Translational insights on developmental origins of metabolic syndrome: Focus on fructose consumption

Abstract

Metabolic syndrome (MetS) is a highly prevalent complex trait despite recent advances in pathophysiology and pharmacological treatment. MetS can begin in early life by so-called the developmental origins of health and disease (DOHaD). The DOHaD concept offers a novel approach to prevent MetS through reprogramming. High fructose (HF) intake has been associated with increased risk of MetS. HF diet becomes one of the most commonly used animal model to induce MetS. This review discusses the maternal HF diet induced programming process and reprogramming strategy to prevent MetS of developmental origin, with an emphasis on: (1) an overview of metabolic effects of fructose consumption on MetS; (2) insight from maternal HF animal models on MetS-related phenotypes; (3) impact of HF consumption induces organ-specific transcriptome changes; and (4) application of reprogramming strategy to prevent maternal HF consumption-induced MetS. Research into the preventions and treatments of MetS that begin early in life will have a lifelong impact and profound savings in disease burden and financial costs.

Post-weaning exposure to high-sucrose diet induces early non-alcoholic fatty liver disease onset and progression in male mice: role of dysfunctional white adipose tissue

“…Many studies have used sugar-rich diets to evaluate metabolic programming of offspring through dams' exposure during gestation or lactation. 5,25 However, the post-weaning period is much less investigated, even being considered a critical window for developmental programming. 26 Moreover, most studies using mono-or disaccharide-rich diets have focused on total energy intake instead of the nutritional composition of such diets.…”

“…2,3 However, increasing evidence has supported that most metabolic disorders are programmed before adulthood, as consequence of environmental and nutritional insults occurring at early stages of life, such as gestation, lactation and childhood. 4,5 For instance, the worldwide epidemic growth of MetS has been directly associated with the exponential rise in sugar consumption during the last decades. 6,7 This issue is particularly important for infants and children, given that sugars are a major component of their diet, representing nearly 25% of total energy intake in the childhood.…”

“…8 Although the accountable mechanisms are barely known, they conceptually fall within the developmental origins of health and disease (DOHaD) theory, which is currently recognised as an important contributor to the epidemic MetS. 5 In the liver, MetS manifests as non-alcoholic fatty liver disease (NAFLD), whose prevalence reaches 25% of general population, but may affect up to 80% of obese subjects. 9 Ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), NAFLD has also been correlated to the elevated dietary intake of sugars.…”

Saliva biomarkers in neurological disorders: A “spitting image” of brain health?

“…Here, Lee et al. [24] review the effects of maternal fructose consumption on the development of MetS, and describe how exposure in utero or early life may bring about transcriptomic reprogramming that leaves individuals vulnerable to developing MetS in later life.…”

Fast quantification of short‐chain fatty acids in rat plasma by gas chromatography

“…In addition, high blood pressure may be associated with gut microbiota dysbiosis in both animals and humans, being specifically accompanied by a decrease in acetate‐ and butyrate‐producing bacteria (Yang et al., 2015). Our previous study has shown that maternal HFD can cause the elevation of blood pressure in adult offspring (Lee, Wu, Leu, & Tain, 2018) that is related to the changes of SCFAs (Hsu, Chang‐Chien, Lin, Hou, & Tain, 2019). Thus, by quantifying SCFAs levels, the characteristics of the gut microbiota can be indirectly evaluated.…”