Maternal High-Fructose Intake Activates Myogenic Program in Fetal Brown Fat and Predisposes Offspring to Diet-Induced Metabolic Dysfunctions in Adulthood

Abstract

Excess dietary fructose intake is a major public health concern due to its deleterious effect to cause various metabolic and cardiovascular diseases. However, little is known about the effects of high-fructose consumption during pregnancy on offspring metabolic health in adulthood. Here, we show that maternal consumption of 20% (w/v) fructose water during pregnancy does not alter the metabolic balance of offspring with a chow diet, but predisposes them to obesity, fatty liver, and insulin resistance when challenged by a high-fat diet. Mechanistically, diet-induced brown fat reprogramming and global energy expenditure in offspring of fructose-fed dams are impaired. RNA-seq analysis of the fetal brown fat tissue reveals that the myogenic pathway is predominantly upregulated in the fructose-treated group. Meanwhile, circulating fructose level is found to be significantly elevated in both fructose-fed dams and their fetuses. Importantly fructose gavage also acutely activates the myogenic program in mice brown fat. Together, our data suggest that maternal high-fructose intake impairs fetal brown fat development, resultantly attenuates diet-induced thermogenesis and causes metabolic disorders in adult offspring probably through inducing myogenic signature in brown fat at the fetal stage.

Effects of Dietary Inclusion of β-Hydroxy-β-Methylbutyrate on Growth Performance, Fat Deposition, Bile Acid Metabolism, and Gut Microbiota Function in High-Fat and High-Cholesterol Diet-Challenged Layer Chickens

“…H&E staining was performed as described previously [ 24 ]. Briefly, the livers and adipose tissues of the layers were dissected and fixed in tissue-fixing solutions overnight at 4 °C.…”

Effect of water-soluble polysaccharides from Morchella esculenta on high-fat diet-induced obese mice: changes in gut microbiota and metabolic functions

“…2F), which helps improve energy metabolism. 43 This phenomenon was not caused by differences in the dietary energy intake (Fig. S1A †).…”

Maternal monosaccharide diets evoke cognitive, locomotor, and emotional disturbances in adolescent and young adult offspring rats

“…Moreover, Sprague–Dawley offspring rats had a higher postnatal body weight after consuming the maternal 13 or 40% water FRU solution ( 46 ). Additionally, in C57BL/6J dam mice, a 20% (w/v) FRU solution increased plasma triglycerides and cholesterol levels during pregnancy and predisposed offspring to obesity and metabolic dysfunction by postnatal high-fat diet intake ( 47 ). In the same mouse strain, pups after maternal GLU or FRU intake before and during pregnancy had less fetal body weight that was enhanced after weaning and correlated with fat mass gain compared to control offspring ( 48 , 49 ).…”