A high-fat diet containing polyunsaturated fatty acids (PUFA: n-3 or n-6) given for 4 wk to 5-wk-old male Wistar rats induced a clear hyperglycemia (10.4 ± 0.001 mmol/l for n-6 rats and 10.1 ± 0.001 for n-3 rats) and hyperinsulinemia (6.6 ± 0.8 ng/ml for n-6 rats and 6.4 ± 1.3 for n-3 rats), signs of insulin resistance. In liver, both diets (n-3 and n-6) significantly reduced insulin receptor (IR) number, IR and IR substrate (IRS)-1 tyrosine phosphorylation, and phosphatidylinositol (PI) 3′-kinase activity. In contrast, in leg muscle, IR density, as determined by Western blotting, was not affected, whereas IR and IRS-1 tyrosine phosphorylation in response to insulin treatment was restored in animals fed with n-3 PUFA to normal; in n-6 PUFA, the phosphorylation was depressed, as evidenced by Western blot analysis using specific antibodies. In addition, PI 3′-kinase activity and GLUT-4 content in muscle were maintained at normal levels in rats fed with n-3 PUFA compared with rats fed a normal diet. In rats fed with n-6 PUFA, both PI 3′-kinase activity and GLUT-4 content were reduced. Furthermore, in adipose tissue and using RT-PCR, we show that both n-3 and n-6 PUFA led to slight or strong reductions in p85 expression, respectively, whereas GLUT-4 and leptin expression was depressed in n-6 rats. The expression was not affected in n-3 rats compared with control rats. In conclusion, a high-fat diet enriched in n-3 fatty acids maintained IR, IRS-1 tyrosine phosphorylation, and PI 3′-kinase activity and total GLUT-44 content in muscle but not in liver. A high-fat diet (n-3) partially altered the expression of p85 but not that of GLUT-4 and leptin mRNAs in adipose tissue.
Background: Factors other than dietary fatty acids could be involved in the variability observed in blood docosahexaenoate (22:6nϪ3) and arachidonate (20:4nϪ6) status in formula-fed infants. Objective: We considered the 22:6nϪ3 and 20:4nϪ6 status at birth to be one of these factors and studied its influence on postnatal changes in term infants fed 4 different diets. Design: The blood phospholipid composition was determined at birth and on day 42 of feeding in 83 term infants fed breast milk, nonsupplemented formula, or 2 different 22:6nϪ3-supplemented formulas. Relations between 22:6nϪ3 and 20:4nϪ6 status at birth and their relative postnatal changes, calculated by the difference between status at the end of the feeding period (6 wk of age) and at birth, were assessed. Results: Postnatal changes in the plasma and erythrocyte phospholipids 22:6nϪ3 and 20:4nϪ6 were negatively related to their respective concentrations at birth (P < 0.01) and the slopes of the regression lines were not significantly affected by the type of milk ingested. Adjusted mean values for phospholipid 22:6nϪ3 in nonsupplemented-formula-fed infants and for 20:4nϪ6 in formula-fed infants decreased significantly more than they did in the other infant groups (P < 0.02). The status at birth and the type of milk ingested explained 33-64% and 7-47%, respectively, of the variability in postnatal changes. Conclusions: The status of 22:6nϪ3 and 20:4nϪ6 at birth in term infants is one of the major determinants of postnatal changes in these fatty acids. This finding indicates that research is required to characterize environmental, genetic, or both factors, which, in addition to maternal diet, could influence fatty acid status at birth.Am J Clin Nutr 1999;70:292-8.
This amino acids solution is efficaciously utilized for protein synthesis in CAPD patients with no effect on protein breakdown. The concomitant ingestion of a carbohydrate-lipid meal inhibits protein breakdown and reinforces a positive effect of the amino acids solution on protein balance.
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