Association of IRS1 gene Pro512Ala polymorphism with nonalcoholic fatty liver disease.

Objective: This study was designed to investigate the possible effect of the insulin receptor substrate 1 (IRS1) gene rs1801276 polymorphism on the risk of nonalcoholic fatty liver disease (NAFLD). Subjects and methods: The rs1801276 polymorphism was investigated in 127 controls and 123 biopsy-proven NAFLD patients using PCR-RFLP. Results: No deviation from Hardy-Weinberg equilibrium was discovered for the rs1801276 variant of IRS1 in either NAFLD patients or controls (P>0.05). The distribution of different rs1801276 genotypes and alleles showed significant variations between controls and NAFLD patients. In comparison to rs1801276 'CC' genotype, the "GG+GC" genotype occurred less frequently in NAFLD patients than in controls, which also persisted after adjustment for confounding factors (P = 0.041, OR = 0.60, 95% CI = 0.45-0.93). In comparison with the IRS1 rs1801276 "C" allele, the "G" allele was significantly less prevalent in NAFLD patients than in controls (P = 0.045, OR = 0.69, 95% CI = 0.58-0.91). Conclusions: For the first time, we reported a significant association between the IRS1 rs1801276 polymorphism and biopsy-proven NAFLD. More studies are required to further elucidate the contribution of the IRS1 gene to NAFLD susceptibility.

The rs2275738 variant of the adiponectin receptor 1 gene is associated with biopsy-proven nonalcoholic fatty liver disease.

Aim: Nonalcoholic fatty liver disease (NAFLD) is a significant health issue worldwide. This study investigated the effect of the adiponectin receptor 1 gene (ADIPOR1) polymorphism on susceptibility to NAFLD.Methods: Data from 330 participants, including 165 biopsy-proven NAFLD patients and 165 healthy controls, were collected. The PCR-RFLP method was used to detect the genotypes of ADIPOR1 rs2275738 or T-106C variant.Results: The "CC" genotype of the ADIPOR1 rs2275738 polymorphism, compared with the "TT" genotype and the "C" allele, compared with the "T" allele, are markers of increased NAFLD susceptibility (p = 0.018; OR = 2.07, 95% CI = 1.43-2.01 and p = 0.041; OR = 1.52, 95% CI = 1.24-2.35, respectively).Conclusion: This research suggests, for the first time, that the ADIPOR1 rs2275738 "CC" genotype is associated with a 107% increased risk for biopsy-proven NAFLD.

[Box: see text].

NAMPT gene rs2058539 variant is a risk factor for nonalcoholic fatty liver disease.

OBJECTIVE: Nonalcoholic fatty liver disease is a chronic liver disease and a growing global epidemic. The aim of this study was to investigate the association between a visfatin gene (NAMPT) variant and nonalcoholic fatty liver disease, owing to the connection between this disease and insulin resistance, obesity, inflammation, and oxidative stress, and the role of visfatin in these metabolic disorders. METHODS: In the present case-control study, we enrolled 312 genetically unrelated individuals, including 154 patients with biopsy-proven nonalcoholic fatty liver disease and 158 controls. The rs2058539 polymorphism of NAMPT gene was genotyped using the PCR-RFLP method. RESULTS: Genotype and allele distributions of NAMPT gene rs2058539 polymorphism conformed to the Hardy-Weinberg equilibrium both in the case and control groups (p>0.05). The distribution of NAMPT rs2058539 genotypes and alleles differed significantly between the cases with nonalcoholic fatty liver disease and controls. The "CC" genotype of the NAMPT rs2058539 compared with "AA" genotype was associated with a 2.5-fold increased risk of nonalcoholic fatty liver disease after adjustment for confounding factors [p=0.034; odds ratio (OR)=2.52, 95% confidence interval (CI)=1.36-4.37]. Moreover, the NAMPT rs2058539 "C" allele was significantly overrepresented in the nonalcoholic fatty liver disease patients than controls (p=0.022; OR=1.77, 95%CI=1.14-2.31). CONCLUSION: Our findings indicated for the first time that the NAMPT rs2058539 "CC" genotype is a marker of increased nonalcoholic fatty liver disease susceptibility; however, it needs to be supported by further investigations in other populations.

