Nutritional investigation of non-obese patients with non-alcoholic fatty liver disease: The significance of dietary cholesterol

Yasutake, Kenichiro; Nakamuta, Makoto; Shima, Yuki; Ohyama, Akiko; Masuda, Kazuyuki; Haruta, Noriko; Fujino, Tatsuya; Aoyagi, Yoko; Fukuizumi, Kunitaka; Yoshimoto, Tsuyoshi; Takemoto, Ryosuke; Miyahara, Toshihiko; Harada, Naohiko; Hayata, Fukuko; Nakashima, Mitsuyoshi; Enjoji, Munechika

doi:10.1080/00365520802588133

Cited by 184 publications

(133 citation statements)

References 26 publications

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“…Statins were used in 4 randomized controlled trials and showed that there was no effect on liver histology and body weight (56)(57)(58)(59)(60)(61)(62)(63). Fibrates have a beneficial effect on liver enzymes in a short period but no effect on liver pathologic scores.…”

Section: Therapy Of Nafld and Nashmentioning

confidence: 99%

Nonalcoholic fatty liver disease: Diagnosis, pathogenesis, and management

Başaranoğlu

Örmeci²

2014

Turk J Gastroenterol

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Nonalcoholic fatty liver disease (NAFLD) is an umbrella term that covers both a relatively benign condition, which is simple steatosis, and nonalcoholic steatohepatitis (NASH). NASH is characterized by a chronic and progressive liver pathology that may progress to cirrhosis, end-stage liver disease, hepatocellular carcinoma, and liver transplantation. Despite the growing body of evidence, one of the important and unresolved problems is the pathogenesis of NASH. It might be a metabolic disturbance as a primary abnormality in NAFLD. Insulin resistance is at the center of these metabolic abnormalities. Then, hepatocyte injury might be induced by oxidative stress. This ongoing process progresses to NASH, even to cirrhosis in some patients. In addition to oxidative stress, possibilities for the next hit are lipid peroxidation, reactive metabolites, adipose tissue products, transforming growth factor-b 1 , Fas ligand, mitochondrial dysfunction, respiratory chain deficiency, and intestinal microbiota. Currently, there is no well-established and approved therapy. Recommendations are to improve existing co-morbidities, such as obesity, hyperlipidemia, or type 2 diabetes, and lifestyle modification with weight loss and exercise.

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Section: Therapy Of Nafld and Nashmentioning

confidence: 99%

Nonalcoholic fatty liver disease: Diagnosis, pathogenesis, and management

Başaranoğlu

Örmeci²

2014

Turk J Gastroenterol

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“…Nutritional investigations implicate certain diets, such as high carbohydrate plus low fat and high fat plus low protein to be causal in NAFLD ( 14,15 ). More recent evidence points towards a possible role for dietary factors in nonobese individuals as well ( 16 ). It is interesting to note that though, Kwon et al ( 6 ) adjusted for lifestyle interventions, including exercise and smoking status between the two groups, they did not factor in dietary variables, which made it diffi cult to delineate the role of nutritional status in the study ' s outcome ( 6 ) ( 14,19 ).…”

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confidence: 99%

“…It is interesting to note that though, Kwon et al ( 6 ) adjusted for lifestyle interventions, including exercise and smoking status between the two groups, they did not factor in dietary variables, which made it diffi cult to delineate the role of nutritional status in the study ' s outcome ( 6 ) ( 14,19 ). More recently, a possible role for dietary cholesterol in the pathogenesis of NAFLD has been suggested ( 16 ). Increased westernization of the Asian diet has resulted in more cholesterol and less n-3 polyunsaturated fatty acids (PUFA) consumption in an already predominant carbohydrate diet.…”

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confidence: 99%

Editorial: Non-Alcoholic Fatty Liver Disease and Obesity: Not All About Body Mass Index

Pagadala

McCullough

2012

American Journal of Gastroenterology

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Patients with nonalcoholic fatty liver (NAFLD) are typically obese and confounded by the metabolic syndrome. The body mass index (BMI) is often used as a surrogate marker of obesity defi ned as a BMI >30 λ kg / m 2 . However, it is now apparent that it is the distribution of body fat (not total fat) that is associated with NAFLD. Many patients (as many as 25 % ) with NAFLD are nonobese. This is particularly true in Asians who have a signifi cantly increased risk of cardiovascular disease and diabetes even among those with a normal BMI. It is important for clinicians to be aware that these " metabolically obese " NAFLD patients should be monitored for the metabolic syndrome and its associated adverse outcomes irrespective of their BMI. Am J Gastroenterol 2012; 107:1859 -1861 doi: 10.1038/ajg.2012 Nonalcoholic fatty liver disease (NAFLD) is recognized worldwide as the most common cause of chronic liver disease. Th e spectrum of the disease ranges from simple steatosis, which has a more benign course to the histological severe steatohepatitis (NASH), a pathological entity associated with an increased risk for developing cirrhosis and hepatocellular carcinoma ( 1 ). Although the precise pathogenesis of NAFLD remains incompletely defi ned and is being investigated, the most widely accepted pathophysiologic model for NAFLD is the " two-hit hypothesis " ( 2 ). Th e fi rst hit involves the development of steatosis, which is closely linked with the development of insulin resistance (IR) ( 3 ). Th e second hit in certain susceptible individuals is associated with the progression of steatosis to NASH, attributed to oxidative stress and lipid peroxidation, which upregulates pro-infl ammatory cytokines and apoptosis further activating hepatic stellate leading to advanced fi brosis. IR is an important pathogenic link in the development of metabolic syndrome (MetS), which is defi ned by: glucose intolerance, arterial hypertension, elevated triglycerides, low highdensity lipoproteins and increased waist circumference (WC). NAFLD is increasingly being considered to be a hepatic manifestation of MetS ( 2 ).Obesity, as classifi ed by the body mass index (BMI), has become a worldwide concern reaching epidemic proportions. While obesity in the United States is defi ned by BMI 30 kg / m 2 , this cutoff is not universal and diff erent classifi cations exist based on racial phenotypic characterizations. Obesity represents a state of chronic low-grade infl ammation that exists in peripheral fat depots. Th is observation is based on the presence of increased circulatory proinfl ammatory cytokines (adipokines), such as: TNF-α , IL-6, IL-8, MCP, CRP, and decreased anti-infl ammatory adipokines such as adiponectin and IL-10. Th is phenomenon is thought to be causal in the development of IR and MetS ( 4 ). Obesity, IR, and MetS (independent of BMI) is strongly associated with NAFLD and severity of the disease ( 5 ). Th e rapidly increasing prevalence of obesity and MetS has also led to the rise in the associated co-morbid condition...

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“…Ezetimibe Growing evidence connects non-esterified cholesterol accumulation in mitochondria to hepatocyte apoptosis, liver injury and NASH development [56][57][58][59][60][61]. On this basis, ezetimibe, a Niemann-Pick C1 like 1 protein inhibitor, was evaluated in two RCTs in NAFLD.…”

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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

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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%

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Nutritional investigation of non-obese patients with non-alcoholic fatty liver disease: The significance of dietary cholesterol

Cited by 184 publications

References 26 publications

Nonalcoholic fatty liver disease: Diagnosis, pathogenesis, and management

Nonalcoholic fatty liver disease: Diagnosis, pathogenesis, and management

Editorial: Non-Alcoholic Fatty Liver Disease and Obesity: Not All About Body Mass Index

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

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