Maternal Broccoli Powder Intake Ameliorates Insulin Resistance and Inflammation via AMPK/mTOR Pathway in the Livers of High-Fructose-Fed Male Rat Offspring Exposed to Maternal Protein Restriction.

SCOPE Sub-optimal prenatal conditions such as maternal undernutrition during pregnancy and lactation posit high risks of adult metabolic diseases. High fructose intake causes insulin resistance and liver inflammation contributing to metabolic diseases. However, food-based preventive measure for these metabolic diseases in the offspring is under-researched. This study aims to investigate the effect of maternal broccoli powder (BP) intake during lactation on insulin resistance and liver inflammation in high-fructose-diet-fed adult male offspring exposed to maternal protein restriction. METHODS AND RESULTS Pregnant Wistar rats are provided normal protein (NP) or low protein (LP) diets and 0% or 0.74% BP-containing NP diets and 0% or 0.74% BP-containing LP diet during lactation. At weaning, offspring receiving water (W) or 10% fructose solution (Fr) are assigned into six groups: NP/NP/W, NP/NP/Fr, NP/NPBP/Fr, LP/LP/W, LP/LP/Fr, and LP/LPBP/Fr. At week 13, plasma insulin, macrophage infiltration, activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) phosphorylation, and autophagy flux markers are examined. LP/LPBP/Fr shows lower insulin levels and Homeostatic model assessment for insulin resistance (HOMA-IR) values than LP/LP/Fr. Liver macrophage infiltration are decreased in LP/LPBP/Fr. LP/LPBP/Fr exhibits upregulated AMPK phosphorylation, downregulated mTOR phosphorylation, and increased Microtubule-associated protein1A/1B-light chain 3B-II (LC3B-II) levels. CONCLUSION Maternal BP intake during lactation ameliorates insulin resistance and inflammation in the livers of adult offspring on a high-fructose diet from LP mothers.