The researchers, working at State University of Rio de Janeiro, experimented with four groups of mice for 12 weeks. A first group got standard food [Control], and a second group was given extra fat in their food [High Fat; HF]. Two other groups of mice, of which one got the standard food [ASE] and the other extra fat [HF+ASE], were given acai extract via a tube every day.
The researchers used an extract made from the seeds of acai. This consisted mainly of anthocyanidin polymers. The human equivalent of the dose, based on a person weighing 80 kg, was about 2.4 g extract per day.
It doesn’t take a genius to work out that the animals on the high fat diet [HF] put on more weight than the ones on standard feed [Control]. Supplementation with acai [ASE] largely prevented the increase in bodyweight.
The mice in the high fat group built up bigger fat reserves, but the increase was noticeably lower in the high fat + acai group. What’s interesting in the table above is that the acai also had a significant effect on the size of the fat reserves in the mice that got standard feed. You don’t see an effect like this so often in animal studies. And that effect is really the reason why we’re writing this post.
The figures above indicate how acai probably works. The extract activated the enzyme AMPK.
The high fat feed increased the concentration of ‘bad cholesterol’ LDL in the blood. The acai supplement reduced the increase.
The figure above reveals how acai improved the cholesterol. The supplement boosted the synthesis of the transport proteins ABCG5 and above all ABCG8 in the liver. These proteins are responsible for removing cholesterol from the body via bile acid.
“Larger multicenter trials with longer term follow-up interventions in more homogenous chronic fatigue syndrome populations are warranted.”
Euterpe oleracea Mart.-Derived Polyphenols Protect Mice from Diet-Induced Obesity and Fatty Liver by Regulating Hepatic Lipogenesis and Cholesterol Excretion
The aim of this study was to investigate the effect of a polyphenol-rich Açaí seed extract (ASE, 300 mg/kg-1d-1) on adiposity and hepatic steatosis in mice that were fed a high-fat (HF) diet and its underlying mechanisms based on hepatic lipid metabolism and oxidative stress. Four groups were studied: C57BL/6 mice that were fed with standard diet (10% fat, Control), 10% fat + ASE (ASE), 60% fat (HF), and 60% fat + ASE (HF + ASE) for 12 weeks. We evaluated the food intake, body weight gain, serum glucose and lipid profile, hepatic cholesterol and triacyglycerol (TG), hepatic expression of pAMPK, lipogenic proteins (SREBP-1c, pACC, ACC, HMG-CoA reductase) and cholesterol excretion transporters, ABCG5 and ABCG8. We also evaluated the steatosis in liver sections and oxidative stress. ASE reduced body weight gain, food intake, glucose levels, accumulation of cholesterol and TG in the liver, which was associated with a reduction of hepatic steatosis. The increased expressions of SREBP-1c and HMG-CoA reductase and reduced expressions of pAMPK and pACC/ACC in HF group were antagonized by ASE. The ABCG5 and ABCG8 transporters expressions were increased by the extract. The antioxidant effect of ASE was demonstrated in liver of HF mice by restoration of SOD, CAT and GPx activities and reduction of the increased levels of malondialdehyde and protein carbonylation. In conclusion, ASE substantially reduced the obesity and hepatic steatosis induced by HF diet by reducing lipogenesis, increasing cholesterol excretion and improving oxidative stress in the liver, providing a nutritional resource for prevention of obesity-related adiposity and hepatic steatosis.