A new British Journal of Nutrition article has revealed that oral supplementation with sodium butyrate (SoB) can protect mice from developing early signs of non-alcoholic fatty liver disease.
Nowadays, Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. Non-alcoholic fatty liver disease includes a wide spectrum of liver diseases from simple inflammation in hepatic cells to steatohepatitis and even liver cirrhosis in the more advanced stages.
Although the exact mechanism of this disease is not well understood, some etiologies have been known as causative factors contributing to the development of NAFLD; insulin resistance is one of the most common causes; chronic hypertension, metabolic syndrome, hypertriglyceridemia, rapid weight gain or rapid weight loss can be of other important contributing causes.
Beside these factors, new studies have revealed that alterations in the barrier function of the gut, leading to increased permeation of intestinal bacterial endotoxin, may be another important factor in the development of NAFLD.
While measures such as gradual weight loss, control of diabetes and hypertension, and supplementation with vitamin E for selected groups are introduced as some methods of treating NAFLD, a well-proven treatment is still lacking.
Recent studies have worked on the protective effects of the oral supplement sodium butyrate (SoB) on the development of NAFLD in animal models, and they revealed that Sodium Butyrate can improve intestinal permeability, thus protecting the liver from intestinal bacterial endotoxins.
The present article, published in the British Journal of Nutrition, has studied the molecular mechanisms involved in the protective effects of an oral supplementation of SoB on the development of NAFLD.
The study conducted on 6-week old male mice models. Models were randomly assigned to three groups of controls, mice fed with a fructose-enriched diet, or mice fed with fructose-enriched diet plus sodium butyrate.
Markers of liver damage, intestinal barrier function, glucose metabolism, toll-like receptor-4 (TLR-4) (this protein is responsible for activating the innate immune system) and melatonin signaling were determined in mice. Differentiated human carcinoma colon-2 cells (Caco-2) (these cells are used to predict the effects of oral intake on the behaviour of intestinal cells in laboratory settings) were also examined.
Results showed that, despite having no effects on markers of intestinal function, glucose metabolism or body weight, SoB supplementation significantly reduced triglyceride accumulation and inflammation in the liver.
Treatment with SoB also increased melatonin levels and expression of enzymes involved in melatonin synthesis in duodenal tissue and Caco-2 cells.
With results suggesting SoB has effects on the melatonin levels in duodenal cells and it plays a role in attenuating development of NAFLD in mice, authors have recommended more studies to be done to delineate the effects of SoB on NAFLD on humans.
Written By: Nima Makhdami, M.D.