Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

Assy, Nimer; Nasser, Gattas; Kamayse, Iad; Nseir, William; Beniashvili, Zaza; Djibre, A.; Grosovski, Maria

doi:10.1155/2008/810961

Cited by 290 publications

(219 citation statements)

References 34 publications

(42 reference statements)

Supporting

Mentioning

194

Contrasting

Unclassified

Order By: Relevance

“…Recently, it has been shown that a diet low in fructose might be beneficial with regard to reduction of liver fat content. 21,22 However, the exact mechanisms involved in sugar and particularly fructose-induced NAFLD are still poorly understood. Here, by feeding mice lacking the endotoxin receptor TLR-4 chronically with a moderate fructose-enhanced diet (e.g., 30% fructose in drinking solutions) we further tested the hypothesis that the endotoxin-induced activation of hepatic Kupffer cells resulting from intestinal bacterial overgrowth and increased intestinal permeability 13,14 is a key factor in the onset of fructose-induced NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

et al. 2009

View full text Add to dashboard Cite

A link between dietary fructose intake, gut-derived endotoxemia, and nonalcoholic fatty liver disease (NAFLD) has been suggested by the results of human and animal studies. To further investigate the role of gut-derived endotoxin in the onset of fructose-induced NAFLD, Toll-like receptor (TLR-) 4-mutant (C3H/HeJ) mice and wildtype (C3H/HouJ) mice were either fed plain water or water enriched with 30% fructose for 8 weeks. Hepatic steatosis, plasma alanine aminotransferase (ALT), and markers of insulin resistance as well as portal endotoxin levels were determined. Hepatic levels of myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and 7, and tumor necrosis factor alpha (TNF␣) as well as markers of lipid peroxidation were assessed. Chronic intake of 30% fructose solution caused a significant increase in hepatic steatosis and plasma ALT levels in wildtype animals in comparison to water controls. In fructose-fed TLR-4 mutant mice, hepatic triglyceride accumulation was significantly reduced by Ϸ40% in comparison to fructose-fed wildtype mice and plasma ALT levels were at the level of water-fed controls. No difference in portal endotoxin concentration between fructose-fed wildtype and TLR-4-mutant animals was detected. In contrast, hepatic lipid peroxidation, MyD88, and TNF␣ levels were significantly decreased in fructose-fed TLR-4-mutant mice in comparison to fructose-fed wildtype mice, whereas IRF3 and IRF7 expression remained unchanged. Markers of insulin resistance (e.g., plasma TNF␣, retinol binding protein 4, and hepatic phospho-AKT) were only altered in fructose-fed wildtype animals. Conclusion: Taken together, these data further support the hypothesis that in mice the onset of fructose-induced NAFLD is associated with intestinal bacterial overgrowth and increased intestinal permeability, subsequently leading to an endotoxin-dependent activation of hepatic Kupffer cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Fructose and high-fructose corn syrup, a common soft drink sweetener, in particular, have been independently connected to the risk and severity of NAFLD in population-based studies and in a randomised crossover trial [115][116][117][118][119].…”

Section: Implications For Future Researchmentioning

confidence: 99%

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

et al. 2012

View full text Add to dashboard Cite

Aims/hypothesis Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH): NAFLD causes an increased risk of cardiovascular disease, diabetes and liverrelated complications (the latter confined to NASH). The effect of proposed treatments on liver disease, glucose metabolism and cardiovascular risk in NAFLD is unknown. We reviewed the evidence for the management of liver disease and cardiometabolic risk in NAFLD. Methods Publications through November 2011 were systematically reviewed by two authors. Outcomes evaluated though standard methods were: histological/radiological/biochemical features of NAFLD, variables of glucose metabolism and cardiovascular risk factors. Seventy-eight randomised trials were included (38 in NASH, 40 in NAFLD): 41% assessed post-treatment histology, 71% assessed glucose metabolism and 88% assessed cardiovascular risk factors. Lifestyle intervention, thiazolidinediones, metformin and antioxidants were most extensively evaluated. Results Lifestyle-induced weight loss was safe and improved cardio-metabolic risk profile; a weight loss ≥7% improved histological disease activity, but was achieved by <50%

show abstract

“…Results of several recent studies suggest that an increased intake of dietary fructose may be associated with the development of NAFLD. 23,25 Further, the CARDIA study has shown that fast-food consumption had a strong positive association with weight gain and insulin resistance in humans. 26 However, aerated drinks or fast-food consumption did not show any association with NAFLD in our study.…”

