher than those of AKP for the diagnosis of coronary artery calcification.