ABSTRACT
PURPOSE: The incidence of non-alcoholic fatty liver disease (NAFLD) in children is gradually increasing. The aim of this study was to investigate the use of serum adiponectin and soluble adiponectin receptor 2 (soluble Adipo R2) levels for the diagnosis of fatty liver disease in obese and overweight children. METHODS: The study included 51 obese and overweight children between the ages of 6 and 18 years diagnosed with NAFLD using ultrasonography and 20 children without fatty liver disease. Patients whose alanine transaminase level was two times higher than normal (≥80 U/L) were included in the non-alcoholic steatohepatitis (NASH) group. RESULTS: NASH was observed in 11 (21.6%) of the patients with NAFLD. The incidence of obesity was higher in patients with NASH (80% and 45%, p=0.021). While the adiponectin levels were similar in patients with NAFLD and those without, they were below the normal level in the whole study group. Adiponectin and soluble Adipo R2 levels of patients with NASH were lower than those in patients without NASH; however, this difference was not statistically significant (p=0.064 and p=0.463). Soluble Adipo R2 levels in obese patients with NAFLD were higher than those in obese children without NAFLD (p<0.001). CONCLUSION: Soluble adiponectin receptor 2 level is a noninvasive marker that can be used for the diagnosis of NAFLD in obese children.
Subject(s)
Child , Humans , Adiponectin , Alanine Transaminase , Diagnosis , Fatty Liver , Incidence , Non-alcoholic Fatty Liver Disease , Obesity , Overweight , Receptors, Adiponectin , UltrasonographyABSTRACT
Prostate cancer is a hormone-associated malignancy and is closely related to obesity in terms of epidemiology and molecular mechanisms.Adiponectin, an adipocytokine produced by adipokine and secreted by adipocyte, exhibits anti-inflammatory, insulin-sensitizing, anti-proliferation, and proapoptosis actions on various organs in an endocrine form. Obesity leads to a decrease in adiponectin level, which is closely associated with the occurrence of many tumors. Studies have showed that prostate cancer patients had lower serum adiponectin levels and decreased expression of adiponectin receptors in tumor tissues, which suggest that functional defects of adiponectin and its receptors may be relevant to the occurrence and development of prostate cancer.This paper reviews adiponectin and its receptors' functions, signaling pathways, and roles in diagnosis, treatment, and prognosis of prostate cancer.
ABSTRACT
Prostate cancer is a hormone-associated malignancy and is closely related to obesity in terms of epidemiology and molecular mechanisms.Adiponectin, an adipocytokine produced by adipokine and secreted by adipocyte, exhibits anti-inflammatory, insulin-sensitizing, anti-proliferation, and proapoptosis actions on various organs in an endocrine form. Obesity leads to a decrease in adiponectin level, which is closely associated with the occurrence of many tumors. Studies have showed that prostate cancer patients had lower serum adiponectin levels and decreased expression of adiponectin receptors in tumor tissues, which suggest that functional defects of adiponectin and its receptors may be relevant to the occurrence and development of prostate cancer.This paper reviews adiponectin and its receptors' functions, signaling pathways, and roles in diagnosis, treatment, and prognosis of prostate cancer.
ABSTRACT
Obesity is a risk factor for colorectal cancer, but the underlying mechanism remains unclear. Adiponectin as an adipocyte-derived protein might play an important role between obesity and colorectal cancer. Here we review the current progress on molecular characteristics of adiponectin, the association of adiponectin with colorectal cancer, and the possible antitumor mechanism.
