Abstract
Background and AimsHigh protein (HP) diets are suggested to positively modulate obesity and associated increased prevalence of non-alcoholic fatty liver (NAFLD) disease in humans and rodents. The aim of our study was to detect mechanisms by which a HP diet affects hepatic lipid accumulation.MethodsTo investigate the acute and long term effect of high protein ingestion on hepatic lipid accumulation under both low and high fat (HF) conditions, mice were fed combinations of high (35 energy%) or low (10 energy%) fat and high (50 energy%) or normal (15 energy%) protein diets for 1 or 12 weeks. Effects on body composition, liver fat, VLDL production rate and the hepatic transcriptome were investigated.ResultsMice fed the HP diets displayed a lower body weight, developed less adiposity and decreased hepatic lipid accumulation, which could be attributed to a combination of several processes. Next to an increased hepatic VLDL production rate, increased energy utilisation due to enhanced protein catabolic processes, such as transamination, TCA cycle and oxidative phosphorylation was found upon high protein ingestion.ConclusionFeeding a HP diet prevented the development of NAFLD by enhancing lipid secretion into VLDL particles and a less efficient use of ingested calories.
Highlights
Within the context of the metabolic syndrome clear links are demonstrated between non-alcoholic fatty liver disease (NAFLD) and insulin resistance, type 2 diabetes mellitus and obesity [1,2]
NAFLD develops from hepatocellular steatosis via non-alcoholic steatohepatitis (NASH) to fibrosis and can eventually end up in irreversible cirrhosis [2,3]
Only mice fed the HFNP, but not those fed the HF-High protein (HP) diet, gained significantly more weight (p,0.0001) compared to the other groups during the entire dietary intervention period (Figure 1 B). This was accompanied by a high fat-induced larger epididymal adipose tissue mass after 12 weeks (p = 0.0003, Figure 1 C)
Summary
Within the context of the metabolic syndrome clear links are demonstrated between non-alcoholic fatty liver disease (NAFLD) and insulin resistance, type 2 diabetes mellitus and obesity [1,2]. NAFLD develops from hepatocellular steatosis via non-alcoholic steatohepatitis (NASH) to fibrosis and can eventually end up in irreversible cirrhosis [2,3]. In obese patients the prevalence of developing NASH or fibrosis was found to be even increased to 60–70% [5,6]. In addition to genetic predisposition, amongst others in apolipoprotein encoding genes [7,8], environment and lifestyle may affect the development of fatty liver. High protein (HP) diets are suggested to positively modulate obesity and associated increased prevalence of non-alcoholic fatty liver (NAFLD) disease in humans and rodents. The aim of our study was to detect mechanisms by which a HP diet affects hepatic lipid accumulation
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