beta-carotene and Fatty-Liver

Much progress has been made in the understanding of the pathogenesis of alcoholic liver disease, resulting in improvement of treatment. Therapy must include correction of nutritional deficiencies, while taking into account changes of nutritional requirements. Methionine is normally activated to S-adenosylmethionine (SAMe). However, in liver disease, the corresponding enzyme is depressed. The resulting deficiencies can be attenuated by the administration of SAMe but not by methionine. Similarly, phosphatidylethanolamine methyltransferase activity is depressed, but the lacking phosphatidylcholine (PC) can be administrated as polyenylphosphatidylcholine (PPC). Chronic ethanol consumption increases CYP2E1, resulting in increased generation of toxic acetaldehyde and free radicals, tolerance to ethanol and other drugs, and multiple ethanol-drug interactions. Experimentally, PPC opposes CYP2E1 induction and fibrosis. Alcoholism and hepatitis C infection commonly co-exist, with acceleration of fibrosis, cirrhosis, and hepatocellular carcinoma. PPC is being tested clinically as a corresponding antifibrotic agent. Available antiviral agents are contraindicated in the alcoholic. Anti-inflammatory agents, such as steroids, may be selectively useful. Finally, anticraving agents, such as naltrexone or acamprosate, should be part of therapy.

Topics: beta Carotene; Ethanol; Fatty Liver; Hepatitis C; Hepatitis, Alcoholic; Humans; Lipid Peroxidation; Liver Cirrhosis; NAD; Nutritional Status; Oxidative Stress; Phosphatidylcholines; S-Adenosylmethionine; Vitamin A

Our aim was to study the effect of 9-cis beta-carotene-rich powder of the alga Dunaliella bardawil on lipid profile, atherogenesis, and liver steatosis in high-fat diet-fed LDL receptor knockout mice. In 4 sets of experiments, mice were distributed into the following groups: control, fed an unfortified diet; Dunaliella 50, fed a diet composed of 50% 9-cis and 50% all-trans beta-carotene; Dunaliella 25, fed a diet containing 25% 9-cis and 75% all-trans beta-carotene; beta-carotene-deficient Dunaliella, fed beta-carotene-deficient Dunaliella powder; and all-trans beta-carotene, fed a synthetic all-trans beta-carotene. All fortified diets contained 0.6% total beta-carotene. Algal 9-cis beta-carotene was absorbed by the mice and accumulated in the liver. Synthetic all-trans beta-carotene was not converted to 9-cis beta-carotene. Dunaliella 50 inhibited high-fat diet-induced plasma cholesterol elevation by 40-63% and reduced cholesterol concentrations in the atherogenic VLDL and LDL. Atherosclerotic lesion area in mice treated with Dunaliella 50 was 60-83% lower compared with mice fed the high-fat diet alone. beta-Carotene-deficient Dunaliella did not influence plasma cholesterol and atherogenesis, suggesting that beta-carotene is essential for a Dunaliella protective effect. Moreover, by administrating Dunaliella powder containing different levels of 9-cis and all-trans beta-carotene isomers, we found that the effect on plasma cholesterol concentration and atherogenesis is 9-cis-dependent. Dunaliella 50 also inhibited fat accumulation and inflammation in the livers of mice fed a high-fat diet, which was accompanied by reduced mRNA levels of inflammatory genes. These results in mice suggest that 9-cis beta-carotene may have the potential to inhibit atherogenesis in humans.

Topics: Animals; Atherosclerosis; beta Carotene; Cholesterol; Diet; Eukaryota; Fatty Liver; Hypercholesterolemia; Intestinal Absorption; Liver; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, LDL; Retinoids

The objective of the present study was to investigate vitamin A nutritional status in individuals with class III obesity through a biochemical indicator (retinol and beta-carotene serum levels), correlating these findings with non-alcoholic fatty liver disease (NAFLD) presence and its risk factors.. The studied population was composed of 145 patients with morbid obesity [body mass index, BMI > or = 40 kg/m(2)) of both sexes. Retinol and beta-carotene serum levels were assessed by high performance liquid chromatography. The cutoff values used for serum retinol and beta-carotene inadequacy were <1.05 micromol/l and < or =40 microg/dl, respectively. Insulin resistance (IR) was assessed through homeostasis model assessment index (HOMA) method. Biochemical parameters of liver enzymes, lipid profile, and glycemia were analyzed. Anthropometric measurements were conducted. NAFLD diagnosis was performed through magnetic resonance.. NAFLD prevalence in the group was 71%. An inadequacy of 11.3 and 41.7% of retinol and beta-carotene serum levels, respectively, was found when NAFLD was present. A significant correlation of serum retinol with albumin liver and total bilirubin was found. As regards beta-carotene, a positive correlation for HDL-c variable and a negative correlation for the HOMA-IR, weight, and BMI variables were observed. There was a significant association between IR presence and retinol and beta-carotene inadequacy.. The high inadequacy of retinol and beta-carotene nutritional status in the sample, with a higher inadequacy in those with NAFLD, suggests an increase in the utilization of vitamin A in this group related to the fight against the oxidative stress to what they are exposed to. The significant association between retinol and beta-carotene with IR supports the hypothesis that vitamin A may have a protector effect on IR pathogenesis.

Topics: Adult; Aged; beta Carotene; Body Mass Index; Cohort Studies; Fatty Liver; Female; Humans; Insulin Resistance; Male; Middle Aged; Nutritional Status; Obesity, Morbid; Risk Factors; Vitamin A

Some studies have indicated that the injury induced by the hepato- and pneumotoxin monocrotaline (MCT) is in part mediated by oxidation. Because beta-carotene is a potent antioxidant, we hypothesized that it would protect the lung and liver parenchyma against MCT-induced injury. Twenty rats were assigned randomly to four groups. All rats were fed a standard AIN93G diet with or without beta-carotene. After 1 week on the purified diets, half of the rats fed the control (standard) diet and half of the rats fed the beta-carotene-supplemented diet were injected subcutaneously with 60 mg MCT/kg body weight or its vehicle (water). All rats were sacrificed at 4 weeks. Histological examination showed that beta-carotene alone did not affect lung or liver structure. On the other hand, lungs of MCT-treated rats had severe focal pneumonia, extensive deposition of collagen in the septa, marked inflammation of the small arteries and arterioles, and arterialization of the small venules. Livers of MCT-treated rats showed some fatty infiltration and diffuse hemorrhages, more prominent sometimes in the centrilobular area and sometimes in the periportal region. Concomitant treatment with beta-carotene protected the lung parenchyma from the inflammatory reaction and the septal fibrosis, but did not prevent cardiac right ventricular hypertrophy and only slightly reduced the thickening of the wall of small arteries and arterioles. Incidence of steatosis and hemorrhages was decreased in the liver. These results indicate that MCT-induced pulmonary vascular remodeling occurs in the absence of inflammatory cell infiltration. Furthermore, beta-carotene prevented inflammation and protected the lung and liver parenchyma of MCT-treated rats.

Topics: Animals; Antidotes; Antioxidants; beta Carotene; Chemical and Drug Induced Liver Injury; Collagen; Diet; Fatty Liver; Hemorrhage; Hypertrophy, Right Ventricular; Liver; Lung; Lung Diseases; Male; Monocrotaline; Poisons; Rats; Rats, Sprague-Dawley