The rs1862513 promoter variant of resistin gene influences susceptibility to nonalcoholic fatty liver disease.

OBJECTIVES: Nonalcoholic fatty liver disease is the term used for a range of conditions in which fat builds up in the liver and exceeds 5% of hepatocytes without inordinate alcohol intake or other causes of lipid accumulation. Regarding the fact that insulin resistance and obesity play key roles in the pathogenesis of nonalcoholic fatty liver disease, as well as the connection between resistin and these metabolic diseases, the association between nonalcoholic fatty liver disease and a resistin gene (RETN) polymorphism was examined. METHODS: In this genetic case-control association study, 150 biopsy-proven nonalcoholic fatty liver disease patients and 154 controls were enrolled and genotyped for the RETN rs1862513 (-420C>G) gene polymorphism using PCR-RFLP method. RESULTS: The -420C>G genotype frequency distributions in both groups were consistent with Hardy-Weinberg equilibrium (HWE; p>0.05). The carriers of the RETN -420C>G "CC" genotype compared with the "GG" genotype occurred less frequently in the cases with nonalcoholic fatty liver disease than in the controls, and the difference remained significant even after adjustment for confounding factors (p=0.030; OR=0.47, 95%CI=0.36-0.93). Interestingly, the RETN -420C>G "C" allele was also associated with a decreased risk for nonalcoholic fatty liver disease too (p=0.042; OR=0.72, 95%CI=0.53-0.95). CONCLUSION: We found for the first time an association between biopsy-proven nonalcoholic fatty liver disease and RETN -420C>G promoter polymorphism. The carriers of the RETN -420C>G "CC" genotype had a 53% decreased risk for nonalcoholic fatty liver disease. Our findings, however, need to be corroborated by further studies.

The Arg/Arg genotype of leptin receptor gene Gln223Arg polymorphism may be an independent risk factor for nonalcoholic fatty liver disease.

BACKGROUND: Given that obesity and insulin resistance play key roles in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and the connection between leptin and these metabolic diseases, the association between NAFLD and a leptin receptor gene (LEPR) polymorphism was examined. METHODS: In this genetic case-control association study, 144 biopsy-proven NAFLD patients and 144 controls were genotyped for the LEPR gene Gln223Arg (rs1137101) polymorphism using the polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: The distributions of genotypes and alleles of Gln223Arg variant were in accordance with the Hardy-Weinberg equilibrium in the study groups (P > .05). Multivariate logistic regression analysis showed that the LEPR Gln223Arg Arg/Arg genotype was an independent risk factor for NAFLD; the Arg/Arg genotype, compared with the Gln/Gln genotype, was associated with a 2.09-fold increased risk for NAFLD (P = .036, odds ratio = 2.09 [95% CI = 1.31-5.95]). CONCLUSIONS: We found that the LEPR Gln223Arg Arg/Arg genotype was independently associated with a more than 2-fold rise in biopsy-proven NAFLD risk. Our findings, however, need to be corroborated by further studies.

Insulin receptor substrate 2 gene Gly1057Asp polymorphism is a risk factor for nonalcoholic fatty liver disease.

OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD), which is an emerging global chronic liver disease, has a close association with insulin resistance. We aimed to determine whether the Gly1057Asp (rs1805097) polymorphism of the insulin receptor substrate 2 (IRS2) gene is associated with NAFLD. METHODS: Using the polymerase chain reaction-restriction fragment length polymorphism method, 135 patients with biopsy-proven NAFLD and 135 controls underwent IRS2 genotype analysis. RESULTS: Genotype and allele distributions of the IRS2 gene Gly1057Asp variant conformed to the Hardy-Weinberg equilibrium in both the case and control groups (P > .05). The Asp/Asp genotype of IRS2 gene Gly1057Asp polymorphism compared with Gly/Gly genotype was associated with a 2.1-fold increased risk for NAFLD after adjustment for confounding factors (P = .029; odds ratio = 2.10, 95% CI = 1.23-3.97). CONCLUSION: Our findings revealed for the first time that the Gly1057Asp Asp/Asp genotype of the IRS2 gene is a marker of increased NAFLD susceptibility; however, studies in other populations are required to confirm the results.

Insulin-like growth factor binding protein 3 promoter variant (rs2854744) is associated with nonalcoholic fatty liver disease

ABSTRACT Objective: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and a growing global epidemic. In NAFLD, liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Given the link between NAFLD and insulin resistance, the possible association between the rs2854744 (−202 G>T) promoter polymorphism of insulin-like growth factor binding protein 3 (IGFBP3) gene and NAFLD was investigated in this study. Materials and methods: In this genetic case-control association study, the IGFBP3 rs2854744 genotypes of 315 unrelated individuals, including 156 patients with biopsy-proven NAFLD and 159 controls, were determined using polymerase chain reaction/restriction fragment length polymorphism analyses. Results: The "GT+TT" genotype of the IGFBP3 rs2854744 polymorphism, compared with the "GG" genotype, was associated with a 2.7-fold increased risk of NAFLD after adjustment for confounding factors (P = 0.009; odds ratio [OR] = 2.71; 95% confidence interval [CI] = 1.19-3.18). Additionally, the IGFBP3 rs2854744 "T" allele, in comparison with the "G" allele, was significantly overrepresented in NAFLD patients than the controls (P = 0.008; OR = 1.85; 95%CI = 1.23-2.94). Conclusion: Our findings first indicated that the IGFBP3 rs2854744 "GT+TT" genotype is a marker of increased NAFLD susceptibility; however, it needs to be supported by further investigations in other populations.

The rs1862513 promoter variant of resistin gene influences susceptibility to nonalcoholic fatty liver disease

SUMMARY OBJECTIVES: Nonalcoholic fatty liver disease is the term used for a range of conditions in which fat builds up in the liver and exceeds 5% of hepatocytes without inordinate alcohol intake or other causes of lipid accumulation. Regarding the fact that insulin resistance and obesity play key roles in the pathogenesis of nonalcoholic fatty liver disease, as well as the connection between resistin and these metabolic diseases, the association between nonalcoholic fatty liver disease and a resistin gene (RETN) polymorphism was examined. METHODS: In this genetic case-control association study, 150 biopsy-proven nonalcoholic fatty liver disease patients and 154 controls were enrolled and genotyped for the RETN rs1862513 (-420C>G) gene polymorphism using PCR-RFLP method. RESULTS: The −420C>G genotype frequency distributions in both groups were consistent with Hardy-Weinberg equilibrium (HWE; p>0.05). The carriers of the RETN −420C>G "CC" genotype compared with the "GG" genotype occurred less frequently in the cases with nonalcoholic fatty liver disease than in the controls, and the difference remained significant even after adjustment for confounding factors (p=0.030; OR=0.47, 95%CI=0.36-0.93). Interestingly, the RETN −420C>G "C" allele was also associated with a decreased risk for nonalcoholic fatty liver disease too (p=0.042; OR=0.72, 95%CI=0.53-0.95). CONCLUSION: We found for the first time an association between biopsy-proven nonalcoholic fatty liver disease and RETN −420C>G promoter polymorphism. The carriers of the RETN −420C>G "CC" genotype had a 53% decreased risk for nonalcoholic fatty liver disease. Our findings, however, need to be corroborated by further studies.

