Hyperglycemia and hypertriglyceridemia were associated with altered hepatic energy regulation in rat offspring from fructose fed dams

Abstract

Maternal nutritional stress acts to program metabolic syndrome in offspring. Dietary fructose is linked to metabolic disorders. We hypothesized that maternal fructose intake would impact energy metabolism in offspring. Future, we hypothesized that these effects would be magnified by postweaning fructose intake. Sprague‐Dawley rats (n=8) were fed either a control (C) or a 63% fructose diet (F). At birth pups were cross‐fostered onto dams fed diet C. Pups within maternal diet group were fed either C or F diet after weaning to give maternal × postweaning diet combinations: CC, CF, FC, and FF. Pups showed greater (P<0.1) blood glucose for FC and FF compared to CC and CF (51.7, 49.0, 45.7, 45.8±2.1 mg/dl) at 114 days of age. Hepatic fatty acid synthase (1.52, 1.90, 0.02, 0.01±0.44), carnitine palmitoyltransferase‐1 (3.9, 5.2, 1.4, 1.0±0.8), pyruvate carboxylase (0.36, 0.48, 0.04, 0.05±0.07) and PPAR? coactivator‐1a (2.3, 3.3, 1.7, 1.2±0.6) mRNA levels were elevated for FC and magnified for FF pups at 130 days compared to CC and CF. Serum triglyceride reflected similar changes (32.0, 43.5, 17.0, 29.2±7.5 mg/dl, FC, FF, CC, CF). Maternal fructose intake leads to hyperglycemia, hypertriglyceridemia and elevated expression of genes for hepatic energy metabolism in offspring; changes that are associated with metabolic syndrome. These effects are further magnified by postweaning fructose intake. Supported by NIH DK077581.