Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An aqueous extract of Platycodi radix inhibited the hydrolysis of triolein emulsified with phosphatidylcholine by pancreatic lipase in vitro and it reduced the elevation of rat plasma triacylglycerol level 2-4 h after oral administration of a lipid emulsion containing corn oil. These preliminary results suggested that the aqueous extract of Platycodi radix may inhibit the intestinal absorption of dietary fat by inhibiting its hydrolysis. Therefore, we examined the antiobesity activity of the aqueous extract of Platycodi radix by testing whether the extract prevented the obesity induced by feeding a high fat diet to mice for 8 wk. Body weights at 3-8 wk and the final parametrial adipose tissue weights were significantly lower in mice fed the high fat diet containing 5% aqueous extract of Platycodi radix than in the controls fed the high fat diet. The aqueous extract of Platycodi radix also significantly reduced hepatic triacylglycerol concentrations that were elevated in mice fed the high fat diet alone. Inulin, which is a major component of Platycodi radix, had no effect on the hydrolysis of triolein emulsified with phosphatidylcholine by pancreatic lipase in vitro, and did not prevent obesity or the fatty liver induced by the high fat diet. On the other hand, the total saponin fraction of the aqueous extract inhibited pancreatic lipase activity in vitro. Therefore, the antiobesity effect of the aqueous extract of Platycodi radix in mice fed a high fat diet may be due in part to the inhibition of intestinal absorption of dietary fat by the saponins of Platycodi radix.
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PMID:Platycodi radix affects lipid metabolism in mice with high fat diet-induced obesity. 1105 18

Inulin enzymatically synthesized from sucrose is a dietary component that completely escapes glucide digestion. Supplementing inulin to a high-fat and high-sucrose diet (HF) ameliorated hypertriglycemia and hepatic steatosis in 8-week-fed rats by suppressing elevated levels of serum triacylglycerols, fatty acids, and glucose, and the accumulation of hepatic triacylglycerols and fatty acids. Inulin intake prevented phenobarbital (PB)- and dexamethasone-induced liver injuries in the HF group. No significant alteration in the baseline expression of CYP2B, CYP2C11, CYP3A, and NADPH-cytochrome P450 (P450) reductase mRNAs and proteins was found. In contrast, baseline and PB-treated expressions of CYP2E1 mRNA were reduced in HF-fed rats. The induction of P450s in response to PB was affected by the nutritional status of the rats; mRNA levels of CYP2B1 and CYP3A1 after PB treatment, as assessed by quantitative real-time polymerase chain reaction analysis were reduced in the inulin-supplemented HF (HF+I) group, compared with those in the HF group. Western blot analysis detected the corresponding changes of CYP2B and CYP3A proteins. These alterations were correlated with changes in hepatic thiobarbituric acid-reactive substances. Furthermore, no significant difference in the expression of nuclear receptors constitutive androstane receptor, pregnane X receptor, and retinoid X receptor alpha and coactivator peroxisome proliferator-activated receptor-gamma coactivator 1alpha proteins was found in the hepatic nucleus between the HF and HF+I groups, but the expression of hepatocyte nuclear factor alpha (HNF4alpha) protein was significantly reduced in the HF+I group. Taken together, these results indicate that inulin intake ameliorates PB-induced liver injury, associated with a decline in lipid accumulation and PB-induced expression of CYP2B and CYP3A, which may be related by a reduction in the nuclear expression of HNF4alpha.
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PMID:Dietary inulin alleviates hepatic steatosis and xenobiotics-induced liver injury in rats fed a high-fat and high-sucrose diet: association with the suppression of hepatic cytochrome P450 and hepatocyte nuclear factor 4alpha expression. 1681 62

Inulin-type fructans have been tested for their capacity to modulate lipid and glucose metabolism in several animal models. Oligofructose (OFS) decreases food intake, fat mass development, and hepatic steatosis in normal and in obese rats; moreover, it exerts an antidiabetic effect in streptozotocin-treated rats and high-fat-fed mice. In most cases, the beneficial effects of OFS are linked to an increase of glucagon-like peptide-1 (GLP-1) level in the portal vein and of GLP-1 and proglucagon mRNA, its precursor, in the proximal colon. In this organ, OFS increases the number of GLP-1-positive L cells by promoting factors (Neurogenin 3 and NeuroD) involved in the differentiation of stem cells into L cells. The chronic administration of GLP-1 receptor antagonist exendin 9-39 totally prevents the beneficial effects of OFS (improved glucose tolerance, fasting blood glucose, glucose-stimulated insulin secretion, insulin-sensitive hepatic glucose production, and reduced body weight gain). Furthermore GLP-1 receptor knockout mice are completely insensitive to the antidiabetic actions of OFS. These findings highlight the potential interest of enhancing endogenous GLP-1 secretion by inulin-type fructans for the prevention/treatment of obesity and type 2 diabetes. Moreover, OFS is also able to modulate other gastrointestinal peptides (such as PYY and ghrelin) that could be involved in the control of food intake. Several studies in humans already support interest in OFS in the control of satiety, triglyceridemia, or steatohepatitis. The link with gut peptides production in humans remains to be proven.
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PMID:Modulation of glucagon-like peptide 1 and energy metabolism by inulin and oligofructose: experimental data. 1795

Polychlorinated biphenyls (PCBs) exposure is closely associated with the prevalence of metabolic diseases, including fatty liver and dyslipidemia. Emerging literature suggests that disturbance of gut microbiota is related to PCB126-induced metabolic disorders. However, the causal role of dysbiosis in PCB126-induced fatty liver is still unknown. To clarify the role of the gut microbiome in the detoxification of PCB126 in intestine or PCB126-induced toxicity in liver, mice were administrated with drinking water containing antibiotics (ampicillin, vancomycin, neomycin, and metronidazole) or Inulin. We showed that PCB126 resulted in significant hepatic lipid accumulation, inflammation, and fibrosis. PCB126, Antibiotics, and Inulin significantly affected the structure and shifted community membership of gut microbiome. 7 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways at level 2 and 39 KEGG pathways at level 3 were significantly affected. Antibiotics alleviated PCB126-induced fibrosis in the liver but increased inflammation. Inulin treatment ameliorated both inflammation and fibrosis in the liver of PCB126-treated mice. Neither Antibiotics nor Inulin had significant effect on PCB126-induced hepatic steatosis. The more specific intervention of gut microbiota is needed to alleviate PCB126-induced fatty liver. These data demonstrate that homeostasis of gut microbiota is critical for the defense against PCB126 toxicity and dysbiosis plays a fundamental role in the development of inflammation and fibrosis in liver of PCB126-treated mice.
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PMID:Homeostasis of gut microbiota protects against polychlorinated biphenyl 126-induced metabolic dysfunction in liver of mice. 3214 51