Nonalcoholic Fatty Liver Disease

Angulo, Paul

doi:10.1002/9780470692189.ch34

Cited by 372 publications

(601 citation statements)

References 63 publications

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“…It is well recognised that obesity is associated with nonalcoholic fatty liver disease (NAFLD) and obese subjects with NAFLD are markedly insulin resistant [8][9][10], although the explanation for the marked insulin resistance with NAFLD is poorly understood [11]. Specifically, it is uncertain whether abnormal cortisol regulation or metabolism is responsible for the marked insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Cortisol clearance and associations with insulin sensitivity, body fat and fatty liver in middle-aged men

et al. 2007

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Aims/hypothesis The regulation of cortisol metabolism in vivo is not well understood. We evaluated the relationship between cortisol metabolism and insulin sensitivity, adjusting for total and regional fat content and for non-alcoholic fatty liver disease. Materials and methods Twenty-nine middle-aged healthy men with a wide range of BMI were recruited. We measured fat content by dual-energy X-ray absorptiometry and magnetic resonance imaging (MRI), liver fat by ultrasound and MRI, the hypothalamic-pituitary-adrenal axis by adrenal response to ACTH 1-24 , unconjugated urinary cortisol excretion, corticosteroid-binding globulin, and cortisol clearance by MS. We assessed insulin sensitivity by hyperinsulinaemic-euglycaemic clamp and by OGTT. Results Cortisol clearance was strongly inversely correlated with insulin sensitivity (M value) (r=−0.61, p=0.002). Cortisol clearance was increased in people with fatty liver compared with those without (mean±SD: 243±10 vs 158± 36 ml/min; p = 0.014). Multiple regression modelling showed that the relationship between cortisol clearance and insulin sensitivity was independent of body fat. The relationship between fatty liver and insulin sensitivity was significantly influenced by body fat and cortisol clearance. Conclusions/interpretation Cortisol clearance is strongly associated with insulin sensitivity, independently of the amount of body fat. The relationship between fatty liver and insulin sensitivity is mediated in part by both fatness and cortisol clearance.

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Section: Introductionmentioning

confidence: 99%

Cortisol clearance and associations with insulin sensitivity, body fat and fatty liver in middle-aged men

et al. 2007

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“…[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.…”

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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

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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 ...

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“…A pproximately 70% of patients who are obese or who have type 2 diabetes mellitus (T2DM) have nonalcoholic fatty liver (NAFL) [1][2][3][4][5] of whom 20% show progression to nonalcoholic steatohepatitis (NASH). 6 Nonalcoholic fatty liver disease (NAFLD) refers to hepatocellular lipid contents of Ͼ5.5% with varying degrees of inflammation in individuals consuming less than 20 g of alcohol per day.…”

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confidence: 99%

“…Combined lipotoxicity, oxidative stress, and proinflammatory mediators, also key factors in the development of muscular insulin resistance, 1 would further damage hepatic mitochondria leading to mitochondrial dysmorphologies and promoting the transition of steatosis to NASH. 2,11 In this context, hyperlipidemia was found to decrease both insulin sensitivity and mitochondrial function at the level of skeletal muscle. 21 However, no data on the association between ectopic fat content, insulin sensitivity, and mitochondrial function are currently available at the level of the liver.…”

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confidence: 99%

Abnormal hepatic energy homeostasis in type 2 diabetes

et al. 2009

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Increased hepatocellular lipids relate to insulin resistance and are typical for individuals with type 2 diabetes mellitus (T2DM). Steatosis and T2DM have been further associated with impaired muscular adenosine triphosphate (ATP) turnover indicating reduced mitochondrial fitness. Thus, we tested the hypothesis that hepatic energy metabolism could be impaired even in metabolically well-controlled T2DM. We measured hepatic lipid volume fraction (HLVF) and absolute concentrations of ␥ATP, inorganic phosphate (Pi), phosphomonoesters and phosphodiesters using noninvasive 1 H/ 31 P magnetic resonance spectroscopy in individuals with T2DM (58 ؎ 6 years, 27 ؎ 3 kg/m 2 ), and age-matched and body mass index-matched (mCON; 61 ؎ 4 years, 26 ؎ 4 kg/m 2 ) and young lean humans (yCON; 25 ؎ 3 years, 22 ؎ 2 kg/m 2 , P < 0.005, P < 0.05 versus T2DM and mCON). Insulin-mediated whole-body glucose disposal (M) and endogenous glucose production (iEGP) were assessed during euglycemic-hyperinsulinemic clamps. Individuals with T2DM had 26% and 23% lower ␥ATP (1.68 ؎ 0.11; 2.26 ؎ 0.20; 2.20 ؎ 0.09 mmol/L; P < 0.05) than mCON and yCON individuals, respectively. Further, they had 28% and 31% lower Pi than did individuals from the mCON and yCON groups (0.96 ؎ 0.06; 1.33 ؎ 0.13; 1.41 ؎ 0.07 mmol/L; P < 0.05). Phosphomonoesters, phosphodiesters, and liver aminotransferases did not differ between groups. HLVF was not different between those from the T2DM and mCON groups, but higher (P ‫؍‬ 0.002) than in those from the yCON group. T2DM had 13-fold higher iEGP than mCON (P < 0.05). Even after adjustment for HLVF, hepatic ATP and Pi related negatively to hepatic insulin sensitivity (iEGP) (r ‫؍‬ ؊0.665, P ‫؍‬ 0.010, r ‫؍‬ ؊0.680, P ‫؍‬ 0.007) but not to whole-body insulin sensitivity. Conclusion: These data suggest that impaired hepatic energy metabolism and insulin resistance could precede the development of steatosis in individuals with T2DM. (HEPATOLOGY

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Nonalcoholic Fatty Liver Disease

Cited by 372 publications

References 63 publications

Cortisol clearance and associations with insulin sensitivity, body fat and fatty liver in middle-aged men

Cortisol clearance and associations with insulin sensitivity, body fat and fatty liver in middle-aged men

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

Abnormal hepatic energy homeostasis in type 2 diabetes

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