scholarly journals Furthering the understanding of maternal obesity in nonalcoholic fatty liver disease

Hepatology ◽  
2013 ◽  
Vol 58 (1) ◽  
pp. 4-5 ◽  
Author(s):  
Miriam B. Vos
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Nonalcoholic Fatty Liver

scholarly journals Oxidative stress and altered lipid homeostasis in the programming of offspring fatty liver by maternal obesity

2014 ◽  
Vol 307 (1) ◽  
pp. R26-R34 ◽  
Author(s):  
Maria Z. Alfaradhi ◽  
Denise S. Fernandez-Twinn ◽  
Malgorzata S. Martin-Gronert ◽  
Barbara Musial ◽  
Abigail Fowden ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Later Life ◽  
Metabolic Complications ◽  
Nonalcoholic Fatty Liver

Changes in the maternal nutritional environment during fetal development can influence offspring's metabolic risk in later life. Animal models have demonstrated that offspring of diet-induced obese dams develop metabolic complications, including nonalcoholic fatty liver disease. In this study we investigated the mechanisms in young offspring that lead to the development of nonalcoholic fatty liver disease (NAFLD). Female offspring of C57BL/6J dams fed either a control or obesogenic diet were studied at 8 wk of age. We investigated the roles of oxidative stress and lipid metabolism in contributing to fatty liver in offspring. There were no differences in body weight or adiposity at 8 wk of age; however, offspring of obese dams were hyperinsulinemic. Oxidative damage markers were significantly increased in their livers, with reduced levels of the antioxidant enzyme glutathione peroxidase-1. Mitochondrial complex I and II activities were elevated, while levels of mitochondrial cytochrome c were significantly reduced and glutamate dehydrogenase was significantly increased, suggesting mitochondrial dysfunction. Offspring of obese dams also had significantly greater hepatic lipid content, associated with increased levels of PPARγ and reduced triglyceride lipase. Liver glycogen and protein content were concomitantly reduced in offspring of obese dams. In conclusion, offspring of diet-induced obese dams have disrupted liver metabolism and develop NAFLD prior to any differences in body weight or body composition. Oxidative stress may play a mechanistic role in the progression of fatty liver in these offspring.

scholarly journals Developmental Programming of Nonalcoholic Fatty Liver Disease: The Effect of Early Life Nutrition on Susceptibility and Disease Severity in Later Life

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Minglan Li ◽  
Clare M. Reynolds ◽  
Stephanie A. Segovia ◽  
Clint Gray ◽  
Mark H. Vickers
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Early Life ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Later Life ◽  
Developmental Programming ◽  
Nonalcoholic Fatty Liver ◽  
Increased Risk

Nonalcoholic fatty liver disease (NAFLD) is fast becoming the most common liver disease globally and parallels rising obesity rates. The developmental origins of health and disease hypothesis have linked alterations in the early life environment to an increased risk of metabolic disorders in later life. Altered early life nutrition, in addition to increasing risk for the development of obesity, type 2 diabetes, and cardiovascular disease in offspring, is now associated with an increased risk for the development of NAFLD. This review summarizes emerging research on the developmental programming of NAFLD by both maternal obesity and undernutrition with a particular focus on the possible mechanisms underlying the development of hepatic dysfunction and potential strategies for intervention.

scholarly journals Transgenerational impact of maternal obesogenic diet on offspring bile acid homeostasis and nonalcoholic fatty liver disease

2019 ◽  
Vol 316 (4) ◽  
pp. E674-E686 ◽  
Author(s):  
Michael D. Thompson ◽  
Alaina Derse ◽  
Jeremie LA Ferey ◽  
Michaela Reid ◽  
Yan Xie ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Maternal Diet ◽  
Nonalcoholic Fatty Liver ◽  
Periportal Fibrosis

Studies show maternal obesity is a risk factor for metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) in offspring. Here we evaluated potential mechanisms underlying these phenotypes. Female C57Bl6 mice were fed chow or an obesogenic high-fat/high-sucrose (HF/HS) diet with subsequent mating of F1 and F2 female offspring to lean males to develop F2 and F3 generations, respectively. Offspring were fed chow or fibrogenic (high transfat, cholesterol, fructose) diets, and histopathological, metabolic changes, and bile acid (BA) homeostasis was evaluated. Chow-fed F1 offspring from maternal HF/HS lineages (HF/HS) developed periportal fibrosis and inflammation with aging, without differences in hepatic steatosis but increased BA pool size and shifts in BA composition. F1, but not F2 or F3, offspring from HF/HS showed increased steatosis on a fibrogenic diet, yet inflammation and fibrosis were paradoxically decreased in F1 offspring, a trend continued in F2 and F3 offspring. HF/HS feeding leads to increased periportal fibrosis and inflammation in chow-fed offspring without increased hepatic steatosis. By contrast, fibrogenic diet-fed F1 offspring from HF/HS dams exhibited worse hepatic steatosis but decreased inflammation and fibrosis. These findings highlight complex adaptations in NAFLD phenotypes with maternal diet.

scholarly journals Maternal obesity programs offspring nonalcoholic fatty liver disease by innate immune dysfunction in mice

Hepatology ◽  
2013 ◽  
Vol 58 (1) ◽  
pp. 128-138 ◽  
Author(s):  
Angelina Mouralidarane ◽  
Junpei Soeda ◽  
Clara Visconti-Pugmire ◽  
Anne-Maj Samuelsson ◽  
Joaquim Pombo ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Maternal Obesity ◽  
Immune Dysfunction ◽  
Innate Immune ◽  
Nonalcoholic Fatty Liver
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