Duodenal flows of hydrogenation intermediates in response to changes in dietary forage:concentrate ratio (F:C) and linseed oil were evaluated using 4 lactating Holstein cows fed a low (65:35 forage to concentrate) or high (35:65) concentrate diet without (LC, HC) added oil or with linseed oil (LCO, HCO) at 3% of DM. A 4 x 4 Latin square design was implemented for 5 wk. Lower hydrogenation of 18:2n-6 and 18:3n-3 was observed with HC, but it increased with LCO or HCO. Duodenal flow of total conjugated linoleic acids (CLA) increased by 1.40 (LCO) to 3.01 (HCO) g/d with linseed oil. This response was associated with greater flows of cis9,trans11- (+0.21 to +0.55 g/d), trans11,cis13- (+0.33 to +0.36), trans11,trans13- (+1.01 to +1.15 g/d), and trans,trans-CLA (+0.12 to +0.72 g/d). Trans10,cis12-CLA flow averaged 0.08 g/d and was not affected by F:C or oil. trans11,cis15-18:2 flow increased by 8.5 (LCO) to 62 (HCO) g/d in response to linseed oil. Total trans-18:1 flow was 37 g/d in cows fed LC and increased to 81 g/d with HC. Feeding oil increased total trans-18:1 to the greatest extent with HCO. Flow of trans10-18:1 was lower with LC than with HC (1.46 vs. 20 g/d). Linseed oil increased trans11-18:1 flow by 40 (LCO) to 113 g/d (HCO). Feeding LCO and HCO also increased flows of trans6+7+8-, trans13+14-, trans15-, and trans16-18:1. Apparent intestinal digestibility of trans-18:1 isomers was largely unaffected by concentrate level and ranged between 67 and 95%. Linseed oil increased digestibility of nearly all isomers by 3 to 16 percentage units. Digestibility of cis9,trans11-CLA was greater in cows fed HC (55%) compared with cows fed LC (32%) and was not affected by linseed oil. Data suggest that high concentrate diets enhanced ruminal outflow of trans10-18:1. We provide initial in vivo evidence that supplemental 18:3n-3 is hydrogenated to trans11,cis15-18:2, trans11-18:1, trans13+14-18:1, trans15-18:1, trans6+7+8-18:1, and trans16-18:1 primarily.

This report was written by the Japanese Society of Dysphagia Rehabilitation, the Japanese Association of Rehabilitation Nutrition, the Japanese Association on Sarcopenia and Frailty, and the Society of Swallowing and Dysphagia of Japan to consolidate the currently available evidence on the topics of sarcopenia and dysphagia. Histologically, the swallowing muscles are of different embryological origin from somatic muscles, and receive constant input stimulation from the respiratory center. Although the swallowing muscles are striated, their characteristics are different from those of skeletal muscles. The swallowing muscles are inevitably affected by malnutrition and disuse; accumulating evidence is available regarding the influence of malnutrition on the swallowing muscles. Sarcopenic dysphagia is defined as dysphagia caused by sarcopenia of the whole body and swallowing‐related muscles. When sarcopenia does not exist in the entire body, the term “sarcopenic dysphagia” should not be used. Additionally, sarcopenia due to neuromuscular diseases should be excluded; however, aging and secondary sarcopenia after inactivity, malnutrition and disease (wasting disorder and cachexia) are included in sarcopenic dysphagia. The treatment of dysphagia due to sarcopenia requires both dysphagia rehabilitation, such as resistance training of the swallowing muscles and nutritional intervention. However, the fundamental issue of how dysphagia caused by sarcopenia of the swallowing muscles should be diagnosed remains unresolved. Furthermore, whether dysphagia can be caused by primary sarcopenia should be clarified. Additionally, more discussion is required on issues such as the relationship between dysphagia and secondary sarcopenia, as well as the diagnostic criteria and means for diagnosing dysphagia caused by sarcopenia. Geriatr Gerontol Int 2019; 19: 91–97.

