Sfrp5 correlates with insulin resistance and oxidative stress

Abstract

In contrast to obese mouse models, serum Sfrp5 was directly related to HOMA-IR and oxidative stress in humans, but not with apolipoproteins, and thus, associations differed from those found for circulating adiponectin. These differences between Sfrp5 and adiponectin might be explained by differences in the investigated species.

SFRP5 acts as a mature adipocyte marker but not as a regulator in adipogenesis

“…In contrast with ours and others' data (Schulte et al 2012, Hu et al 2013a, Carstensen et al (2013) have reported a much wider range of circulating SFRP5 concentrations in mostly overweight and obese Caucasians. It is likely that this disparity is partly related to the different clinical characteristics of these studies, including glycaemia levels, blood pressure, certain medications, other diseases and the variance in the definition of obesity.…”

“…As SFRP5 has been reported to be highly expressed in retinal pigment epithelium and be moderately expressed in the pancreas (Chang et al 1999), the circulating SFRP5 concentrations might not reflect their expression levels in WAT. This notion is corroborated by our findings that the serum SFRP5 levels were clearly measurable but could not be used to distinguish obese patients from non-obese subjects, which is consistent with the findings of two other studies on Caucasians (Schulte et al 2012, Carstensen et al 2013.…”

“…It is likely that this disparity is partly related to the different clinical characteristics of these studies, including glycaemia levels, blood pressure, certain medications, other diseases and the variance in the definition of obesity. Although both positive (Carstensen et al 2013) and negative (Hu et al 2013a,b) associations between circulating SFRP5 concentrations and HOMA-IR have been reported, we did not observe a statistically significant correlation between serum SFRP5 levels and HOMA-IR in our cohort consisting of a total of 160 young adults with a broad range of BMI. The reasons for this discrepancy might be a comparatively healthier glucose metabolic state (only 21 obese patients had impaired glucose regulation), a much younger age and a higher degree of obesity in our study population.…”

“…Similarly, Mori et al (2012) demonstrated that SFRP5 is not easily detectable in whole-cell lysates or extracellular matrix (ECM) fractions except when overexpressed in HEK293T and 3T3L1 cells. Results from several studies have indicated that circulating SFRP5 is detectable in humans (Schulte et al 2012, Carstensen et al 2013, Hu et al 2013a,b, Lu et al 2013. However, both positive (Carstensen et al 2013) and negative (Hu et al 2013a,b) associations between circulating SFRP5 concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) were reported, whereas no statistically significant correlation between plasma SFRP5 levels and HOMA-IR was found in a Chinese cohort (Lu et al 2013).…”

“…Results from several studies have indicated that circulating SFRP5 is detectable in humans (Schulte et al 2012, Carstensen et al 2013, Hu et al 2013a,b, Lu et al 2013. However, both positive (Carstensen et al 2013) and negative (Hu et al 2013a,b) associations between circulating SFRP5 concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) were reported, whereas no statistically significant correlation between plasma SFRP5 levels and HOMA-IR was found in a Chinese cohort (Lu et al 2013). Moreover, Ehrlund et al (2013) reported that SFRP1, SFRP2 and SFRP4, but not SFRP3 or SFRP5, were actively secreted from human WAT and constituted adipokines.…”