Non-alcoholic fatty liver disease and insulin resistance: importance of risk factors and histological spectrum

Siqueira, Ana Cristina; Cotrim, Helma Pinchemel; Rocha, Raquel; Carvalho, Fernando Martins; Freitas, Luiz Antônio Rodrigues de; Barrêto, Danyella da Silva; Gouveia, Leandro; Landeiro, Luciana

doi:10.1097/00042737-200508000-00010

Cited by 32 publications

(24 citation statements)

References 19 publications

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“…Third, the smoking data was collected by binary criteria in this study so the effects of smoking on metabolic syndrome components might be underestimated [35] . In summary, fatty liver and smoking were closely related to insulin resistance [1][2][3][4][5][6][7][8][9][11][12][13][14]16,[21][22][23]25,32] , and our study provided evidence that fatty liver and smoking had a synergistic effect on metabolic syndrome and its components, especially for triglyceride and HDL-C levels. We suggested that smoking cessation would have the great benefit of reducing the risk of metabolic syndrome, especially for subjects with fatty liver.…”

Section: Discussionmentioning

confidence: 55%

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Synergistic effect of fatty liver and smoking on metabolicsyndrome

Chiang¹,

Chang²,

Chen³

2009

WJG

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AIM:To investigate the association of fatty liver and smoking on metabolic syndrome and its components. METHODS:This cross-sectional study enrolled participants who attended annual health screening at Shin Kong Wu Ho-Su Memorial Hospital from January to December 2005. A total of 3455 (1981 men and 1474 women) subjects were included in final analyses. Fatty liver was diagnosed using abdominal ultrasonography by trained gastroenterologists. The modified National Cholesterol Education Program Adult Treatment Panel Ⅲ was used to define metabolic syndrome. The associations between smoking, fatty liver and metabolic syndrome were analyzed using multiple logistic regression. RESULTS:Subjects with fatty liver, and who smoked tobacco, had the highest odds ratios (ORs) for high waist circumference [OR, 4.5 (95% CI: 3.3-6.1), P < 0.05], hypertriglyceridemia [OR, 8.1 (95% CI: 6.0-10.9), P < 0.05], low serum high-density lipoprotein cholesterol (HDL-C) [OR, 8.3 (95% CI: 6.1-11.3), P < 0.05], and metabolic syndrome [OR, 9.5 (95% CI: 6.7-13.4), P < 0.05] compared to subjects without fatty liver who did not smoke tobacco. We also found that the ORs for hypertriglyceridemia, low serum HDL-C, and metabolic syndrome for subjects with fatty liver who smoked tobacco had greater than the sum of the ORs for subjects with fatty liver who did not smoke plus those who did not have fatty liver and who did smoke.CONCLUSION: Fatty liver and smoking had a synergistic effect on metabolic syndrome and its components, especially for hypertriglyceridemia and low serum HDL-C.

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Section: Discussionmentioning

confidence: 55%

“…The association between fatty liver and metabolic syndrome was broadly discussed in previous studies [1][2][3][4][5][6][7][8][9] . Fatty liver is often associated with central obesity, type 2 diabetes mellitus, dyslipidemia, and hypertension.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effect of fatty liver and smoking on metabolicsyndrome

Chiang¹,

Chang²,

Chen³

2009

WJG

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“…Patients with fatty liver seem to have lower c-peptid and insulin levels than those with NASH [47,51] . Recent studies claimed that metabolic risk factors and insulin resistance could influence liver histology [52] . Sobhonslidsuk et al [11] represented that insulin resistance and elevated visceral fat are risk factors for the presence of NASH.…”

mentioning

confidence: 99%

“…Bahrami et al [41] found the rate of insulin resistance was only 54.7% in 53 patients with NASH. Guidorizzi de Siqueira et al [52] said that insulin resistance was detected in only 33% of NAFLD patients but there was a high frequency of IR in patients with advanced fibrosis. Sakurai et al [56] have specified that only steatosis was significantly and independently associated with elevated HOMA values but there was no similar association with the grade or stage of NASH.…”

mentioning

confidence: 99%

Noninvasive predictors for liver fibrosis in patients with nonalcoholic steatohepatitis

