Abstract
We aimed to elucidate the effects of caloric and non-caloric sweeteners on liver lipid metabolism in rats using in vivo magnetic resonance spectroscopy (MRS) and to determine their roles in the development of liver steatosis. Wistar rats received normal chow and either normal drinking water, or solutions containing 13% (w/v) glucose, 13% fructose, or 0.4% aspartame. After 7 weeks, in vivo hepatic dietary lipid uptake and de novo lipogenesis were assessed with proton-observed, carbon-13-edited MRS combined with 13C-labeled lipids and 13C-labeled glucose, respectively. The molecular basis of alterations in hepatic liver metabolism was analyzed in detail ex vivo using immunoblotting and targeted quantitative proteomics. Both glucose and fructose feeding increased adiposity, but only fructose induced hepatic lipid accumulation. In vivo MRS showed that this was not caused by increased hepatic uptake of dietary lipids, but could be attributed to an increase in de novo lipogenesis. Stimulation of lipogenesis by fructose was confirmed by a strong upregulation of lipogenic enzymes, which was more potent than with glucose. The non-caloric sweetener aspartame did not significantly affect liver lipid content or metabolism. In conclusion, liquid fructose more severely affected liver lipid metabolism in rats than glucose, while aspartame had no effect.
Highlights
In 2013, an estimated 2.1 billion people were overweight or obese compared with 857 million people in 1980 [1]
The rats received the diets for a period of 7 weeks, after which each dietary group was divided into two subgroups: experimental group 1 (n = 9 per diet group) for magnetic resonance spectroscopy (MRS) measurements to determine dietary lipid uptake and for an oral glucose tolerance test (OGTT), and experimental group 2 (n = 6 per diet group) for MRS to determine de novo lipogenesis and for hepatic biochemical analyses
We showed that fructose and not glucose consumption led to an increase in hepatic lipid content, which was accompanied by an increased conversion of 13 C-labeled glucose to lipids in the liver as determined in vivo by MRS
Summary
In 2013, an estimated 2.1 billion people were overweight or obese compared with 857 million people in 1980 [1]. Nutrients 2017, 9, 476 consumption of fructose, as opposed to glucose, has been linked to the development of obesity, insulin resistance, dyslipidemia, and hepatic steatosis [6,7,8,9,10]. The metabolism of fructose to triose phosphate bypasses phosphofructokinase, a key regulatory step of glycolysis, allowing unregulated entry of fructose into glycolysis independent of hepatic energy status. This leads to an excess production of triose phosphates, which serve as precursors for de novo lipogenesis [9,11,12]
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