Jae Kyung Lee, Kyunga Kim, Younjhin Ahn, Mihi Yang, and Jung Eun Lee
The association between coffee intake and type 2 diabetes may be modulated by common genetic variation.
The purpose of this study was to examine the association between habitual coffee intake and the risk of type 2 diabetes and to determine whether this association varied by genetic polymorphisms related to type 2 diabetes in Korean adults.
Design and methods
A population-based cohort study over a follow-up of 4 years was conducted. A total of 4077 Korean men and women aged 40–69 years with a normal glucose level at baseline were included. Coffee intake was assessed using a validated food frequency questionnaire, and incident type 2 diabetes or prediabetes was defined by oral glucose tolerance test or fasting blood glucose test. The genomic DNA samples were genotyped with the Affymetrix Genome-Wide Human SNP Array 5.0, and nine single-nucleotide polymorphisms related to type 2 diabetes in East Asian populations were extracted.
A total of 120 cases of type 2 diabetes and 1128 cases of prediabetes were identified. After adjustment for potential confounding factors, we observed an inverse association, but without any clear linear trend, between coffee intake and the combined risk of type 2 diabetes and prediabetes. We found that inverse associations between habitual coffee intake and the combined risk of type 2 diabetes and prediabetes were limited to those with the T-allele (GT/TT) of rs4402960 in IGF2BP2, those with the G-allele (GG/GC) of rs7754840 in CDKAL1, or those with CC of rs5215 in KCNJ11.
We found a lower risk of prediabetes and type 2 diabetes combined with coffee intake among individuals with the GT/TT of IGF2BP2 rs4402960, GG/GC of CDKAL1 rs7754840, or CC of KCNJ11 rs5215, which are known to be related to type 2 diabetes in East Asians.
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.