Fructose and metabolic syndrome

Ying Cheng Lin, Ta Jen Wu, Horng Yih Ou

Research output: Contribution to journalArticle

Abstract

There has been a marked increase in the consumption of dietary sugar during the past decades. Many randomized clinical trials and epidemiologic studies have shown that individuals who consume higher amounts of added sugar tend to gain more weight and have a higher risk of obesity, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease (CVD). Thus, the World Health Organization recommends those added sugar make up less than 10% of total calories. As for the mechanisms of sugar-related health hazard, increasing evidences suggested that fructose from sugar may play a pivotal role. Without negative feedback by energy status as seen in the metabolism of glucose, fructose is associated with increased de novo lipogenesis and the consumption of intracellular ATP. The fast depletion in ATP level further leads to accumulation of uric acid. Increased intracellular uric acid is associated with increased oxidative stress, insulin resistance, and hypertriglyceridemia. Malonyl CoA acts as a signal molecule in the satiety center in hypothalamus. Opposite to the effect of. glucose consumption, fructose metabolism leads to lowered malonyl CoA level and increased food intake. Based on the above reasons and the lack of nutritional values, a further reduction of sugar consumption to below 5% of total energy intake per day may have additional benefits.

Original languageEnglish
Pages (from-to)410-416
Number of pages7
JournalJournal of Internal Medicine of Taiwan
Volume25
Issue number6
Publication statusPublished - 2014 Dec 1

All Science Journal Classification (ASJC) codes

  • Internal Medicine

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