Pathophysiological basis for compromised health beyond generations: role of maternal high-fat diet and low-grade
1Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign.
Insights
Maternal high-fat diet induces chronic inflammation in offspring, increasing susceptibility to obesity and related diseases. This review explores inflammation
Area of Science:
- Developmental Biology
- Nutritional Science
- Immunology
Background:
- Maternal high-fat diet (HFD) exposure during development programs offspring for disease.
- HFD-induced chronic low-grade inflammation affects multiple fetal organs and systems.
- Inflammation is linked to obesity, cardiovascular disease, fatty liver disease, and brain damage.
Purpose of the Study:
- To review how maternal HFD impacts offspring inflammatory status.
- To summarize the pathogenic effects of this inflammation on offspring development.
- To highlight the need for research into epigenetic regulation of inflammation by maternal HFD.
Main Methods:
- Literature review of studies on maternal HFD and offspring inflammation.
- Analysis of research linking inflammation to developmental outcomes.
- Identification of knowledge gaps in epigenetic mechanisms.
Main Results:
- Maternal HFD consistently triggers inflammatory responses in offspring.
- Inflammation is a key mediator of HFD-induced developmental pathologies.
- Limited data exists on epigenetic modifications by maternal HFD.
Conclusions:
- Maternal HFD-induced inflammation poses significant risks to offspring health.
- Further research is crucial to understand epigenetic regulation and develop interventions.
- This review provides a foundation for future mechanistic and clinical studies.
Abstract:
Early exposure to a fat-enriched diet programs the developmental profile and thus is associated with disease susceptibility in subsequent generations. Chronic low-grade inflammation, resulting from maternal high-fat diet, is activated in the fetal environment and in many organs of offspring, including placenta, adipose, liver, vascular system and brain. The prevalence of an inflammatory response is highly associated with obesity incidence, cardiovascular diseases, nonalcoholic fatty liver disease and brain damage. Substantial studies using high-fat model have consistently demonstrated the incidence of such inflammatory reactions; however, the potential contribution of active inflammation toward the physiological outcomes and developmental diseases is neither discussed in depth nor systemically integrated. Therefore, we aim to summarize the current findings in regards to how a maternal high-fat diet influences the inflammatory status, and probable pathogenic effects on the offspring. More importantly, since limited research has been conducted to reveal the epigenetic regulation of these inflammatory markers by maternal high-fat diet, we sincerely hope that our review will not only outline the pathophysiological relevance of inflammation but also identify a future direction for mechanistic investigation and clinical application.
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