The Effect of Dietary Fish Oil in addition to Lifestyle Counselling on Lipid Oxidation and Body Composition in Slightly Overweight Teenage Boys

Objective. n-3 long-chain polyunsaturated fatty acids (LCPUFAs) have shown potential to increase lipid oxidation and prevent obesity. Subjects. Seventy-eight boys aged 13–15 y with whole-body fat% of 30 ± 9% were randomly assigned to consume bread with fish oil (FO) (1.5 g n-3 LCPUFA/d) or vegetable oil for 16 weeks. All boys were counselled to improve diet and exercise habits. Results. Lifestyle counselling resulted in decreased sugar intake but did not change the physical activity level. Whole-body fat% decreased 0.7 ± 2.5% and 0.6 ± 2.2%, resting metabolic rate after the intervention was 7150 ± 1134 kJ/d versus 7150 ± 1042 kJ/d, and the respiratory quotient was 0.89 ± 0.05 versus 0.88 ± 0.05, in the FO and control group, respectively. No group differences were significant. Conclusion. FO-supplementation to slightly overweight teenage boys did not result in beneficial effects on RMR, lipid oxidation, or body composition

Fish intake, erythrocyte n-3 fatty acid status and metabolic health in Danish adolescent girls and boys

Marinen-3 long-chain PUFA (n-3 LCPUFA) may have a beneficial effect on several aspects of the metabolic syndrome (dyslipidaemia, insulin resistance, hypertension and abdominal obesity). The metabolic syndrome is increasing in prevalence during adolescence, but only few studies have investigated the effects ofn-3 LCPUFA in adolescence. The present study examines associations between fish intake (assessed by a 7 d pre-coded food diary), erythrocyte (RBC) DHA status (analysed by GC) and metabolic syndrome measures (anthropometry, blood pressure and plasma lipids, insulin and glucose) in 109 17-year-old children from the Copenhagen Birth Cohort Study. Of the children, 8 % were overweight or obese and few showed signs of the metabolic syndrome, but all the metabolic syndrome variables were correlated. Median fish intake was 10·7 (interquartile range 3·6–21·2) g/d. Boys tended to have a higher fish intake (P = 0·052), but girls had significantly higher RBC levels of DHA (P = 0·001). Sex and fish intake explained 37 % of the variance in RBC-DHA (P &lt; 0·001). After adjusting for confounders, high DHA status was found to be significantly correlated with higher systolic blood pressure (P = 0·014) and increased fasting insulin (P = 0·018), but no adverse association was observed with the mean metabolic syndromez-score. Overall, the present study showed the expected association between fish intake and RBC-DHA, which in contrast to our expectations tended to be associated with a poorer metabolic profile. Whether these results reflect the physiological function ofn-3 LCPUFA, lifestyle factors associated with fish intake in Denmark, or mere chance remains to be investigated.</jats:p

N-glycosylation proteome enrichment analysis in kidney reveals differences between diabetic mouse models

Background: Diabetic nephropathy (DN) is a late complication in both type 1 diabetes mellitus (T1DM) and T2DM. Already at an early stage of DN morphological changes occur at the cell surface and in the extracellular matrix where the majority of the proteins carry N-linked glycosylations. These glycosylated proteins are highly important in cell adhesion and cell-matrix processes but not much is known about how they change in DN or whether the distinct etiology of T1DM and T2DM could have an effect on their abundances. Method: We enriched for the N-glycosylated kidney proteome in db/db mice dosed with insulin or vehicle, in streptozotocin-induced (STZ) diabetic mice and healthy control mice dosed with vehicle. Glycopeptides were analyzed with label-free shotgun mass spectrometry and differential protein abundances identified in both mouse models were compared using multivariate analyses. Results: The majority of the N-glycosylated proteins were similarly regulated in both mouse models. However, distinct differences between the two mouse models were for example seen for integrin-β1, a protein expressed mainly in the glomeruli which abundance was increased in the STZ diabetic mice while decreased in the db/db mice and for the sodium/glucose cotransporter-1, mainly expressed in the proximal tubules which abundance was increased in the db/db mice but decreased in the STZ diabetic mice. Insulin had an effect on the level of both glomerular and tubular proteins in the db/db mice. It decreased the abundance of G-protein coupled receptor-116 and of tyrosine-protein phosphatase non-receptor type substrate-1 away from the level in the healthy control mice. Conclusions: Our finding of differences in the N-glycosylation protein profiles in the db/db and STZ mouse models suggest that the etiology of DN could give rise to variations in the cell adhesion and cell-matrix composition in T1DM and T2DM. Thus, N-glycosylated protein differences could be a clue to dissimilarities in T1DM and T2DM at later stages of DN. Furthermore, we observed insulin specific regulation of N-glycosylated proteins both in the direction of and away from the abundances in healthy control mice