Increased hepatic fat in overweight Hispanic youth influenced by interaction between genetic variation in PNPLA3 and high dietary carbohydrate and sugar consumption

Davis, Jaimie N.; Lê, Kim-Anne; Walker, Ryan W.; Vikman, Susanna; Spruijt‐Metz, Donna; Weigensberg, Marc J.; Allayee, Hooman; Goran, Michael I.

doi:10.3945/ajcn.2010.30185

Cited by 180 publications

(173 citation statements)

References 27 publications

(30 reference statements)

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“…This observation is likely multifactorial and may include a greater prevalence of the PNPLA3 gene, which is associated with higher liver fat content in the presence of dietary sugar (46) , higher overweight and obesity rates (6) , as well as higher abdominal obesity, consistent with prior findings among US adolescent and adult populations (47,48) . Our findings have a number of limitations.…”

Section: Discussionsupporting

confidence: 78%

Added sugar intake and metabolic syndrome in US adolescents: cross-sectional analysis of the National Health and Nutrition Examination Survey 2005–2012

Rodríguez¹,

Madsen²,

Cotterman³

et al. 2016

Public Health Nutr.

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Objective: To examine the association between added sugar intake and metabolic syndrome among adolescents. Design: Dietary, serum biomarker, anthropometric and physical activity data from the US National Health and Nutrition Examination Survey cycles between 2005 and 2012 were analysed using multivariate logistic regression models. Added sugar intake in grams per day was estimated from two 24 h standardized dietary recalls and then separated into quintiles from lowest to highest consumption. Multivariate logistic regression analyses were adjusted for physical activity, age, BMI Z-score and energy intake, and their interactions with race were included. Setting: Nationally representative sample, USA. Subjects: US adolescents aged 12-19 years (n 1623). Results: Added sugar was significantly associated with metabolic syndrome. The adjusted prevalence odds ratios for having metabolic syndrome comparing adolescents in the third, fourth and fifth quintiles v. those in the lowest quintile of added sugar were 5·3 (95 % CI 1·4, 20·6), 9·9 (95 % CI 1·9, 50·9) and 8·7 (95 % CI 1·4, 54·9), respectively. Conclusions: Our findings suggest that higher added sugar intake, independent of total energy intake, physical activity or BMI Z-score, is associated with increased prevalence of metabolic syndrome in US adolescents. Further studies are needed to determine if reducing intake of added sugar may help US adolescents prevent or reverse metabolic syndrome.

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Section: Discussionsupporting

confidence: 78%

Added sugar intake and metabolic syndrome in US adolescents: cross-sectional analysis of the National Health and Nutrition Examination Survey 2005–2012

Rodríguez¹,

Madsen²,

Cotterman³

et al. 2016

Public Health Nutr.

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“…This leads to development of macrovesicular steatosis ( 26,30 ), simple steatosis to steatohepatitis and progressive cirrhosis ( 31 ), and hepatic fi brinogenesis by a sterol regulatory element-binding protein (SREBP)-1c-PNPLA3 pathway ( 32 ). A greater impact of the L148M variant on hepatic lipid content is unmasked in the presence of other risk factors such as obesity ( 33 ), visceral adiposity ( 34 ), increased intake of sugars ( 35 ), omega-6 PUFAs ( 36 ), glucokinase regulatory protein gene variant ( 37 ), chronic hepatitis B ( 38 ), and hepatocellular carcinoma ( 39 ). In contrast to these reports, PNPLA3 has been reported to restore lipid homeostasis ( 40 ) by mediating acylation of lysophospholipids and hydrolyzing TGs in the liver in a direct manner or by regulation by cofactors ( 41,42 ).…”

mentioning

confidence: 99%

Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Ramanadham

Ali

Ashley

et al. 2015

Journal of Lipid Research

166

190

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The Ca 2+ -independent phospholipases A 2 (iPLA 2 s) are part of a diverse family of PLA 2 s that hydrolyze the sn -2 substituent from membrane phospholipids to release a free fatty acid and a lysolipid ( 1, 2 ). These enzymes are ubiquitously expressed, and in contrast to secretory PLA 2 s (sPLA 2 s) and cytosolic PLA 2 s (cPLA 2 s), do not require Ca 2+ for either translocation or activity. Some of the fi rst descriptions of iPLA 2 activity were in the mid-to late-1980s with the identifi cation of a plasmalogen-selective PLA 2 in Abstract Among the family of phospholipases A 2 (PLA 2 s) are the Ca 2+ -independent PLA 2 s (iPLA 2 s) and they are designated group VI iPLA 2 s. In relation to secretory and cytosolic PLA 2 s, the iPLA 2 s are more recently described and details of their expression and roles in biological functions are rapidly emerging. The iPLA 2 s or patatin-like phospholipases (PNPLAs) are intracellular enzymes that do not require Ca 2+ for activity, and contain lipase (GXSXG) and nucleotide-binding (GXGXXG) consensus sequences. Though nine PNPLAs have been recognized, PNPLA8 (membraneassociated iPLA 2 ␥ ) and PNPLA9 (cytosol-associated iPLA 2 ␤ ) are the most widely studied and understood. The iPLA 2 s manifest a variety of activities in addition to phospholipase, are ubiquitously expressed, and participate in a multitude of biological processes, including fat catabolism, cell differentiation, maintenance of mitochondrial integrity, phospholipid remodeling, cell proliferation, signal transduction, and cell death. As might be expected, increased or decreased expression of iPLA 2 s can have profound effects on the metabolic state, CNS function, cardiovascular performance, and cell survival; therefore, dysregulation of iPLA 2 s can be a critical factor in the development of many diseases. This review is aimed at providing a general framework of the current understanding of the iPLA 2 s and discussion of the potential mechanisms of action of the iPLA 2 s and related involved lipid mediators. -Ramanadham, S

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“…The relevance of this SNP in conferring human susceptibility to NASH and fibrosis progression has been shown in several studies as illustrated by an Italian study in 253 patients with NAFLD (28). Furthermore, it has been reported that the association between the I148M variant of PNPLA3 and serum levels of liver enzymes was associated with the size of the abdominal fat depot and high dietary carbohydrate and sugar consumption (29,30).…”

Section: Genetic Susceptibilitymentioning

confidence: 98%

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

2016

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Increased hepatic fat in overweight Hispanic youth influenced by interaction between genetic variation in PNPLA3 and high dietary carbohydrate and sugar consumption

Cited by 180 publications

References 27 publications

Added sugar intake and metabolic syndrome in US adolescents: cross-sectional analysis of the National Health and Nutrition Examination Survey 2005–2012

Added sugar intake and metabolic syndrome in US adolescents: cross-sectional analysis of the National Health and Nutrition Examination Survey 2005–2012

Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

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