Risk factors associated with non-alcoholic fatty liver disease in subjects from primary care units. A case-control study

Caballería, Llorenç; Auladell, Maria; Pera, Guillem; Miranda, Dolores; Alumà, Alba; Casas, José Dario; Muñoz, Laura; Sánchez, C.; Tibau, Albert; Birulés, M; Canut, Santiago; Bernad, Jesús; Aubà, Josep; Aizpurua, Miren; Alcaraz, Enriqueta

doi:10.1186/1471-230x-8-44

Cited by 23 publications

(27 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In this work, TG deposition in liver increased with the aggravation of fatty changes (P <O.OS), indicating that more serious degree of fatty liver corresponded to greater possibility of abnormal blood fat. The AFLD patients always suffered from TG metabolic disorder, and the increased TG was closely related to NALFD, which was in accordance to the notion that fatty liver primarily manifested as increased fatty acid and TG [9]. Contents of LDL-C and HDL-C in blood showed slight increase and decrease (without significant difference), respectively, with the aggravation of fatty changes, which was consistent with the previous report [10], suggesting that metabolism of HDL-C and LDL-C might be linked to fatty liver.…”

Section: Disccusionsupporting

confidence: 82%

Liver mitochondrial DNA<sup>4977</sup> deletion in alcoholic fatty liver disease and relation to ultrasound

Liu

Liang

2011

The 2011 IEEE/ICME International Conference on Complex Medical Engineering

View full text Add to dashboard Cite

Aim To screen for the mitochondrial DNA 4977bp (mtDNA 4977 ) deletion in the patients with alcoholic fatty liver disease (AFLD). Methods Po}fmerase chain reaction (PCR) was carried out to detect mtDNA 49 deletion within 90 cases of AFLD plus 90 of normal controls. The ultrasound examination was conducted for the liver tissues of AFLD to compare liver function, blood fat level, body weight, and mtDNA 4977 deletion among different ultrasound grades of AFLD. Results With the aggravation of fatty change in live tissues of AFLD, deposition of both triglyceride (TG) and body mass index (BMI) in liver increased significantly (P

show abstract

Section: Disccusionsupporting

confidence: 82%

Liver mitochondrial DNA<sup>4977</sup> deletion in alcoholic fatty liver disease and relation to ultrasound

Liu

Liang

2011

The 2011 IEEE/ICME International Conference on Complex Medical Engineering

View full text Add to dashboard Cite

show abstract

“…In particular, there has been an increasing frequency of nonalcoholic hepatic steatosis in subjects with obesity or insulin resistance that may progress to chronic liver disease [2], [3].…”

Section: Introductionmentioning

confidence: 99%

Counteracting Roles of AMP Deaminase and AMP Kinase in the Development of Fatty Liver

et al. 2012

View full text Add to dashboard Cite

Fatty liver (hepatic steatosis) is associated with nucleotide turnover, loss of ATP and generation of adenosine monophosphate (AMP). It is well known that in fatty liver, activity of the AMP-activated kinase (AMPK) is reduced and that its stimulation can prevent hepatic steatosis by both enhancing fat oxidation and reducing lipogenesis. Here we show that another AMP dependent enzyme, AMPD2, has opposing effects on fatty acid oxidation when compared to AMPK. In human hepatocytres, AMPD2 activation –either by overexpression or by lowering intracellular phosphate levels with fructose- is associated with a significant reduction in AMPK activity. Likewise, silencing of AMPK spontaneously increases AMPD activity, demonstrating that these enzymes counter-regulate each other. Furthermore, we show that a downstream product of AMP metabolism through AMPD2, uric acid, can inhibit AMPK activity in human hepatocytes. Finally, we show that fructose-induced fat accumulation in hepatocytes is due to a dominant stimulation of AMPD2 despite stimulating AMPK. In this regard, AMPD2-deficient hepatocytes demonstrate a further activation of AMPK after fructose exposure in association with increased fatty acid oxidation, and conversely silencing AMPK enhances AMPD-dependent fat accumulation. In vivo, we show that sucrose fed rats also develop fatty liver that is blocked by metformin in association with both a reduction in AMPD activity and an increase in AMPK activity. In summary, AMPD and AMPK are both important in hepatic fat accumulation and counter-regulate each other. We present the novel finding that uric acid inhibits AMPK kinase activity in fructose-fed hepatocytes thus providing new insights into the pathogenesis of fatty liver.

show abstract

“…Nonalcoholic fatty liver disease (NAFLD) consists of the accumulation of fat vacuoles in the cytoplasm of hepatocytes and is characterized by development of hepatic lesions similar to those caused by alcohol in subjects without significant alcohol consumption 1. The prevalence of NAFLD is reported to be 3%–24% in the general population in various countries, and is increasing in parallel with the rising prevalence of obesity 2.…”

Section: Introductionmentioning

confidence: 99%

Relationship between obesity, metabolic syndrome, and nonalcoholic fatty liver disease in the elderly agricultural and fishing population of Taiwan

Shen¹,

Zhao²,

Hu³

et al. 2014

CIA

View full text Add to dashboard Cite

BackgroundThe purpose of this study was to explore the relationship between obesity, the metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD) in the elderly agricultural and fishing population of Taipei, Taiwan.MethodsThe study participants comprised 6,511 (3,971 male and 2,540 female) healthy elderly subjects voluntarily attending a teaching hospital for a physical check-up in 2010. Blood samples and real-time ultrasound-proven fatty liver sonography results were collected.ResultsThe prevalence of NAFLD in this elderly population was 27.2%, including mild NAFLD (16.0%), moderate NAFLD (10.3%), and severe NAFLD (0.9%). The prevalence of moderate or severe NAFLD for metabolic syndrome proved to be substantially greater (P<0.0001, χ2 test) for one or two metabolic factors. Using multinomial logistic regression analysis, age, sex, metabolic syndrome, and higher body mass index had a statistically significant association with mild NAFLD. Age, sex, metabolic syndrome, higher body mass index, and higher alanine aminotransferase were significantly related to moderate NAFLD. In addition, higher body mass index, higher uric acid, and higher alanine aminotransferase levels were significantly related to severe NAFLD. The sensitivity and specificity of body mass index and waist circumference as markers of NAFLD were estimated to be 81% and 84%, respectively, and 77% and 69%, respectively.ConclusionThe prevalence of mild or moderate NAFLD was related to obesity and metabolic syndrome. Higher body mass index was also related to severe NAFLD but not to metabolic syndrome. Targeting this population for control of obesity and improved metabolic function is important.

show abstract

Risk factors associated with non-alcoholic fatty liver disease in subjects from primary care units. A case-control study

Cited by 23 publications

References 17 publications

Liver mitochondrial DNA<sup>4977</sup> deletion in alcoholic fatty liver disease and relation to ultrasound

Liver mitochondrial DNA<sup>4977</sup> deletion in alcoholic fatty liver disease and relation to ultrasound

Counteracting Roles of AMP Deaminase and AMP Kinase in the Development of Fatty Liver

Relationship between obesity, metabolic syndrome, and nonalcoholic fatty liver disease in the elderly agricultural and fishing population of Taiwan

Contact Info

Product

Resources

About