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Inflammatory response in visceral fat tissue and liver is prenatally programmed: experimental research
L Bezpalko1, O Gavrilyuk, O Zayachkivska
1Department of Normal Physiology, Lviv National Medical University, Ukraine. ozayachkivska@gmail.com.
Insights
Maternal stress and high sugar/fat diets during pregnancy significantly alter offspring
Area of Science:
- Developmental programming and metabolic disorders
- Endocrinology and immunology of adipose tissue and liver
- Toxicology and nutritional science
Background:
- Developmental programming links early-life exposures to adult health outcomes.
- Maternal stress and diet are critical factors influencing offspring development.
- Adipose tissue and liver are key metabolic organs susceptible to programming.
Purpose of the Study:
- To investigate how maternal stress and diet impact offspring adipose tissue and liver.
- To analyze changes in pro- and anti-inflammatory cytokines and adipokines.
- To establish a rat model for studying nonalcoholic fatty liver disease development.
Main Methods:
- Pregnant rats exposed to stress (Pratt's model) and diets (HSD, HFD, HSFD).
- Analysis of visceral fat and liver histology in male offspring.
- Measurement of serum cytokines (IL-1β, GRO/CINC-1) and adipokines (leptin, adiponectin).
Main Results:
- Combined maternal stress and HSFD caused significant liver and visceral fat inflammation and cell reorganization.
- Offspring exposed to HSFD showed marked increases in IL-1β, GRO/CINC-1, and leptin, with decreased adiponectin.
- The leptin/adiponectin index was elevated across all diet groups, particularly in the HSFD group.
Conclusions:
- Maternal stress and diet profoundly influence offspring metabolic health and organ integrity.
- Cytokine profiles and the leptin/adiponectin index may serve as early biomarkers for metabolic liver disease.
- Prenatal interventions focusing on nutrition and stress management can prevent adult metabolic disorders.
Abstract:
To investigate the mechanisms of developmental programming we analyzed the effects of maternal stress and food intake on physiological activity of adipose tissue and hepatocellular organization in the offsprings. The experiments were conducted in nonlinear female rats (n=20) and their male offsprings (n=28). During their pregnancy female rats were exposed to social and emotional stress using Pratt's model, and nutritional insults: high sugar diet (HSD) with chronic access to 30% solution of saccharose in drinking water ad libitum, high fat diet (HFD) containing 45% calories from fat or their combination - high sugar and high fat diet (HSFD). The effects of maternal stress and nutrition on severity of visceral fat and liver changes were then examined in offsprings, along with changes in serum levels of the pro- and anti-inflammatory cytokines: IL-1b, IL-8 (in rats known as GRO/CINC-1), leptin and adiponectin, respectively. Maternal exposure to stress in combination with HSFD resulted in the most prominent changes in the offsprings: histological changes in the visceral fat tissue and liver with cell reorganization and signs of inflammation, 217% increase in IL-1β level, 99% increase in GRO/CINC-1 level, 79% increase in leptin level and 41% decrease in adiponectin level. The leptin/adiponectin index was elevated in all study groups and reached 158% in HSD group, 138% in HFD group and was two times higher in HSFD group vs control. The rat model used in this study provides novel insight into development of nonalcoholic fatty liver disease. Expressed pro- and anti-inflammatory cytokines may indicate early changes in liver and adipose tissue functioning and leptin/adiponectin index could be a novel non-invasive marker of metabolic-related liver alteration. Healthy nutrition and stress management during prenatal period may serve as a valid strategy to prevent liver and adipose tissue inflammation/alteration and metabolic disorders in adulthood.
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