Background/Aims: We investigated whether the tissue transglutaminase inhibitor cystamine is able to inhibit remodelling of small arteries in vivo, a possibility suggested by recent in vitro experiments. Methods: Using osmotic minipumps, phenylephrine, cystamine and/or amlodipine were infused for 1–2 weeks into 9-week-old Wistar rats. Small arteries were then removed for pressure myograph investigation. Results: Phenylephrine infusion caused inward remodelling of the small arteries compared to vehicle infusion. The remodelling was abolished by concomitant infusion with cystamine; blood pressure was unaffected. Second, we investigated whether cystamine was able to inhibit outward remodelling. Rats were first infused with phenylephrine for 1 week, and some were infused for a further week with amlodipine with or without cystamine. Amlodipine caused 24% outward remodelling compared to vessels from rats at completion of the phenylephrine infusion. The outward remodelling was attenuated 86% by concomitant cystamine infusion. A series of in vitro experiments supported the inhibitory action of cystamine on tissue transglutaminase. Conclusion: The ability of cystamine to inhibit inward remodelling independent of blood pressure is consistent with a role of tissue transgluaminase in this process. It remains to be determined if the ability of cystamine to inhibit outward remodelling also involves inhibition of tissue transglutaminase.

Biomarkers of inflammation vary in parallel with the intake of traditional Inuit diet. A diet based on marine mammals from the Arctic does not reduce inflammatory activity and it may be speculated that markers of inflammation reflect the disease rather than the cause of the disease.

The traditional Inuit diet in Greenland consists mainly of fish and marine mammals, rich in vitamin D. Vitamin D has anti-inflammatory capacity but markers of inflammation have been found to be high in Inuit living on a marine diet. Yet, the effect of vitamin D on inflammation in Inuit remains unsettled. This led us to investigate the association between vitamin D and markers of inflammation in a population with a high intake of a marine diet. We studied 535 Inuit and non-Inuit living in West and East Greenland. Information concerning dietary habits was obtained by interview-based FFQ. Blood samples were drawn for analysis of 25-hydroxyvitamin D, high-sensitivity C-reactive protein (hsCRP) and chitinase-3-like protein 1(YKL-40). Participants were divided into three groups based on degree of intake of the traditional Inuit diet. The diet groups (Inuit diet/mixed diet/imported foods) were associated with vitamin D levels in serum (74·2, 69·8 and 52·9 nm; P < 0·001), hsCRP (1·6, 1·4 and 1·3 mg/l; P = 0·002) and YKL-40 (130, 95 and 61 ng/ml; P < 0·001), respectively. YKL-40 level decreased with rising vitamin D level in Inuit (Inuit diet P = 0·002; mixed diet P = 0·011). YKL-40 was lower in groups with higher vitamin D levels after adjusting for other factors known to influence inflammation (P < 0·001). This was not seen for hsCRP. In conclusion, vitamin D and markers of inflammation vary in parallel with the intake of the marine Inuit diet. Vitamin D levels were inversely associated with YKL-40 levels, but no association with hsCRP was found. The hypothesised anti-inflammatory effect of vitamin D was not supported. Other factors in the marine diet may be speculated to influence inflammation.

No abstract