The effect of linseed oil (LSO) supplementation on total-tract and ruminal nutrient digestibility, N metabolism, and ruminal fluid characteristics was investigated in dairy cows fed diets containing different forage to concentrate ratios (F:C). The experimental design was a 4 x 4 Latin square with 2 x 2 factorial arrangement of treatments. Four lactating Holstein cows were fed a forage-rich diet without LSO (F; F:C = 65:35, dry matter basis), a forage-rich diet with LSO (FO; F:C = 65:32, 3% LSO), a concentrate-rich diet without LSO (C; F:C = 35:65), or a concentrate-rich diet with LSO (CO; F:C = 35:62, 3% LSO). Total-tract digestibility of DM and OM was greater with supplemental LSO. A tendency for greater total-tract digestibility of NDF and ADF also was observed in cows fed LSO. Ruminal digestibility of NDF or ADF decreased when CO was fed compared with C. In contrast, feeding FO increased NDF or ADF digestibility compared with F. Although ruminal starch digestion was nearly complete with all diets, digestibility was greater when cows were fed C or CO compared with F or FO. Bacterial N flow to the duodenum decreased when FO was fed compared with F. In contrast, feeding CO increased bacterial-N flow compared with C. Neither F:C nor LSO supplementation affected ruminal pH or total VFA concentration in ruminal fluid. However, molar proportion of propionate was greater with C or CO compared with F or FO and increased with LSO supplementation regardless of F:C. Molar proportion of n-butyrate decreased with LSO supplementation. Total protozoal numbers in ruminal fluid decreased markedly only when CO was fed. Overall, data show that feeding LSO had no negative effects on total-tract digestion in dairy cows but may decrease ruminal fiber digestibility when fed with high-concentrate diets. The widely spread idea that LSO decreases digestibility, arising from studies with sheep, did not seem to apply to lactating cows fed 3% LSO.

No abstract

Three Holstein cows were fed a high-concentrate diet (65:35 concentrate to forage) supplemented with either 5% sunflower oil (SO), 5% linseed oil (LO), or 2.5% fish oil (FO) to examine effects on biohydrogenation and fatty acid profiles in rumen, blood plasma, and milk. Diets were fed in a 3 x 3 Latin square with 4-wk periods with grass hay as the forage. Milk yield, dry matter intake, and percentages of milk fat (2.64) and protein (3.22) did not differ. All diets resulted in incomplete hydrogenation of unsaturated fatty acids as indicated by the profiles of 18:1 isomers, conjugated 18:2 isomers, nonconjugated 18:2 isomers, and 18:0 in ruminal fluid. Percentages of 8:0-14:0 and 16:0 in milk fat were greater with FO. Percentage and yield of trans10,cis12-18:2 were small and greater in cows fed SO (0.14%, 0.57 g/d) than FO (0.03%, 0.15 g/d) or LO (0.04%, 0.12 g/d). Percentage and yield of trans10-18:1, however, increased with FO (6.16%) and SO (6.47%) compared with LO (1.65%). Dietary FO doubled percentage of cis11-18:1 in rumen, plasma, and milk fat. Despite a lack of difference in ruminal percentage of trans11-18:1 (10.5%), cows fed FO had greater plasma trans11-18:1 (116 vs. 61.5 microg/mL) but this response did not result in greater trans11-18:1 percentage in milk fat, which averaged 5.41% across diets. Percentage (2.2%) and yield (14.3 g/d) of cis9,trans11-18:2 in milk fat did not differ due to oils. Unique responses to feeding LO included greater than 2-fold increases in percentages of trans13+14-18:1, trans15-18:1, trans16-18:1, cis15-18:1, cis9,trans12-18:2 and trans11,cis15 -18:2 in umen, plasma, and milk, and cis9,trans13-18:2 in plasma and milk. Ruminal 18:0 percentage had the highest positive correlation with milk fat content (r = 0.82) across all diets. When compared with previous data with cows fed high-concentrate diets without oil supplementation, results suggest that greater production of trans10-18:1, cis11-18:1, and trans11,cis15-18:2 coupled with low production of 18:0 in the rumen may be associated with low milk fat content when feeding high-concentrate diets and fish oil. In contrast, SO or LO could lead to low milk fat content by increasing ruminal trans10-18:1 (SO) or trans11,cis15-18:2 and trans9,trans12-18:2 (LO) along with a reduction in mammary synthesis of 8:0-16:0. Simultaneous increases in ruminal trans11-18:1 with fish oil, at a fraction of sunflower oil supplementation, may represent an effective strategy to maintain cis9,trans11-18:2 synthesis in mammary while reducing milk fat output and sparing energy.