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Structural differences in dietary fatty acids modify their rate of oxidation and effect on satiety, endpoints that may influence the development of obesity. This study tests the hypothesis that meals containing fat sources with elevated unsaturated fats will result in greater postprandial energy expenditure, fat oxidation, and satiety than meals containing fats with greater saturation. In a randomized, 5-way crossover design, healthy men and women (n = 23, age: 25.7 ± 6.6 years, BMI: 27.7 ± 3.8 kg/m2) consumed liquid meals containing 30 g of fat from heavy cream (HC), olive oil (OO), sunflower oil (SFO), flaxseed oil (FSO), and fish oil (FO). Energy expenditure and diet-induced thermogenesis (DIT) were determined by metabolic rate over a 240 min postprandial period. Serum concentrations of ghrelin, glucose, insulin, and triacylglycerol (TAG) were assessed. DIT induced by SFO was 5% lower than HC and FO (p = 0.04). Energy expenditure and substrate oxidation did not differ between fat sources. Postprandial TAG concentrations were significantly affected by fat source (p = 0.0001). Varying fat sources by the degree of saturation and PUFA type modified DIT but not satiety responses in normal to obese adult men and women.

Dietary n-3 polyunsaturated fatty acids (PUFA) influence postnatal brain growth and development. However, little data exist regarding the impacts of dietary n-3 PUFA in juvenile animals post weaning, which is a time of rapid growth. We tested the hypothesis that depleting dietary n-3 PUFA would result in modifications to the cerebellar transcriptome of juvenile rats. To test this hypothesis, three week old male rats (an age that roughly corresponds to an 11 month old child in brain development) were fed diets containing either soybean oil (SO) providing 1.1% energy from &alpha, linolenic acid (ALA, 18:3n-3, ALA-sufficient) or corn oil (CO) providing 0.13% energy from ALA (ALA-deficient) for four weeks. Fatty acids (FAs) in the cerebellum were analyzed and revealed a 4-fold increase in n-6 docosapentaenoic acid (DPA, 22:5n-6), increases in arachidonic acid (AA, 20:4n-6) and docosatetraenoic acid (DTA, 22:4n-6), but no decrease in docosahexaenoic acid (DHA, 22:6n-3), in animals fed CO versus SO. Transcript abundance was then characterized to identify differentially expressed genes (DEGs) between the two diets. Upper quartile (UQ) scaling and transcripts per million (TPM) data normalization identified 100 and 107 DEGs, respectively. Comparison of DEGs from the two normalization methods identified 70 genes that overlapped, with 90% having abundance differences less than 2-fold. Nr4a3, a transcriptional activator that plays roles in neuroprotection and learning, was elevated over 2-fold from the CO diet. These data indicate that expression of Nr4a3 in the juvenile rat cerebellum is responsive to dietary n-3 PUFA, but additional studies are needed clarify the neurodevelopmental relationships between n-3 PUFA and Nr4a3 and the resulting impacts.

Metallothioneins (MTs) perform important regulatory and cytoprotective functions in tissues including the brain. While it is known that energy restriction (ER) and dietary n-3 polyunsaturated fatty acid (PUFA) deficiency impact postnatal brain growth and development, little data exist regarding the impact of undernutrition upon MT expression in growing animals. We tested the hypothesis that ER with and without dietary n-3 PUFA deficiency reduces MT expression in juvenile rats. ER rats were individually pair-fed at 75% of the ad libitum (AL) intake of control rats provided diets consisting of either soybean oil (SO) that is α-linolenic acid (ALA; 18:3n-3) sufficient or corn oil (CO; ALA-deficient). Fatty acids (FA) and metal concentrations of liver and brain regions were analyzed. Tissue expression of MTs (Mt1-3) and modulators of MT expression including glucocorticoid receptors (Nr3c1 and Nr3c2) and several mediators of thyroid hormone regulation (Dio1-3, Mct8, Oatp1c1, Thra, and Thrb) were measured. Plasma corticosterone and triiodothyronine levels were also evaluated. ER, but not metal deficiency, reduced Mt2 expression in the cerebellum (50%) and cerebral cortex (23%). In liver, a reduction in dietary n-3 PUFA reduced Mt1, Mt2, Nr3c1, Mct8, and Thrb. ER elevated Nr3c1, Dio1, and Thrb and reduced Thra in the liver. Given MT’s role in cellular protection, further studies are needed to evaluate whether ER or n-3 PUFA deficiency may leave the juvenile brain and/or liver more susceptible to endogenous or environmental stressors.

Current US federal dietary guidance recommends regular consumption of seafood (fish + shellfish) to promote health, however, little is known about how well Americans meet the guideline, particularly population subgroups that may be at risk for inadequate intake. The purposes of this study were to describe the prevalence of seafood consumption and, among consumers, the amounts of seafood eaten by sex, age group, income and education level, and race-ethnicity. Data from 15,407 adults aged 19+ participating in the 2005–2010 National Health and Nutrition Examination Surveys were analyzed using methods to account for sporadic intake of seafood. Over 80% of Americans reported consuming any seafood over the past 30 days, 74% reported consuming fish, and 54% reported eating shellfish. The percentages varied by socio-demographic group. Younger age and lower income and education levels were associated with lower odds of being a seafood consumer (p &lt, 0.0001). Among those who reported eating seafood, the average amount eaten of any seafood was 158.2 ± 5.6 g/week. Among seafood consumers, women and individuals of lower age and education levels consumed less seafood. Approximately 80%–90% of seafood consumers did not meet seafood recommendations when needs were estimated by energy requirements. A great deal of work remains to move Americans toward seafood consumption at current recommended levels.

Increasing fish consumption is recommended for intake of omega-3 (n-3) fatty acids and to confer benefits for the risk reduction of cardiovascular disease (CVD). Most Americans are not achieving intake levels that comply with current recommendations. It is the goal of this review to provide an overview of the issues affecting this shortfall of intake. Herein we describe the relationship between fish intake and CVD risk reduction as well as the other nutritional contributions of fish to the diet. Currently recommended intake levels are described and estimates of fish consumption at a food disappearance and individual level are reported. Risk and benefit factors influencing the choice to consume fish are outlined. The multiple factors influencing fish availability from global capture and aquaculture are described as are other pertinent issues of fish nutrition, production, sustainability, and consumption patterns. This review highlights some of the work that needs to be carried out to meet the demand for fish and to positively affect intake levels to meet fish intake recommendations for CVD risk reduction.