Background: Non-alcoholic fatty liver disease (NAFLD) is an important cause of liver disease burden worldwide. The gastrointestinal microbiota has a close relationship with the liver as the liver is most exposed to intestinal bacteria. Microbial manipulation is a potential and effective therapy as an alternative in the management of NAFLD/NASH. It has been found that probiotics prevent NAFLD/NASH. However, the study about the protective effect of probiotics on NAFLD/NASH is still limited. Objective: The objective of this study is to evaluate the effect of probiotics on liver histopathology Sprague Dawley rats which given high-fat high fructose (HFHFr) dietMethods: This study is a murine-model post-test-only control study group design. The samples were 21 Sprague Dawley male rats in 7 – 8 weeks of age and were divided into three groups. The Control Group (C) was provided with a standard chow diet for eight weeks. The Non-Probiotic (NP) group was given a High-Fat High Fructose (HFHFr) diet for eight weeks. The Probiotic group (P) was given a HFHFr diet for eight weeks, and a combination of HFHFr and probiotic supplementation consisted of Lactobacillus acidophilus, Bifidobacterium longum, and Streptococcus thermophilus for the next eight weeks. Histopathological samples were obtained from liver biopsy to assess steatosis, NAFLD activity score (NAS), and fibrosis stages. Wilcoxon test was done to analyze body weight before and after treatment. We analyzed the difference in histopathological results using the Mann-Whitney test.Results: We found a significant difference in NAFL and NAS Score between NP and P group. The P group was shown to have lower trends for NAFLD and NASH than the NP group, but not for fibrosis. There is no significant difference between pre and post-test body weight. Conclusion: Probiotics supplementation has a protective effect on liver histopathology against disturbances caused by the HFHFr diet.

Intestinal barrier function, critical for maintaining optimal gut health, is achieved primarily through mucins and tight junction proteins (i.e., zonula occludens-1 and occludin). An aberrant expression of these proteins results in increased paracellular permeability, leading to nonalcoholic steatohepatitis. Furthermore, enhanced expression of the inflammasome’s nucleotide-binding domain, leucine-rich repeat-containing protein 3 (cryopyrin), and Toll-like receptor 4 are also associated with nonalcoholic steatohepatitis. To understand the role of probiotic supplementation (Lactobacillus acidophilus, Bifidobacterium longum, and Streptococcus thermophilus) in rats on a high-fat, high-fructose diet with nonalcoholic steatohepatitis, the expression of occludin, cryopyrin, and Toll-like receptor 4 was evaluated. A comparison of the results between the control, nonalcoholic steatohepatitis group, and probiotic-treated nonalcoholic steatohepatitis groups showed (a) a lack of any significant difference in occluding expression (P = 0.724) and (b) a significant reduction in serum Toll-like receptor 4 (P = 0.012) and cryopyrin (P = 0.025) by probiotics. Furthermore, only one rat developed nonalcoholic steatohepatitis in the probiotic group, compared to six rats in the non-probiotic group. In conclusion, there were hepatoprotective effects of probiotic administration on high-fat, high-fructose diet-induced nonalcoholic steatohepatitis in Sprague-Dawley rats.

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. Histopathological diagnosis has been the gold standard for diagnosing and determining the severity of non-alcoholic steatohepatitis (NASH). However, this method is invasive, especially for diagnosing NASH in children. This research aimed to study the effect of probiotics on the De Ritis ratio, TGF-β levels, and histopathological changes in rats given High Fat, High Fructose (HFHFr) diet to look at the correlation between the De Ritis ratio and liver histopathology in diagnosing NAFLD. Method: Twenty-one male Sprague Dawley rats were included and divided into three groups. In the first group, as control only received a normal chow diet for eight weeks. The second group received an HFHFr diet for eight weeks, and the last group received HFHFr for eight weeks and a combination of HFHFr and probiotics for another eight weeks. After decapitation, we took 3 ml of serum from each rat to measure AST, ALT, and TGF-β. A 4 μm thick liver tissue slide was taken and stained with Hematoxylin – Eosin Stain for histopathological analysis. We used the Non-Alcoholic Steatohepatitis (NAS) Score for measuring liver damage progression. Results: De Ritis ratio and TGF-β level did not significantly differ between probiotic and non-probiotic groups (p = 0.064 and 0.383), but there was a significant NAS score difference (p = 0.001) in probiotic and non-probiotic groups. This was followed by a significant correlation between the De Ritis ratio and the NAS score (r = 0.613, p = 0.003). Conclusion: Probiotic supplementation alleviated liver damage caused by the HFHFr diet but did not successfully reduce the De Ritis ratio or improve TGF-β.

Background: Children with Down Syndrome (DS) have been associated with obesity. Leptin and adiponectin were also significant predictors of obesity and its comorbidity in DS. However, there was limited data regarding leptin and adiponectin in children with DS, particularly who were undernutrition. This study aimed to seek the role of leptin levels, adiponectin levels, and nutritional status in children with DS. Methods: This cross-sectional study was conducted on 40 children with DS aged 1 - 5 years. Height and weight were measured, and then the growth was interpreted using a DS growth chart. The Weight for Height Z-Score (WHZ) and Height for Age Z-Score (HAZ) were determined, and Mid-Upper Arm Circumference (MUAC) was measured. Leptin and adiponectin serum were analyzed using the enzyme-linked immunosorbent assay (ELISA) method. Mann-Whitney test was done to compare leptin and adiponectin levels in normal and wasted groups, while Spearman’s analysis was carried out to correlate laboratory results and anthropometric parameters. Results: Forty children participated (23 males, 17 females) with a median age was 25.5 months. Ten out of 40 children with DS (25%) were wasted and leptin was significantly lower in wasted compared to normal children. In addition, leptin was significantly correlated with WHZ (r = 0.415; p = 0.008), and MUAC (r = 0.427; p = 0.006), while adiponectin did not significantly correlate with those anthropometric variables in both wasted or non-wasted groups. Conclusion: Leptin is associated with WHZ and MUAC, and it decreases in wasted children with DS.