NAMPT gene rs2058539 variant is a risk factor for nonalcoholic fatty liver disease

SUMMARY OBJECTIVE: Nonalcoholic fatty liver disease is a chronic liver disease and a growing global epidemic. The aim of this study was to investigate the association between a visfatin gene (NAMPT) variant and nonalcoholic fatty liver disease, owing to the connection between this disease and insulin resistance, obesity, inflammation, and oxidative stress, and the role of visfatin in these metabolic disorders. METHODS: In the present case-control study, we enrolled 312 genetically unrelated individuals, including 154 patients with biopsy-proven nonalcoholic fatty liver disease and 158 controls. The rs2058539 polymorphism of NAMPT gene was genotyped using the PCR-RFLP method. RESULTS: Genotype and allele distributions of NAMPT gene rs2058539 polymorphism conformed to the Hardy-Weinberg equilibrium both in the case and control groups (p>0.05). The distribution of NAMPT rs2058539 genotypes and alleles differed significantly between the cases with nonalcoholic fatty liver disease and controls. The "CC" genotype of the NAMPT rs2058539 compared with "AA" genotype was associated with a 2.5-fold increased risk of nonalcoholic fatty liver disease after adjustment for confounding factors [p=0.034; odds ratio (OR)=2.52, 95% confidence interval (CI)=1.36-4.37]. Moreover, the NAMPT rs2058539 "C" allele was significantly overrepresented in the nonalcoholic fatty liver disease patients than controls (p=0.022; OR=1.77, 95%CI=1.14-2.31). CONCLUSION: Our findings indicated for the first time that the NAMPT rs2058539 "CC" genotype is a marker of increased nonalcoholic fatty liver disease susceptibility; however, it needs to be supported by further investigations in other populations.

Insulin-like growth factor binding protein 3 promoter variant (rs2854744) is associated with nonalcoholic fatty liver disease.

Objective: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and a growing global epidemic. In NAFLD, liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Given the link between NAFLD and insulin resistance, the possible association between the rs2854744 (-202 G>T) promoter polymorphism of insulin-like growth factor binding protein 3 (IGFBP3) gene and NAFLD was investigated in this study. Materials and methods: In this genetic case-control association study, the IGFBP3 rs2854744 genotypes of 315 unrelated individuals, including 156 patients with biopsy-proven NAFLD and 159 controls, were determined using polymerase chain reaction/restriction fragment length polymorphism analyses. Results: The "GT+TT" genotype of the IGFBP3 rs2854744 polymorphism, compared with the "GG" genotype, was associated with a 2.7-fold increased risk of NAFLD after adjustment for confounding factors (P = 0.009; odds ratio [OR] = 2.71; 95% confidence interval [CI] = 1.19-3.18). Additionally, the IGFBP3 rs2854744 "T" allele, in comparison with the "G" allele, was significantly overrepresented in NAFLD patients than the controls (P = 0.008; OR = 1.85; 95%CI = 1.23-2.94). Conclusion: Our findings first indicated that the IGFBP3 rs2854744 "GT+TT" genotype is a marker of increased NAFLD susceptibility; however, it needs to be supported by further investigations in other populations.

The effectiveness of walking exercise on the bowel preparation before colonoscopy: a single blind randomized clinical trial study.

