Se Eun Park, Won Jun Kim, Sung Woo Park, Ji Woo Park, Namseok Lee, Cheol-Young Park, and Byung-Soo Youn
Angiotensin-converting enzyme 2 (ACE2) plays an important role in glucose metabolism and renal function. However, the relationship between ACE2 and hyperglycemia or microalbuminuria has not been established in humans. We investigated whether urinary ACE2 levels are associated with abnormal glucose homeostasis and urinary albumin excretion.
We developed an ELISA for quantifying ACE2 in urine. The ELISA was used to measure urinary ACE2 levels in 621 subjects with: normal glucose tolerance (NGT; n=77); impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) (n=132); and type 2 diabetes mellitus (T2DM, n=412). Insulin resistance was assessed by homeostasis model assessment for insulin resistance (HOMA-IR) index and urinary albumin excretion by urine albumin-to-creatinine ratio (ACR). Other biochemical and anthropometric parameters were measured.
Urinary ACE2 levels were significantly higher in insulin-resistant subjects with IFG, IGT, and T2DM than in the NGT group (P<0.001). Urinary ACE2 concentrations appeared to correlate with HOMA-IR, fasting blood glucose, triglyceride, high-sensitivity C-reactive protein, serum creatinine, urinary ACR, and systolic blood pressure (all P<0.05). After adjustment for impaired renal function and other metabolic parameters, urinary ACE2 concentration was still associated with a higher risk for T2DM (OR 1.80, 95% CI 1.05–3.08, P=0.02). In addition, urinary ACE2 levels were highly predictive of microalbuminuria after adjusting for clinical risk factors (OR 2.68, 95% CI 1.55–4.64, P<0.001).
Our data suggest that the urinary ACE2 level is closely associated with T2DM and is an independent risk factor for microalbuminuria.
Ji Eun Jun, Mira Kang, Sang-Man Jin, Kyunga Kim, You-Cheol Hwang, In-Kyung Jeong, and Jae Hyeon Kim
We aimed to investigate the interaction of reduced skeletal muscle mass and abdominal obesity on coronary artery calcification (CAC).
Design and methods
A total of 19 728 adults free of cardiovascular disease (CVD) who contemporaneously underwent cardiac tomography and bioelectrical impedance analysis were enrolled in a cross-sectional and longitudinal cohort. Skeletal muscle mass index (SMI) was calculated using the following formula: SMI (%) = total appendicular muscle mass (kg)/body weight (kg) × 100 according to sex. CAC presence or incidence was defined as CAC score > 0, and CAC progression was defined as √CAC score (follow-up) – √CAC score (baseline)>2.5. Pre-sarcopenia was defined as SMI ≤ −1.0 s.d. of the sex-specific mean of a young reference group. Abdominal obesity was defined as waist circumference ≥ 90 cm for men and ≥85 cm for women. All individuals were further classified into four groups: normal, abdominal obesity alone, pre-sarcopenia alone, and pre-sarcopenic obesity.
Individuals with pre-sarcopenic obesity showed the highest adjusted odds ratio (AOR) for CAC presence (AOR 2.16, 95% CI : 1.98–2.36, P < 0.001) as well as total CAC incidence and progression (adjusted hazard ratio: 1.54, 95% CI: 1.37–1.75, P < 0.001), compared with normal individuals. Pre-sarcopenic obesity significantly increased CAC incidence and progression compared to either pre-sarcopenia or abdominal obesity alone.
Pre-sarcopenia and abdominal obesity together were significantly associated with a higher CAC presence and increased risk of CAC incidence and progression, independent of traditional CVD risk factors.