Abstract
Background:We have previously reported that dietary ketogenic amino acids (KAAs) modulate hepatic de novo lipogenesis (DNL) and prevent hepatic steatosis in mice. However, the dependence of the metabolic phenotypes generated by KAA on the type of dietary lipid source remains unclear.Objective:The aim of this study was to assess the effect of KAA combined with different dietary lipid sources on hepatic DNL and tissue lipid partitioning in mice.Design:We compared three different KAA-supplemented diets, in which a portion of the dietary protein was replaced by five major essential amino acids (Leu, Ile, Val, Lys and Thr) in high-fat diets based on palm oil (PO), high-oleic safflower oil (FO) or soy oil (SO). To compare the effects of these diets in C57B6 mice, the differential regulation of DNL and dietary lipid partitioning due to KAA was assessed using stable isotopic flux analysis.Results:The different dietary oils showed strikingly different patterns of lipid partitioning and accumulation in tissues. High-PO diets increased both hepatic and adipose triglycerides (TG), whereas high-FO and high-SO diets increased hepatic and adipose TG, respectively. Stable isotopic flux analysis revealed high rates of hepatic DNL in high-PO and high-FO diets, whereas it was reduced in the high-SO diet. KAA supplementation in high-PO and high-FO diets reduced hepatic TG by reducing the DNL of palmitate and the accumulation of dietary oleate. However, KAA supplementation in the high-SO diet failed to reduce hepatic DNL and TG. Interestingly, KAA reduced SO-induced accumulation of hepatic linoleate and enhanced SO-induced accumulation of dietary oleate.Conclusions:Overall, the reduction of hepatic TG by KAA is dependent on dietary lipid sources and occurs through the modulation of DNL and altered partitioning of dietary lipids. The current results provide further insight into the underlying mechanisms of hepatic lipid reduction by amino acids.
Highlights
The rising prevalence of obesityFa major health concern worldwideFhas been linked to a number of cardiovascular and metabolic disorders, such as hypertension, insulin resistance, hyperlipidemia and, more recently, non-alcoholic fatty liver disease, known as hepatic steatosis.[1,2] Physical inactivity, dietary behavior and inherited predisposition are the predominant causes of excessive fat accumulation in 2 a high-protein diet may have beneficial effects on body fat maintenance by inducing satiety or reducing hepatic lipid deposition.[8]
In pre-high-fat diet (HFD) conditions, the high-ketogenic amino acid (KAA) diet reduced body weight gain (BWG) only in low-fat diet (LFD), but no clear reduction was seen in HFD
This study found that dietary lipids and amino acids reciprocally affect fat accumulation in mice through the regulation of de novo lipogenesis (DNL) and tissue lipid distribution
Summary
The rising prevalence of obesityFa major health concern worldwideFhas been linked to a number of cardiovascular and metabolic disorders, such as hypertension, insulin resistance, hyperlipidemia and, more recently, non-alcoholic fatty liver disease, known as hepatic steatosis.[1,2] Physical inactivity, dietary behavior and inherited predisposition are the predominant causes of excessive fat accumulation in 2 a high-protein diet may have beneficial effects on body fat maintenance by inducing satiety or reducing hepatic lipid deposition.[8]. Using gas chromatography–mass spectrometry (GC-MS)-based lipid profiling and stable isotopic metabolic flux analysis, we assessed the dependence of the effect of KAA on the type of dietary lipid in terms of both the regulation of hepatic DNL and the dietary lipid partitioning to tissues. Design: We compared three different KAA-supplemented diets, in which a portion of the dietary protein was replaced by five major essential amino acids (Leu, Ile, Val, Lys and Thr) in high-fat diets based on palm oil (PO), high-oleic safflower oil (FO) or soy oil (SO). To compare the effects of these diets in C57B6 mice, the differential regulation of DNL and dietary lipid partitioning due to KAA was assessed using stable isotopic flux analysis. Nutrition and Diabetes (2011) 1, e5; doi:10.1038/nutd.2011.1; published online 28 March 2011
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