BACKGROUND AND AIM: Bowel preparation is a crucial factor affecting the diagnostic accuracy of colonoscopy, and few randomized control trials evaluated enhancement in bowel preparation. In this study, we aimed to evaluate the effectiveness of walking exercises on bowel preparation before a colonoscopy procedure. METHODS: The present study is a single-blind randomized controlled trial involving 262 patients scheduled for colonoscopy procedures. These patients were randomly assigned to two groups: an intervention group (n = 131) and a control group (n = 131). In the intervention group, participants followed a predetermined plan that included the consumption of specific liquids and foods, bisacodyl pills, polyethylene glycol powder, and a regimen of walking exercises in preparation for their colonoscopy. Conversely, individuals in the control group followed the same regimen but were not instructed to engage in walking exercises. On the day of the colonoscopy, both groups were assessed for their level of physical activity using a foot counter. Additionally, an experienced gastroenterologist evaluated and compared the bowel preparation between the two groups using the Boston Bowel Preparation Scale (BBPS). RESULTS: The number of footsteps recorded in the two groups exhibited a significant difference (P < 0.001). Although there was no statistically significant difference between the intervention and control groups in terms of mean BBPS scores (6.26 ± 1.9 vs. 6.29 ± 1.9, P = 0.416), individuals who took more than 6900 steps had significantly higher BBPS scores compared to those with fewer than 6900 footsteps (6.62 ± 1.8 vs. 5.92 ± 1.9, P = 0.003).In the univariate analysis, BBPS was found to be significantly associated with individuals under the age of 50 (OR: 2.45, 95% CI: 1.30-4.61, P = 0.006) and smoking status (OR: 0.41, 95% CI: 0.17-0.94, P = 0.043). In the multivariate analysis, the relationship between BBPS and age below 50 and smoking remained significant (OR: 2.50, 95% CI: 1.30-4.70, P = 0.005, and OR: 0.38, 95% CI: 0.16-0.93, P = 0.034, respectively). CONCLUSION: A higher number of footsteps taken especially more than 6900 can significantly enhance bowel preparation; however, walking exercise as an intervention before colonoscopy is not significantly associated with BBPS. Also, older people and smokers seem to have fewer benefits from walking exercises for bowel preparation. TRIAL REGISTRATION: ISRCTN32724024 (Registration date:22/08/2018).

A visfatin gene promoter polymorphism (rs1319501) is associated with susceptibility to nonalcoholic fatty liver disease.

Background: Considering the role of visfatin in nonalcoholic fatty liver disease (NAFLD), a growing global epidemic, this article explores the potential association between the visfatin gene (NAMPT) and NAFLD. Methods: We used the PCR-restriction fragment length polymorphism method to genotype the rs1319501 promoter variant of the NAMPT gene in 154 patients with biopsy-proven NAFLD and 158 controls in this case-control genetic association study. Results: The 'CC+TC' genotype of NAMPT rs1319501 in comparison to the 'TT' genotype occurred less frequently in the cases with NAFLD than the controls, and the difference remained significant after adjustment for confounding factors (p = 0.029; odds ratio = 0.55; 95% CI = 0.31-0.82). Conclusion: This study showed, for the first time, that the carriers of the NAMPT rs1319501 'CC+TC' genotype had a 45% decreased risk for NAFLD.

The common variant of rs6214 in insulin like growth factor 1 (IGF1) gene: a potential protective factor for non-alcoholic fatty liver disease.

PURPOSE: Regarding the central role of insulin resistance in NAFLD, we explored whether insulin-like growth factor 1 (IGF1) and insulin-like growth factor-binding protein 3 (IGFBP3) gene variants were associated with NAFLD susceptibility. METHODS: IGF1 (rs6214) and IGFBP3 (rs3110697) gene variants were genotyped in 154 cases with biopsy-proven NAFLD and 156 controls using PCR-RFLP method. RESULTS: The IGF1 rs6214 "AA + AG" genotype compared with the "GG" genotype appeared to be a marker of decreased NAFLD susceptibility (p = .006; OR = 0.47, 95%CI = 0.28-0.80). Furthermore, the IGF1 rs6214 "A" allele was underrepresented in the cases than controls (p = .024; OR = 0.61, 95%CI = 0.40-0.94). However, we observed no significant difference in genotype or allele frequencies between the cases and controls for IGFBP3 gene. CONCLUSIONS: To our knowledge, these findings suggest, for the first time, that the IGF1 rs6214 "A" allele and "AA + AG" genotype have protective effects for NAFLD susceptibility. Nonetheless, further studies are needed to validate our findings.

