Elevated whole blood viscosity is associated with insulin resistance and non-alcoholic fatty liver.

BACKGROUND: Accumulating evidences demonstrate that abnormalities in whole blood viscosity (WBV) have been implicated in insulin resistance which may lead to non-alcoholic fatty liver disease (NAFLD). However, epidemiological studies exploring the association between WBV and NAFLD were not available. OBJECTIVE: Our objective was to evaluate the association between WBV levels and risk of prevalent NAFLD. DESIGN: This was a cross-sectional population-based study performed in Shanghai, China. PATIENTS: A total of 8673 participants aged 40 years or older were included. MEASUREMENTS: WBV was calculated from haematocrit and plasma protein concentration, at a shear rate of 208(-1) s, by a validated equation. NAFLD was diagnosed by hepatic ultrasound after the exclusion of alcohol abuse and other liver diseases. Insulin resistance (IR) was assessed by homeostasis model assessment (HOMA-IR). RESULTS: The overall prevalence of NAFLD was 30·2% in this population. With the increase of WBV level, participants have larger waist circumference (WC), more severe insulin resistance and the prevalence of NAFLD increased significantly with elevated WBV quartiles. Compared with those in the lowest quartiles, adults in the highest quartile of WBV levels have higher prevalence of NAFLD (adjusted odds ratio 1·77, 95% confidence interval [CI] 1·48-2·13) and IR (2·72, 95% CI 2·26-3·27). CONCLUSIONS: Elevated WBV is associated with prevalence of NAFLD and IR in middle-aged and elderly Chinese population.

Phenylalanine impairs insulin signaling and inhibits glucose uptake through modification of IRß.

Whether amino acids act on cellular insulin signaling remains unclear, given that increased circulating amino acid levels are associated with the onset of type 2 diabetes (T2D). Here, we report that phenylalanine modifies insulin receptor beta (IRß) and inactivates insulin signaling and glucose uptake. Mice fed phenylalanine-rich chow or phenylalanine-producing aspartame or overexpressing human phenylalanyl-tRNA synthetase (hFARS) develop insulin resistance and T2D symptoms. Mechanistically, FARS phenylalanylate lysine 1057/1079 of IRß (F-K1057/1079), inactivating IRß and preventing insulin from promoting glucose uptake by cells. SIRT1 reverse F-K1057/1079 and counteract the insulin-inactivating effects of hFARS and phenylalanine. F-K1057/1079 and SIRT1 levels in white blood cells from T2D patients are positively and negatively correlated with T2D onset, respectively. Blocking F-K1057/1079 with phenylalaninol sensitizes insulin signaling and relieves T2D symptoms in hFARS-transgenic and db/db mice. These findings shed light on the activation of insulin signaling and T2D progression through inhibition of phenylalanylation.

Seroprevalence of Bartonella henselae and Identification of Risk Factors in China.

Serum samples were tested for Bartonella henselae IgG antibodies using indirect immunofluorescence assays. We then analyzed associated risk factors. Serum samples were considered positive when reactive at a dilution of more than 1:320. Differences between groups and risk factors associated with Bartonella exposure were statistically analyzed using Chi-square tests and the generalized linear model. 122 of 1,260 samples (9.68%) were positive for B. henselae infection. The infection rate ranged from 0% to 30.43% and differed significantly among age groups ( P < 0.01); infection rate in the 50-59 years group was significantly higher than that in other age groups. The seroprevalence of Bartonella varied significantly among sites within the four provinces, and the infection rate of field workers was significantly higher than that of urban workers.