Hepatic fatty acid composition differs between chronic hepatitis C patients with and without steatosis.

Hepatic fatty acid (FA) composition may influence steatosis development in patients with chronic hepatitis C (CHC). In a cross-sectional study, we compared the hepatic FA profile in hepatitis C patients with (n = 9) and without (n = 33) steatosis (> or =5% of hepatocytes involved). FA composition of hepatic and RBC total lipids was measured by gas chromatography. Lipid peroxidation and antioxidants in liver and plasma, blood biochemistry, and nutritional status were also assessed. Patients with steatosis had more fibrosis, higher necroinflammatory activity of their hepatitis C infection, were more often infected with genotype 3, and had lower serum cholesterol. Monounsaturated FA in the liver were higher and trans FA were lower in patients with steatosis. Lower stearic acid and higher oleic acid in hepatic total lipids suggested higher Delta9-desaturase activity. alpha-Linolenic acid in the liver was higher and the ratios of long-chain PUFA:essential FA precursors were lower for (n-3) and (n-6) PUFA. Plasma vitamin C was lower in steatosis, but RBC FA composition and other parameters did not differ. We conclude that hepatic FA composition is altered in patients with hepatitis C and steatosis, probably due to modulation of enzymatic elongation and desaturation. Oxidative stress or nutritional status does not seem to play a predominant role for development of steatosis in CHC.

Seizure resistance in fat-1 transgenic mice endogenously synthesizing high levels of omega-3 polyunsaturated fatty acids.

N-3 polyunsaturated fatty acids (PUFA), derived from marine oils, have been shown to protect against various neurological diseases. However, very little is known about their potential anticonvulsant properties. The objective of the present study was to determine whether enrichment of brain lipids with n-3 PUFA inhibits seizures induced by pentylenetetrazol. We demonstrate that increased brain levels of n-3 PUFA in transgenic fat-1 male mice, which are capable of de novo synthesis of n-3 PUFA from n-6 PUFA, increases latency to seizure onset by 45%, relative to wildtype controls (p = 0.08). Compared with wildtype littermates, transgenic fat-1 mice have significantly (p < 0.05) higher levels of docosahexaenoic acid and total n-3 PUFA in brain total lipid extracts and phospholipids. Levels of brain docosahexaenoic acid were positively correlated to seizure latency (p < 0.05). These findings demonstrate that n-3 PUFA have anticonvulsant properties and suggest the possibility of a novel, non-drug dietary approach for the treatment of epilepsy.

Nutritional assessment and hepatic fatty acid composition in non-alcoholic fatty liver disease (NAFLD): a cross-sectional study.

BACKGROUND/AIMS: Low hepatic n-6 and n-3 polyunsaturated fatty acid (PUFA) may contribute to steatosis and steatohepatitis and can be affected by diet and oxidative stress. METHODS: Seventy-three patients referred for elevated liver enzymes and suspected NAFLD were assessed. Nutritional assessment, hepatic FA composition and oxidative stress were compared between these groups: simple steatosis (SS, n=18), steatohepatitis (NASH, n=38) and minimal findings on liver biopsy (MF, n=17). RESULTS: Patients with NASH had higher: BMI, central obesity, body fat, insulin resistance, dyslipidemia and lower physical activity compared to the other groups. They also had relatively lower hepatic n-3 and n-6 PUFA, a decrease in the ratio of metabolites to essential FA precursors for both n-6 and n-3 FA (eicosapentaenoic+docosahexaenoic/linolenic and arachidonic/linoleic acid ratios) and higher liver lipid peroxides with lower antioxidant power, when compared to MF. Overall, there was no significant difference between SS and NASH in FA composition. Self-reported dietary intake and red blood cell FA composition were similar among the three groups. CONCLUSIONS: NASH patients have more metabolic abnormalities. This is associated with higher oxidative stress and lower n-3 and n-6 PUFA in the liver in the absence of any differences in dietary FA composition.