RESISTIN GENE POLYMORPHISM AND NONALCOHOLIC FATTY LIVER DISEASE RISK.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and one of the main global health issues in which liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Owing to the link between NAFLD and insulin resistance (IR) and obesity and the role of resistin in theses metabolic disorders, we explored the possible association between resistin gene (RETN) variant and NAFLD. METHODS: A total of 308 unrelated subjects, including 152 patients with biopsy-proven NAFLD and 156 controls were enrolled and genotyped for the RETN gene rs3745367 variant using PCR-RFLP method. RESULTS: NAFLD patients had higher liver enzymes, systolic blood pressure (SBP), and diastolic blood pressure (DBP) than the controls (P<0.001). However, we observed no significant difference in genotype and allele frequencies between the cases with NAFLD and the controls for the RETN rs3745367 polymorphism either before or after adjustment for confounding factors including age, BMI, sex, smoking status, SBP, and DBP. CONCLUSION: To our knowledge, this study is the first one that investigated the association between RETN gene rs3745367 variant and biopsy-proven NAFLD. Our findings do not support a role for this gene polymorphism in NAFLD risk in Iranian population; nonetheless, they need to be further investigated in other populations.

Risco de polimorfismo genético resistina e doença hepática gordurosa não alcoólica / Resistin gene polymorphism and nonalcoholic fatty liver disease risk

ABSTRACT Background Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease and one of the main global health issues in which liver fat surpasses 5% of hepatocytes without the secondary causes of lipid accumulation or excessive alcohol consumption. Owing to the link between NAFLD and insulin resistance (IR) and obesity and the role of resistin in theses metabolic disorders, we explored the possible association between resistin gene (RETN) variant and NAFLD. Methods A total of 308 unrelated subjects, including 152 patients with biopsy-proven NAFLD and 156 controls were enrolled and genotyped for the RETN gene rs3745367 variant using PCR-RFLP method. Results NAFLD patients had higher liver enzymes, systolic blood pressure (SBP), and diastolic blood pressure (DBP) than the controls (P<0.001). However, we observed no significant difference in genotype and allele frequencies between the cases with NAFLD and the controls for the RETN rs3745367 polymorphism either before or after adjustment for confounding factors including age, BMI, sex, smoking status, SBP, and DBP. Conclusion To our knowledge, this study is the first one that investigated the association between RETN gene rs3745367 variant and biopsy-proven NAFLD. Our findings do not support a role for this gene polymorphism in NAFLD risk in Iranian population; nonetheless, they need to be further investigated in other populations.

RESUMO Contexto: A doença hepática gordurosa não alcoólica (DHGNA) é uma doença hepática crônica e um dos principais problemas de saúde global em que a gordura hepática ultrapassa 5% dos hepatócitos sem as causas secundárias de acúmulo lipídico ou consumo excessivo de álcool. Devido à ligação entre a DHGNA e resistência à insulina (IR) e obesidade e o papel da resistina em distúrbios metabólicos, exploramos a possível associação entre a variante do gene resistina (RETN) e a DHGNA. Metodos Foram selecionados 308 indivíduos não relacionados, incluindo 152 pacientes com DHGNA comprovada por biópsia e 156 controles para a variante do gene RETN rs3745367 usando o método PCR-RFLP. Resultados Pacientes com DHGNA apresentaram enzimas hepáticas mais elevadas, assim como pressão arterial sistólica e pressão arterial diastólica maiores do que os controles (P<0,001). No entanto, não se observou diferença significativa nas frequências genótipo e alelo entre os casos com DHGNA e os controles para o polimorfismo RETN rs3745367 antes ou depois do ajuste para fatores de confusão, incluindo idade, índice de massa corporal, sexo, estado de tabagismo, pressão arterial sistólica e pressão arterial diastólica. Conclusão Para nosso conhecimento, este estudo foi o primeiro que investigou a associação entre a variante do gene RETN rs3745367 e a DHGNA comprovada em biópsia. Nossas descobertas não suportam um papel para este polimorfismo genético no risco DHGNA na população iraniana; no entanto, eles precisam ser mais investigados em outras populações.

