Maternal Protein Restriction Altered Insulin Resistance and Inflammation-Associated Gene Expression in Adipose Tissue of Young Adult Mouse Offspring in Response to a High-Fat Diet.

Juhae Kim,Young Hye Kwon,Alee Choi

doi:10.3390/nu12041103

Juhae Kim, Young Hye Kwon + Show 1 more

Open Access

https://doi.org/10.3390/nu12041103

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Abstract

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.

Highlights

Nutritional status during fetal and neonatal periods can lead to adverse fetal growth and render offspring vulnerable to metabolic diseases in later life [1]
Epidemiological investigations on adult offspring conceived during the Dutch famine of 1944–1945 have highlighted the association between maternal undernutrition and later disease development [2]. It is not clear which nutritional deficiencies are responsible for causing offspring to become nutritionally ‘thrifty’, maternal protein intake has been extensively studied based on the pivotal roles of amino acids in fetal growth and production and secretion of insulin [3]
Each set of up-regulated and down-regulated differentially expressed genes (DEGs) was further submitted to Gene ontology (GO) enrichment analysis

Summary

Introduction

Nutritional status during fetal and neonatal periods can lead to adverse fetal growth and render offspring vulnerable to metabolic diseases in later life [1]. Epidemiological investigations on adult offspring conceived during the Dutch famine of 1944–1945 have highlighted the association between maternal undernutrition and later disease development [2]. It is not clear which nutritional deficiencies are responsible for causing offspring to become nutritionally ‘thrifty’, maternal protein intake has been extensively studied based on the pivotal roles of amino acids in fetal growth and production and secretion of insulin [3]. A maternal low-protein animal model has been mostly used to explore the underlying mechanisms of epidemiological findings, linking the early-life nutritional environment to the susceptibility to developing the metabolic syndrome in later life [4]. In a low-protein animal model, the fetus of dams

Results

Discussion

Conclusion