Preliminary report: circulating levels of the adipokine vaspin in gestational diabetes mellitus and preeclampsia.

The objective of the study was to investigate serum levels of the insulin-sensitizing adipokine vaspin in patients with gestational diabetes mellitus (GDM) and preeclampsia (PE) as compared with healthy controls of similar gestational age. Vaspin serum levels were quantified by enzyme-linked immunosorbent assay in control (n = 102), GDM (n = 40), and PE (n = 22) subjects. Median maternal vaspin concentrations were not significantly different in GDM, PE, and control subjects. Furthermore, vaspin did not significantly correlate to clinical and biochemical measures of renal function, glucose, and lipid metabolism, as well as inflammation. Circulating vaspin levels are not significantly different between GDM, PE, and control subjects and do not correlate with insulin sensitivity in pregnant subjects.

Fibrosis rather than blood pressure determines cardiac BNP expression in mice.

BACKGROUND: Since first reports demonstrated interactions between the natriuretic peptide (NPS) and renin-angiotensin system (RAS), our experiments should clarify whether cardiac brain natriuretic peptide (BNP) is regulated in mice genetically altered for components of the RAS. METHODS AND RESULTS: The study was carried out in hypotensive AT1- and angiotensinogen (ANG)-, and normotensive AT2-knockout mice, and in hypertensive animals overexpressing ANG and wildtype controls of each genotype. Ventricular BNP expression was analyzed by RNase-protection assay (RPA) (n=6). Cardiac fibrosis was visualized by Sirius red staining. While ANG overexpression increases cardiac BNP-mRNA expression (1035+/-210 vs. wildtype: 405+/-95 in PSL/mm(2), P<0.01), its deficiency had no influence. Both AT1- and AT2-knockouts showed significantly decreased BNP-mRNA concentrations (AT1: 21+/-6 vs. wildtype: 139+/-28 in PSL/mm(2), P<0.001; AT2: 8+/-2 vs. 19+/-3 in PSL/mm(2), P<0.05). These alterations correlate to reduced cardiac fibrosis in AT2-deficient animals, and an unchanged matrix content in ANG knockouts. CONCLUSIONS: Increased BNP-mRNA levels in hypertensive ANG-overexpressing mice and decreased BNP in hypotensive AT1-deficient animals suggest that this mRNA expression is blood pressure-dependent. However, the observed alterations of fibrosis and the unchanged BNP in hypotensive ANG knockouts and impaired BNP-mRNA expression in normotensive AT2-deficient mice demonstrate a direct interaction of the RAS and NPS that is fibrosis- rather than blood pressure-dependent.