Association of rs5742612 Polymorphism in the Promoter Region of IGF1 Gene with Nonalcoholic Fatty Liver Disease: A Case-Control Study.

OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) is an emerging global chronic liver disease encompassing a wide spectrum of disorders ranging from simple steatosis to nonalcoholic steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Considering the strong association between NAFLD and insulin resistance, and the vital role of insulin-like growth factor 1 (IGF1) in IR, we hypothesized that IGF1 gene polymorphism might be associated with NAFLD. METHODS: A total of 302 subjects, including 149 patients with biopsy-proven NAFLD and 153 controls, were enrolled in this case-control study. All the subjects were genotyped for the rs5742612 polymorphism of the IGF1 gene using the polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: The distribution of IGF1 rs5742612 genotypes and alleles differed significantly between the cases with NAFLD and controls. The IGF1 rs5742612 CC genotype compared with the TT genotype or the TT+TC genotype occurred more frequently in the cases than the controls and the differences remained significant after adjustment for confounding factors such as age and body mass index (P = .011, OR = 2.71, 95%CI = 1.16-5.85; and P = .032, OR = 2.29, 95% CI = 1.10-5.24, respectively). CONCLUSION: For the first time, this study uncovered that the IGF1 rs5742612 CC genotype compared with the TT genotype or the TT+TC genotype had a 2.71-fold or 2.29-fold increased risk for NAFLD, respectively.

Effects of Vitamin D Supplementation on Bone Health and Bone-related Parameters in HIV-infected Patients: A Systematic Review and Meta-analysis.

PURPOSE: There is growing evidence that bone health is decreased in individuals with HIV infection. Vitamin D deficiency is also highly prevalent among HIV-infected patients. The literature was systematically reviewed to determine whether bone health and bone-related parameters may improve with vitamin D supplementation in HIV-infected individuals. METHODS: Four databases were systematically searched for randomized clinical trials of vitamin D supplementation in HIV infection, published from January 1990 to September 2021. No language or publication restrictions were applied. Standardized mean differences (SMD) with 95% CIs are reported. A random-effects model was used to perform meta-analysis. FINDINGS: Ten studies met the inclusion criteria (N = 733 participants at study completion). The mean ages of the patients in the included trials ranged from 10 to 49 years. The meta-analysis indicated that with vitamin D supplementation, serum 25-hydroxy vitamin D (25[OH]D) level was significantly increased (SMD, 1.86; 95% CI, 1.02 to 2.70; I2 = 94.4%), but there were no significant effects on levels of serum 1,25-dihydroxy vitamin D (1,25-[OH]2D) (SMD, 0.29; 95% CI, -0.07 to 0.64; I2 = 67.4%), total bone mineral density (SMD, 0.07; 95% CI, -0.23 to 0.37; I2 = 00.0%), spine bone mineral density (SMD, 0.15; 95% CI, -0.19 to 0.49; I2 = 17.3%), and parathyroid hormone level (SMD, -0.18; 95% CI, -0.37 to 0.02; I2 = 1.2%) in HIV-infected patients. IMPLICATIONS: This study showed that vitamin D supplementation can improve serum 25(OH)D in HIV-infected patients. The effects of vitamin D supplementation on other bone health-related parameters such as bone mineral density and parathyroid hormone in HIV-infected patients need to be further investigated in larger-scale, well-designed randomized, controlled trials.

The effect of chromium intake on oxidative stress parameters: A systematic review and meta-analysis.

