Abstract
Non-alcoholic fatty liver diseases (NAFLDs) along with metabolic syndrome and Type-2 diabetes (T2D) are increasingly prevalent worldwide. Without an effective resolution, simple hepatic steatosis may lead to non-alcoholic steatohepatitis (NASH), characterized by hepatocyte damage, chronic inflammation, necrosis, fatty degeneration, and cirrhosis. The gut microbiome is vital for metabolic homeostasis. Conversely, dysbiosis contributes to metabolic diseases including NAFLD. Specifically, diet composition is critical for the enterotype of gut microbiota. We reasoned that green pigment rich in vegetables may modulate the gut microbiome for metabolic homeostasis. In this study, C57BL/6 mice under a high fat diet (HFD) were treated with sodium copper chlorophyllin (CHL), a water-soluble derivative of chlorophyll, in drinking water. After 28 weeks of HFD feeding, liver steatosis was established accompanied by gut microbiota dysbiosis, intestinal impairment, endotoxemia, systemic inflammation, and insulin resistance. Administration of CHL effectively alleviated systemic and intestinal inflammation and maintained tight junction in the intestinal barrier. CHL rebalanced gut microbiota in the mice under high fat feeding and attenuated hepatic steatosis, insulin resistance, dyslipidemia, and reduced body weight. Fecal flora transplants from the CHL-treated mice ameliorated steatosis as well. Thus, dietary green pigment or the administration of CHL may maintain gut eubiosis and intestinal integrity to attenuate systemic inflammation and relieve NASH.
Highlights
Non-alcoholic fatty liver diseases (NAFLDs) are defined as fatty liver disorders while the subjects are without significant alcohol consumption
About 20% of NAFLD in simple steatosis may further progress into non-alcoholic steatohepatitis (NASH), featured as persistent liver inflammation, hepatic fat degeneration, liver injury and necrosis, and hepatic fibrosis and cirrhosis, while some may eventually progress into hepatocellular carcinoma (HCC) (Pais et al, 2013; Calzadilla Bertot and Adams, 2016)
After 1 week of adaptation, the mice were randomly divided into three groups: (1) control group, by which mice were fed with ANI93 chow for 28 weeks, (2) high fat diet (HFD) group, of which 65% calorie in the chow was derived from animal fat, (3) high fat diet feeding plus chlorophyllin treatment (HFD+CHL), by which the mice under HFD feeding were treated with CHL in drinking water (30 mg/L) from the 17th week for consecutive 12 weeks (n = 8– 10 for each group)
Summary
Non-alcoholic fatty liver diseases (NAFLDs) are defined as fatty liver disorders while the subjects are without significant alcohol consumption. It is believed that NAFLD comes from complex interactions among excessive calorie intake, malnutrition, genetic susceptibility, environmental factors, and insulin resistance (Arab et al, 2017). The interaction of these risk factors may lead to abnormal lipid metabolism and excessive lipid accumulation in hepatocytes, which can further convert to NAFLD. Changing lifestyles, such as the control of body weight and diet balance, may delay or prevent the development of NASH from simple steatosis (Johnson and George, 2010; Vilar-Gomez et al, 2015). At present, there are numerous potential drugs in clinical trials for NASH treatment, none of them is approved by FDA or Abbreviations: CHL, Chlorophyllin; NAFLDs, non-alcoholic fatty liver diseases; NASH, non-alcoholic steatohepatitis; TNF-alpha, tumor necrosis factor-alpha
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