Increasing Dietary alpha-linolenic acid enhances tissue levels of long-chain n-3 PUFA when linoleic acid intake is low in hamsters.

BACKGROUND/AIMS: We tested whether feeding hamsters diets varying in alpha-linolenic acid (ALA) content and low in linoleic acid (LA) could increase the tissue levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) to the same extent as a fish oil-supplemented diet. METHODS: For 5 weeks, 60 hamsters were fed 1 of the following 5 diets containing 2% of total dietary energy (TE) as LA and either 0.5% (diet A), 1% (diets B and E), 2% (diet C), or 4% (diet D) ALA of TE, so that the ratio of LA/ALA was 4:1, 2:1, 1:1, or 1:2. Diet E was supplemented with fish oil at the level of 0.2% of total energy intake. At the end of the study, overnight-fasted hamsters were sacrificed, and blood and tissues were collected. RESULTS: Tissue levels of ALA, EPA, DPA, and DHA rose in proportion to the increase in the dietary ALA level (p < 0.01); however, the levels of DHA reached a plateau at ALA intakes above 1% (p < 0.01). These changes were accompanied by decreases in arachidonic acid with or without increases in LA levels (p < 0.01). Hamsters fed diet D had similar or higher EPA, DPA, and DHA tissue levels to those fed diet E (p < 0.01). CONCLUSIONS: In hamsters, diets containing 4% energy as ALA and 2% energy as LA can increase the tissue levels of EPA, DPA, and DHA to the same extent as feeding 0.2% energy as fish oil.

Dietary starch type affects body weight and glycemic control in freely fed but not energy-restricted obese rats.

This study comprised 2 experiments that tested the hypothesis that a high-amylose starch diet (AMO) would improve body weight and glycemic control relative to a high-amylopectin starch diet (AMN) in rats with diet-induced obesity. After inducing obesity with a high-fat and -energy diet (Expt. 1), male Sprague-Dawley rats (n = 46) were divided into 4 groups and given free or restricted access to either an AMN or an AMO diet for 4 wk (Expt. 2). After 3 wk, rats from each group underwent an oral glucose tolerance test. At the end of the experiment, food-deprived rats were killed by decapitation and blood and tissues were collected for analyses. AMO led to lower total energy intake, weight gain, fat pad mass, and glycemic response but higher insulin sensitivity index than AMN, only when consumed ad libitum (AL) (P < 0.05). AMO led to higher glucagon-like peptide-1 and peptide YY responses and mRNA levels, independent of feeding paradigm (P < 0.01). The mRNA levels of key neuropeptide systems involved in the regulation of food intake were affected only by energy restriction. On the other hand, AMO resulted in higher expression of uncoupling protein-1 in the brown adipose tissue than AMN in rats that consumed food AL (P < 0.05). The effects of AMO appear to be mediated by its high resistant starch content rather than its glycemic index. We conclude that starches high in AMO can be effective in weight and glycemic control in obesity.