BACKGROUND: Trivalent chromium is a trace element thought to have a beneficial effect on oxidative stress (OS) parameters and inflammation. This review aimed to investigate the dose-response of chromium and summarize the effects of chromium supplementation on OS parameters in the literature. METHODS: MEDLINE, Scopus, Web of Science and Cochrane CENTRAL databases were searched for RCTs published from inception to January 2021 evaluating the effect of chromium supplementation on OS parameters, namely MDA, TBARS, SOD, TAS, CAT, GPx, and GSH. A random-effects model was used to pool data and calculated standard mean difference and 95 % confidence intervals. Quantified heterogeneity among studies was assessed through Cochrane's I2 values. RESULTS: Nine studies enrolling 550 participants met the inclusion criteria. The obtained results indicate that chromium supplementation significantly increases TAC (SMD: 0.46; 95 % CI: 0.08, 0.84; I2 = 00.0 % n = 2) and significantly decreases MDA levels (SMD: -0.46; 95 % CI: -0.86, -0.07; I2 = 52.4 % n = 5). Supplementation did not significantly change CAT, GPx, GSH, SOD, TAS, and TBARS. CONCLUSION: Chromium supplementation may improve OS parameters, however, due to high heterogeneity observed in the included studies, these findings should be interpreted with caution. Large RCTs on various patient groups evaluating the impact of chromium supplementation are needed to allow an adequate generalization of the benefits of chromium on human health.

Effect of omega-3 fatty acids supplementation on adipokines: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Although a large body of literature reported the beneficial effects of omega-3 fatty acids (omega-3 FAs) consumption on adipokines levels, but recent findings from clinical trials are not univocal. The aim of this systematic review and meta-analysis was to evaluate the effect of omega-3 FAs supplements on adipokines. METHODS: We searched Medline, Web of Science, Scopus, Embase, and Cochrane Library from inception to August 2020 without any particular language limitations. Outcomes were summarized as standardized mean difference (SMD) with 95% confidence intervals (CIs) estimated from Hedge's g and random effects modeling. RESULTS: Fifty-two trials involving 4,568 participants were included. Omega-3 FAs intake was associated with a significant increase in plasma adiponectin levels (n = 43; 3,434 participants; SMD: 0.21, 95% CI: 0.04, 0.37; p = 0.01; I2= 80.14%). This meta-analysis indicates that supplementing participants with omega-3 fatty acids more than 2000 mg daily and more than 10 weeks resulted in a significant and more favorable improvement in plasma adiponectin levels. However, omega-3 FAs intake had no significant effect on leptin levels (SMD: -0.02, 95% CI: -0.20, 0.17, I2= 54.13%). CONCLUSION: The evidence supports a beneficial effect of omega-3 FAs intake on serum adiponectin levels but does not appear to impact on leptin concentrations. Larger well-designed RCTs are still required to evaluate the effect of omega-3 FAs on leptin in specific diseases.

CIRCULATING GHRELIN LEVELS AND SUSCEPTIBILITY TO COLORECTAL CÂNCER.

BACKGROUND AND OBJECTIVE: Considering the association between colorectal cancer (CRC) and both insulin resistance and obesity, and the prominent role of ghrelin in these metabolic disorders, we explored whether plasma levels of ghrelin were associated with CRC. Moreover, in the patients with CRC the possible correlations between ghrelin and insulin, insulin resistance, and body mass index (BMI) as an indicator of obesity were examined. METHODS: A total of 170 subjects, including 82 cases with CRC and 88 controls were enrolled in this study. Plasma levels of ghrelin, insulin, and glucose were measured in all the subjects using ELISA and glucose oxidase methods. Furthermore, insulin resistance was assessed by calculating HOMA-IR index. RESULTS: The cases with CRC had decreased ghrelin levels (P<0.001) and a higher HOMA-IR index (P<0.001) than controls. Interestingly, when CRC patients were stratified based on tumor site, lower ghrelin levels and a higher HOMA-IR index were observed in the patients with either colon or rectal cancer vs. controls too. Additionally, there were an age and BMI-independent negative correlation between ghrelin levels and HOMA-IR (r=-0.365, P<0.05), and an age-independent negative correlation between ghrelin levels and BMI (r=-0.335, P<0.05) in the rectal subgroup. CONCLUSION: Our findings support a role for ghrelin in connection with insulin resistance and obesity in CRC susceptibility; however, it needs to be corroborated by further studies.