The Prevalence and Pathobiology of Nonalcoholic Fatty Liver Disease in Patients of Different Races or Ethnicities

Kalia, Harmit; Gaglio, Paul J.

doi:10.1016/j.cld.2015.10.005

Cited by 70 publications

(52 citation statements)

References 32 publications

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“…Consistent with other reports, 43 high liver fat was significantly more prevalent in Latino children compared with African-Americans. However, even with a habitual diet high in fructose, 37% of the children appeared to be protected against NAFLD.…”

Section: Discussionsupporting

confidence: 92%

Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity

et al. 2017

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Background & Aims Consumption of sugar is associated with obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease, and cardiovascular disease. The conversion of fructose to fat in liver (de novo lipogenesis, DNL) may be a modifiable pathogenetic pathway. We determined the effect of 9 days of isocaloric fructose restriction on DNL, liver fat, visceral fat (VAT), subcutaneous fat, and insulin kinetics in obese Latino and African American children with habitual high sugar consumption (fructose intake more than 50 g/day). Methods Children (9–18 years old; n = 41) had all meals provided for 9 days with the same energy and macronutrient composition as their standard diet, but with starch substituted for sugar, yielding a final fructose content of 4% of total kcal. Metabolic assessments were performed before and after fructose restriction. Liver fat, VAT, and subcutaneous fat were determined by magnetic resonance spectroscopy and imaging. The fractional DNL area under the curve value was measured using stable isotope tracers and gas chromatography/mass spectrometry. Insulin kinetics were calculated from oral glucose tolerance tests. Paired analyses compared change from day 0 to day 10 within each child. Results Compared with baseline, on day 10, liver fat decreased from a median of 7.2% (inter-quartile range, 2.5%–14.8%) to 3.8% (inter-quartile range, 1.7%–15.5%)(P<.001) and VAT decreased from 123 cm3 (inter-quartile range, 85–145 cm3) to 110 cm3 (inter-quartile range, 84–134 cm3) (P<.001). The DNL area under the curve decreased from 68% (inter-quartile range, 46%–83%) to 26% (inter-quartile range, 16%–37%) (P<0.001). Insulin kinetics improved (P<.001). These changes occurred irrespective of baseline liver fat. Conclusions Short-term (9 day) isocaloric fructose restriction decreased liver fat, VAT, and DNL, and improved insulin kinetics in children with obesity. These findings support efforts to reduce sugar consumption. ClinicalTrials.gov no: NCT01200043

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Section: Discussionsupporting

confidence: 92%

Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity

et al. 2017

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“…The rate at which NAFLD develops has been shown to be greatest in Hispanic patients[13]. Also, NAFLD in the Asian population has been increasing, and interestingly, can be seen in those who have a normal body mass index[13].…”

Section: Risk Factors and Etiologymentioning

confidence: 99%

Non-alcoholic fatty liver disease: An expanded review

Benedict

Zhang

2017

WJH

597

494

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Non-alcoholic fatty liver disease (NAFLD) encompasses the simple steatosis to more progressive steatosis with associated hepatitis, fibrosis, cirrhosis, and in some cases hepatocellular carcinoma. NAFLD is a growing epidemic, not only in the United States, but worldwide in part due to obesity and insulin resistance leading to liver accumulation of triglycerides and free fatty acids. Numerous risk factors for the development of NAFLD have been espoused with most having some form of metabolic derangement or insulin resistance at the core of its pathophysiology. NAFLD patients are at increased risk of liver-related as well as cardiovascular mortality, and NAFLD is rapidly becoming the leading indication for liver transplantation. Liver biopsy remains the gold standard for definitive diagnosis, but the development of noninvasive advanced imaging, biochemical and genetic tests will no doubt provide future clinicians with a great deal of information and opportunity for enhanced understanding of the pathogenesis and targeted treatment. As it currently stands several medications/supplements are being used in the treatment of NAFLD; however, none seem to be the “magic bullet” in curtailing this growing problem yet. In this review we summarized the current knowledge of NAFLD epidemiology, risk factors, diagnosis, pathogenesis, pathologic changes, natural history, and treatment in order to aid in further understanding this disease and better managing NAFLD patients.

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“…alpha-1 antitrypsin, Wilson’s, hemachromatosis, glycogen storage diseases, autoimmune chronic active hepatitis, primary biliary cirrhosis) in addition to HBV) can cause HCC [107]. New nucleotide/nucleoside and protease inhibitors that clear HCV viral loads theoretically should reduce HCC over time for those who can obtain the expensive treatment [108,109], but other conditions such as NAFLD will likely become the dominant etiology among populations in the U.S. Rates of NAFLD are highest among Hispanic patients compared to NHWs and Blacks [110,111], and without a clear definitive treatment path for NAFLD to date, a relative increased disparity could develop for HCC in Hispanics in the future. Variants for NAFLD risk exist in single nucleotide polymorphisms in or near PNPLA3 and PPP1R3B genes in Hispanic Americans and PNPLA3 , NCAN , GCKR , and PPP1R3B genes in Blacks [112].…”

Section: Introductionmentioning

confidence: 99%

Racial Disparity in Gastrointestinal Cancer Risk

et al. 2017

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Cancer from the gastrointestinal tract and its associated excretory organs will occur in over 300,000 Americans in 2017, with colorectal cancer responsible for over forty percent of that burden; there will be over 150,000 deaths from this group of cancers in the same time period. Disparities among subgroups related to these cancers’ incidence and mortality exist. The epidemiology and risk factors associated with each cancer bear out differences for racial groups in the United States. Esophageal adenocarcinoma is more frequent in Non-Hispanic Whites, whereas esophageal squamous cell carcinoma with risk factors of tobacco and alcohol is more frequent among Blacks. Liver cancer has been most frequent among Asian/Pacific Islanders chiefly due to hepatitis B vertical transmission, but other racial groups show increasing rates due to hepatitis C and emergence of cirrhosis from non-alcoholic fatty liver disease. Gastric cancer incidence remains highest among Asian/Pacific Islanders likely due to gene-environment interaction. In addition to esophageal squamous cell carcinoma, cancers of the small bowel, pancreas and colorectum show the highest rates among Blacks, where the explanations for the disparity are not as obvious and are likely multifactorial, including socio-economic and health care access, treatment and prevention (vaccination and screening) differences, dietary and composition of the gut microbiome, as well as biological and genetic influences. Cognizance of these disparities in gastrointestinal cancer risk, as well as approaches that apply precision medicine methods to populations with the increased risk, may reduce the observed disparities for digestive cancers.

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The Prevalence and Pathobiology of Nonalcoholic Fatty Liver Disease in Patients of Different Races or Ethnicities

Cited by 70 publications

References 32 publications

Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity

Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity

Non-alcoholic fatty liver disease: An expanded review

Racial Disparity in Gastrointestinal Cancer Risk

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