Uslusoy¹

2011

WJH

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AIM:To evaluate certain anthropometric, clinical and laboratory features indicating liver fibrosis in nonalcoholic steatohepatitis and to establish the noninvasive markers for liver fibrosis. METHODS:Eighty-one patients (40 male, 41 female) who were diagnosed with fatty liver by ultrasonographic examination and fulfilled the inclusion criteria participated in the study. Anamnesis, anthropometric, clinical and laboratory features of all cases were recorded and then liver biopsy was performed after obtaining patient consent. Steatosis, necroinflammation and liver fibrosis were examined according to age ≥ 45, gender, body mass index, central obesity, aspartate aminotransferase (AST)/alanine aminotransferase (ALT) > 1, γ-glutamyltransferase (GGT)/ALT > 1, platelet count, insulin, c-peptide levels and the presence of hypertension, diabetes, hypertriglyceridemia and insulin resistance. RESULTS:Eighty-one patients with non-alcoholic steatohepatitis (NASH) enrolled in the study. 69 of 81 patients were diagnosed with NASH, 11 were diagnosed with simple fatty liver and 1 was diagnosed with cirrhosis. AST/ALT > 1, GGT/ALT > 11, high serum ferritin and fasting insulin levels, the presence of diabetes, hypertension, hypertriglyceridemia and insulin resistance seemed to enhance the severity of steatosis, necroinflammation and fibrosis but these results were not statistically significant. CONCLUSION:Liver steatosis and fibrosis can occur in individuals with normal weight. There was no significant concordance between severity of liver histology and the presence of predictors for liver fibrosis including metabolic risk factors.

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“…Earlier studies of NAFLD have focused on histological or molecular analyses of the liver tissue. [26][27][28] We used a systematic assessment of the influences of WAT on liver pathology to reveal new insights into the biological mechanisms of NAFLD and new therapeutic targets for treatment. We chose to focus this initial study on the global analysis of phosphorylation-driven cellular signaling within the WAT itself.…”

Section: Discussionmentioning

confidence: 99%

A systems biology approach to the pathogenesis of obesity-related nonalcoholic fatty liver disease using reverse phase protein microarrays for multiplexed cell signaling analysis

et al. 2007

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Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease. Omental adipose tissue, a biologically active organ secreting adipokines and cytokines, may play a role in the development of NAFLD. We tested this hypothesis with reverse-phase protein microarrays (RPA) for multiplexed cell signaling analysis of adipose tissue from patients with NAFLD. Omental adipose tissue was obtained from 99 obese patients. Liver biopsies obtained at the time of surgery were all read by the same hepatopathologist. Adipose tissue was exposed to rapid pressure cycles to extract protein lysates. RPA was used to investigate intracellular signaling. Analysis of 54 different kinase substrates and cell signaling endpoints showed that an insulin signaling pathway is deranged in different locations in NAFLD patients. Furthermore, components of insulin receptor-mediated signaling differentiate most of the conditions on the NAFLD spectrum. For example, PKA (protein kinase A) and AKT/mTOR (protein kinase B/mammalian target of rapamycin) pathway derangement accurately discriminates patients with NASH from those with the non-progressive forms of NAFLD. PKC (protein kinase C) delta, AKT, and SHC phosphorylation changes occur in patients with simple steatosis. Amounts of the FKHR (forkhead factor Foxo1)phosphorylated at S256 residue were significantly correlated with AST/ALT ratio in all morbidly obese patients. Furthermore, amounts of cleaved caspase 9 and pp90RSK S380 were positively correlated in patients with NASH. Specific insulin pathway signaling events are altered in the adipose tissue of patients with NASH compared with patients with nonprogressive forms of NAFLD. Conclusion: These findings provide evidence for the role of omental fat in the pathogenesis, and potentially, the progression of NAFLD. (HEPATOLOGY 2007;46:166-172.)

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Non-alcoholic fatty liver disease and insulin resistance: importance of risk factors and histological spectrum

Abstract: IR occurred in 33% of the NAFLD patients, being more frequent among those with MC than among those with exposure to petrochemicals. The presence of IR in cases with advanced fibrosis suggests that it may influence the prognosis of NAFLD.

Cited by 32 publications

References 19 publications

Synergistic effect of fatty liver and smoking on metabolicsyndrome

Synergistic effect of fatty liver and smoking on metabolicsyndrome

Noninvasive predictors for liver fibrosis in patients with nonalcoholic steatohepatitis

A systems biology approach to the pathogenesis of obesity-related nonalcoholic fatty liver disease using reverse phase protein microarrays for multiplexed cell signaling analysis

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