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Background: Overnutrition in utero may increase offspring risk of nonalcoholic fatty liver disease (NAFLD), but the specific contribution of maternal diet quality during pregnancy to this association remains understudied in humans.
Objectives: This study aimed to examine the associations of maternal diet quality during pregnancy with offspring hepatic fat in early childhood (median: 5 y old, range: 4-8 y old).
Methods: Data were from 278 mother-child pairs in the longitudinal, Colorado-based Healthy Start Study. Multiple 24-h recalls were collected from mothers during pregnancy on a monthly basis (median: 3 recalls, range: 1-8 recalls starting after enrollment), and used to estimate maternal usual nutrient intakes and dietary pattern scores [Healthy Eating Index-2010 (HEI-2010), Dietary Inflammatory Index (DII), and Relative Mediterranean Diet Score (rMED)]. Offspring hepatic fat was measured in early childhood by MRI. Associations of maternal dietary predictors during pregnancy with offspring log-transformed hepatic fat were assessed using linear regression models adjusted for offspring demographics, maternal/perinatal confounders, and maternal total energy intake.
Results: Higher maternal fiber intake and rMED scores during pregnancy were associated with lower offspring hepatic fat in early childhood in fully adjusted models [Back-transformed β (95% CI): 0.82 (0.72, 0.94) per 5 g/1000 kcal fiber; 0.93 (0.88, 0.99) per 1 SD for rMED]. In contrast, higher maternal total sugar and added sugar intakes, and DII scores were associated with higher offspring hepatic fat [Back-transformed β (95% CI): 1.18 (1.05, 1.32) per 5% kcal/d added sugar; 1.08 (0.99, 1.18) per 1 SD for DII]. Analyses of dietary pattern subcomponents also revealed that lower maternal intakes of green vegetables and legumes and higher intake of "empty calories" were associated with higher offspring hepatic fat in early childhood.
Conclusions: Poorer maternal diet quality during pregnancy was associated with greater offspring susceptibility to hepatic fat in early childhood. Our findings provide insights into potential perinatal targets for the primordial prevention of pediatric NAFLD.
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http://dx.doi.org/10.1016/j.tjnut.2023.01.039 | DOI Listing |
Life Sci
September 2025
Department of Experimental Medical Science, Faculty of Medicine, Lund University, 221 84, Lund, Sweden; Wallenberg Center for Molecular Medicine, Faculty of Medicine, Lund University, 221 84, Lund, Sweden. Electronic address:
Aims: Experimental evidence suggests an important role for sphingosine-1-phosphate (S1P) and its generating enzymes sphingosine kinase 1/2 (SphK1/2) in obesity. We and others have shown that plasma S1P levels are elevated in obese mice and humans. Preclinical studies suggest that genetic SphK2 ablation in mice protects from age- and diet-induced obesity and metabolic dysfunction.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Shanxi Medical University, Taiyuan 030001, China. Electronic address:
Metabolic dysfunction-associated steatohepatitis (MASH) affects a large proportion of the global population and is widely regarded as the fastest growing cause of hepatocellular carcinoma. Currently, approved therapeutic strategies for MASH are limited. Therefore, this study used the Connectivity Map (CMap) database to identify a candidate compound for MASH, evaluate its efficacy in experimental models, and explore its mechanism of action.
View Article and Find Full Text PDFCell Metab
August 2025
Section of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA. Electronic address:
Diet and obesity contribute to insulin resistance and type 2 diabetes, in part via the gut microbiome. To explore the role of gut-derived metabolites in this process, we assessed portal/peripheral blood metabolites in mice with different risks of obesity/diabetes, challenged with a high-fat diet (HFD) + antibiotics. In diabetes/obesity-prone C57BL/6J mice, 111 metabolites were portally enriched and 74 were peripherally enriched, many of which differed in metabolic-syndrome-resistant 129S1/129S6 mice.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
September 2025
Department of Biological Sciences, The University of Texas at Dallas, Richardson, Texas. Electronic address:
Background & Aims: Binge drinking causes fat accumulation in the liver and is a known risk factor for more severe forms of alcohol-associated liver disease (ALD). Although adipocyte-released free fatty acids (FFA) have been shown to contribute to alcohol-induced liver damage, the signaling pathways that trigger lipolytic activity in adipose tissues following acute alcohol overconsumption is largely unknown. Notably, activation of sympathetic nerve-β3 adrenergic receptor (Adrb3) plays a central role in sustained adipocyte lipolysis.
View Article and Find Full Text PDFTransplant Cell Ther
September 2025
Division of Pharmacy, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Background: Pediatric patients undergoing hematopoietic stem cell transplant (HSCT) are at high risk for fungal infections including Candida, Aspergillus, and Mucorales necessitating the use of broad-spectrum antifungal agents such as posaconazole for prophylaxis and at times for treatment of invasive fungal infections. When first approved, posaconazole was limited to an immediate release oral suspension, which exhibited unreliable absorption dependent on co-administration with high fat meals. During HSCT, patients commonly have significant nausea, vomiting, and decreased enteral intake making this formulation particularly challenging.
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