Section: Singh Et Al Risk Factors Associated With Non-alcoholic Fattymentioning

confidence: 99%

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Singh

Misra

et al. 2015

Journal of Clinical and Experimental Hepatology

View full text Add to dashboard Cite

Background/Aims: NAFLD has today emerged as the leading cause of liver disorder. There is scanty data on risk factors associated with NAFLD emanating from India. The present study was conducted to identify the risk factors associated with NAFLD. Methods: 464 consecutive NAFLD patients and 181 control patients were subjected to detailed questionnaire regarding their lifestyle and dietary risk factors. Anthropometric measurements were obtained and biochemical assays were done. Comparison of different variables was made between NAFLD patients and controls using principal component analysis (PCA). Results: NAFLD patients had higher BMI [26.25 AE 3.80 vs 21.46 AE 3.08 kg/m 2 , P = 0.000], waist-hip ratio [0.96 AE 0.12 vs 0.90 AE 0.08, P = 0.000] and waist-height ratio [0.57 AE 0.09 vs 0.50 AE 0.06, P = 0.000] compared to controls. Fasting blood sugar [101.88 AE 31.57 vs 90.87 AE 10.74 mg/dl] and triglyceride levels [196.16 AE 102.66 vs 133.20 AE 58.37 mg/dl] were significantly higher in NAFLD group. HOMA-IR was also higher in NAFLD group [2.53 AE 2.57 vs 1.16 AE 0.58, P = 0.000]. Majority (90.2%) of NAFLD patients were sedentary. Family history of metabolic syndrome (MS) was positively correlated with NAFLD. Dietary risk factors associated with NAFLD were non-vegetarian diet [35% vs 23%, P = 0.002], fried food [35% vs 9%, P = 0.000], spicy foods [51% vs 15%, P = 0.001] and tea [55% vs 39%, P = 0.001]. Diabetes, hypertension, snoring and sleep apnoea syndrome were common factors in NAFLD. On multivariate PCA, waist/height ratio and BMI were significantly higher in the NAFLD patients. Conclusion: The risk factors associated with NAFLD are sedentary lifestyle, obesity family history of MS, consumption of meat/fish, spicy foods, fried foods and tea. Other risk factors associated with NAFLD included snoring and MS. ( J CLIN EXP HEPATOL 2015;5:295-302) N on-alcoholic fatty liver disease (NAFLD) is a distinct clinico-pathologic entity characterized histologically by a spectrum ranging from simple steatosis to steatohepatitis (NASH), cirrhosis and even hepatocellular carcinoma (HCC). 1,2 NAFLD (steatosis of the liver) is highly prevalent in Western countries. 1 With the introduction of westernized lifestyle and the increasing frequency of obesity in the Asia-Pacific region, the prevalence of NAFLD has increased over the past two decades.Studies from different regions of India have shown that NAFLD is very common in Indians. [3][4][5] Risk factors implicated in the development of NAFLD are obesity and metabolic syndrome (MS). 6,7 However, it is obvious that NAFLD is multifactorial and identifying the various risk factors associated with NAFLD in our population could help us to intervene in order to prevent its progression to more severe forms of the disease.The few studies identifying the risk factors associated with NAFLD have emanated from the West, where the profiles of NAFLD patients appear to be different. [8][9][10] The observed differences in Indian NAFLD patients include a lower frequency of MS, 9,11 lesser degree ...

show abstract

Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

Cited by 290 publications

References 34 publications

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Contact Info

Product

Resources

About