Copper, iron, zinc and tannin concentrations throughout the digestive tract of tropical goats and sheep fed a high-fibre tannin-rich diet.

The dry season in tropical regions urges livestock to feed on nutritionally very poor diets. It has not been explored how tropical sheep-assumed grazers-and tropical goats-intermediate browsers-cope with a high-fibre tannin-rich diet. This study was designed to determine the effects of a high-fibre and tannin-rich diet on the flow of important microminerals iron (Fe), zinc (Zn) and copper (Cu) throughout the digestive tract of tropical sheep and goats. The feeding trial was set up with twelve adult male animals, six sheep with mean body weight (BW) of 30.3 ± 1.6 kg and six goats with mean BW of 26.4 ± 2.2 kg. The feed consisted of 36% leaves of Millettia ferruginea, 61% hay and 3% concentrate and was offered at 3% of BW (all on dry matter (DM) basis). The total faecal collection was carried out for 7 consecutive days. At the end of the experimental period, the animals were slaughtered to collect liver and digesta samples from the gastrointestinal tract. Feed, digesta and faecal samples underwent analysis of Fe, Zn, and Cu and total tannins (TT). Goats had significantly higher reticulum Cu concentrations expressed on DM as compared to sheep. Faecal Cu concentrations were higher for goats compared to sheep. Reticulum and colon digesta Zn levels were higher in goats than sheep. Abomasum and colon Fe levels were higher in sheep than goats when expressed on DM. These results suggest differences in feed intake, micromineral absorption, secretion and excretion between sheep and goats, pointing to a divergent mineral metabolism as an adaptation to the challenge of a dry season diet having very low nutritive value.

Blood Flow Suppresses Vascular Anomalies in a Zebrafish Model of Cerebral Cavernous Malformations.

RATIONALE: Pathological biomechanical signaling induces vascular anomalies including cerebral cavernous malformations (CCM), which are caused by a clonal loss of CCM1/KRIT1 (Krev interaction trapped protein 1), CCM2/MGC4607, or CCM3/PDCD10. Why patients typically experience lesions only in lowly perfused venous capillaries of the cerebrovasculature is completely unknown. OBJECTIVE: In contrast, animal models with a complete loss of CCM proteins lack a functional heart and blood flow and exhibit vascular anomalies within major blood vessels as well. This finding raises the possibility that hemodynamics may play a role in the context of this vascular pathology. METHODS AND RESULTS: Here, we used a genetic approach to restore cardiac function and blood flow in a zebrafish model of CCM1. We find that blood flow prevents cardiovascular anomalies including a hyperplastic expansion within a large Ccm1-deficient vascular bed, the lateral dorsal aorta. CONCLUSIONS: This study identifies blood flow as an important physiological factor that is protective in the cause of this devastating vascular pathology.