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Association studies between ADIPOR1 genetic variants and predisposition to type 2 diabetes (DM2) have provided contradictory results. We determined if two single nucleotide polymorphisms (SNP c.-8503G>A and SNP c.10225C>G) in regulatory regions of ADIPOR1 in 567 Brazilian individuals of European (EA; N = 443) or African (AfA; N = 124) ancestry from rural (quilombo remnants; N = 439) and urban (N = 567) areas. We detected a significant effect of ethnicity on the distribution of the allelic frequencies of both SNPs in these populations (EA: -8503A = 0.27; AfA: -8503A = 0.16; P = 0.001 and EA: 10225G = 0.35; AfA: 10225G = 0.51; P < 0.001). Neither of the polymorphisms were associated with DM2 in the case-control study in EA (SNP c.-8503G>A: DM2 group -8503A = 0.26; control group -8503A = 0.30; P = 0.14/SNP 10225C>G: DM2 group 10225G = 0.37; control group 10225G = 0.32; P = 0.40) and AfA populations (SNP c.-8503G>A: DM2 group -8503A = 0.16; control group -8503A = 0.15; P = 0.34/SNP 10225C>G: DM2 group 10225G = 0.51; control group 10225G = 0.52; P = 0.50). Similarly, none of the polymorphisms were associated with metabolic/anthropometric risk factors for DM2 in any of the three populations, except for HDL cholesterol, which was significantly higher in AfA heterozygotes (GC = 53.75 ± 17.26 mg/dL) than in homozygotes. We conclude that ADIPOR1 polymorphisms are unlikely to be major risk factors for DM2 or for metabolic/anthropometric measurements that represent risk factors for DM2 in populations of European and African ancestries.
Subject(s)
Female , Humans , Male , Middle Aged , Body Mass Index , /genetics , Polymorphism, Single Nucleotide/genetics , Receptors, Adiponectin/genetics , Black People/genetics , Brazil , Case-Control Studies , White People/genetics , Gene Frequency , Genotype , Genetic Predisposition to Disease/genetics , Risk FactorsABSTRACT
Objective To explore genes expression of adiponectin receptors during differentiation of SW872 preadipocytes. Met-(hods) SW872 preadipocytes were cultured in vitro and induced to differentiate by 0.6 mmol/L oleic acid. During the progress of diffe-(rentiation), the morphological changes of SW872 cells were observed and the differentiation rate was assayed by oil-red O staining. Adiponectin receptors mRNA was measured by reverse transcription-polymerase chain reaction during differentiation of SW872 preadipocytes. Results 1.After stimulated by 0.6 mmol/L oleic acid for 72 hours, almost all SW872 cells were differentiated,and there were lots of fat droplets in the cells.2.There were adiponectin receptors genes expressions in SW872 preadipocytes.After 72 hours,and the levels of adiponectin receptor(AdipoR) 1 mRNA and AdipoR 2 mRNA were markedly increased up to 2.54 and 4.09 times,respectively. Conclusion There are AdipoR1 and AdipoR2 genes expressions in fat cells and the expressions are differentiation-dependent.
ABSTRACT
Adiponectin is one of the adipocytokines that are derived from adipose tissue. It has anti-inflammatory, anti-diabetic, anti-atherogenic and insulin-sensitizing effects. Its receptors AdipoR1 and (AdipoR2) mediate the function of adiponectin. Recent researches show that AdipoR1 is abundantly expressed in skeletal muscles, whereas AdipoR2 is predominantly expressed in the liver. Both AdipoR1 and AdipoR2 are found to be expressed in human and rat pancreatic ? cells and the expression levels are similar to those in liver and higher than those in muscles; AdipoR1 and AdipoR2 can also be found in monocytes and macrophages. GH and agonists of PPAR-?, PPAR-? and LXR also affect the exprssion and regulation of adiponectin receptors.
ABSTRACT
Obesity is a risk factor for colorectal cancer,but the underlying mechanism remains unclear.Adiponectin as an adipocyte-derived protein might play an important role between obesity and colorectal cancer.Here we review the current progress on molecular characteristics of adiponectin,the association of adiponectin with colorectal cancer,and the possible anti-tumor mechanism.
ABSTRACT
The mRNA levels of adiponectin in adipose tissue and adiponectin receptor R1 in skeletal muscle of type 2 diabetic rats were examined by semi-quatitative RT-PCR.The expression of adiponectin receptor R1 was not altered in the skeletal muscle of type 2 diabetic rats as compared with normal rats.The serum adiponectin level was decreased in diabetic rats due to the decline of adiponectin mRNA level in adipose tissue and rosiglitazone improved the adiponectin deficiency.