Intake of traditional Inuit diet vary in parallel with inflammation as estimated from YKL-40 and hsCRP in Inuit and non-Inuit in Greenland.

BACKGROUND: Chronic low-grade inflammation is involved in the initiation and progression of atherosclerosis and ischemic heart disease. This was rare in pre-western Inuit who lived on a diet that consisted mainly of marine mammals rich in n-3 fatty acids. OBJECTIVES: To assess the association between biomarkers of inflammation and the intake of traditional Inuit diet in addition to Inuit ethnicity. METHODS: YKL-40 and hsCRP were measured in serum from 535 Inuit and non-Inuit living in the capital city Nuuk in West Greenland or in the main town or a settlement in rural East Greenland. Dietary habits were assessed by an interview-based food frequency questionnaire. RESULTS: The participation rate was 95%. YKL-40 was higher in Inuit than in non-Inuit (p < 0.001), in Inuit with a higher intake of traditional Inuit diet (p < 0.001), and in Inuit from rural compared to urban areas (p < 0.001). It also rose with age (p < 0.001), alcohol intake (0.019) and smoking (p < 0.001). Inuit had higher hsCRP compared to non-Inuit (p = 0.003) and hsCRP increased in parallel with intake of traditional Inuit foods (p < 0.001). Alcohol associated with a decrease in hsCRP in Inuit (p = 0.004). YKL-40 and hsCRP increased with higher intakes of traditional Inuit diet after adjusting for ethnicity, gender, age, smoking, alcohol intake and BMI. CONCLUSIONS: 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.

YKL-40, a new inflammatory marker with relation to insulin resistance and with a role in endothelial dysfunction and atherosclerosis.

Substantial evidence supports a role of chronic subclinical inflammation and activation of the innate immune system in the pathogenesis of insulin resistance and endothelial dysfunction and the development of type 2 diabetes (T2D) and atherosclerosis. Several proinflammatory cytokines, acute phase-reactants and cell adhesion molecules play a pivotal role in this chronic subclinical inflammation but a comprehensive understanding of the interrelations of these molecules is still needed. YKL-40 is a new inflammatory marker with relation to acute and chronic inflammation as well as cancer. It is secreted in vitro from a variety of human cells, including vascular smooth muscle cells (VSMCs), activated macrophages and macrophages during late stages of differentiation and is found in vivo in subpopulations of macrophages in tissues with inflammation and extracellular tissue remodelling, such as macrophages in atherosclerotic plaques. YKL-40 promotes chemotaxis, cell attachment and migration of VSMCs and the formation of branching tubules suggesting that YKL-40 plays a role in angiogenesis. Latest studies reveal that YKL-40 is elevated in patients with T2D and is related to insulin resistance. This article reviews the studies of YKL-40 with focus on a possible role of YKL-40 in insulin resistance, endothelial dysfunction and atherosclerosis.

YKL-40, a biomarker of inflammation, is elevated in patients with type 2 diabetes and is related to insulin resistance.

OBJECTIVE AND DESIGN: YKL-40 participates in inflammatory states and vascular processes, which implies that comparison can be made with other inflammatory markers associated with insulin resistance and type 2 diabetes (T2D). In the present study levels of plasma YKL-40 and serum hsCRP were evaluated in patients with T2D. MATERIALS AND METHODS: Patients with T2D and age-matched healthy controls participated in the study. Insulin resistance was estimated using HOMA-IR model. Biochemical parameters were measured in venous blood after a 10 h fast. RESULTS: Patients with T2D were insulin resistant (p<0.001) and had raised levels of plasma YKL-40 (p<0.001) and serum hsCRP (p<0.001). YKL-40 was correlated with HOMA-IR (r=0.23, p<0.01), NEFA (r=0.32, p<0.001) and triglycerides (r=0.24, p<0.05). YKL-40 and hsCRP were not correlated (r=0.17, p=NS). All participants with hsCRP<1 mg/l had higher insulin sensitivity (p<0.05 and p<0.01, respectively). HsCRP were predicted by HOMA-IR and BMI (r2=0.48, p<0.01). Plasma YKL-40 was predicted by HOMA-IR and triglycerides (r2=0.27, p<0.01). CONCLUSIONS: YKL-40 and hsCRP are elevated in patients with T2D and are related to insulin resistance. No correlation was found between YKL-40 and hsCRP indicating that increased levels of YKL-40 occur independently from elevated plasma hsCRP.