The association between retinol-binding protein 4 and risk of type 2 diabetes: A systematic review and meta-analysis.

Retinol-binding protein 4 (RBP4) was controversially associated with type 2 diabetes mellitus (T2DM). This meta-analysis aimed at evaluating the association between RBP4 level and T2DM risk. MEDLINE and EMBASE were searched to identify relevant studies up to 3 December 2022. Random effects model was used to pool multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Publication bias was estimated by Funnel plot and Egger's test, it was considered to be significant when P < 0.05. Eight studies including 8087 participants were finally included. Compared to those with the lowest level, subjects with the highest level of RBP4 have a higher risk of T2DM (OR = 1.47, 95% CI: 1.16-1.78, P < 0.001, I2 = 86.9%). No publication bias among the included studies was found (t = 0.94, P = 0.377). This meta-analysis indicated that high RBP4 level was associated with increasing risk of T2DM.

Physical activity diminished adverse associations of obesity with lipid metabolism in the population of rural regions of China.

The interactive effects of obesity and physical inactivity on lipid metabolism and prevalent dyslipidemia are scarcely reported in rural regions. 39029 subjects were obtained from the Henan Rural Cohort, and their metabolic equivalents (METs) of physical activity (PA) were computed. Independent associations of the obesity indices and PA with either lipid indices or prevalent dyslipidemia were analyzed by generalized linear models, and additive effects of obesity and PA on prevalent dyslipidemia were further quantified. Each obesity index was positively associated with total cholesterol, triglyceride, low-density lipoprotein or prevalent dyslipidemia but negatively associated with high-density lipoprotein, whereas the opposite association of PA with either each lipid index or prevalent dyslipidemia was observed. Joint association of PA and each obesity index with each lipid index and prevalent dyslipidemia was observed. Furthermore, the association of each obesity index in association with each lipid index was attenuated by increased PA levels.

Naringenin activates beige adipocyte browning in high fat diet-fed C57BL/6 mice by shaping the gut microbiota.

Naringenin is a kind of natural citrus flavonoid with various biological and pharmacological functions. Several studies have reported the anti-obesity effect of naringenin, but its potential mechanism of action (MoA) on beige adipose browning remains unclear. Here, we investigated whether naringenin induces gut microbe-host interactions to promote beige adipose thermogenesis and browning. Naringenin treatment alleviated obesity, increased body's energy expenditure and activated inguinal white adipose tissue thermogenesis and browning in high fat diet (HFD) fed mice. In addition, naringenin improved HFD-induced gut microbiota dysbiosis and increased short-chain fatty acid (SCFA) levels (especially acetic acid) in a host's cecum and serum. Furthermore, using antibiotic treatment and gut microbe transplantation, we found that gut microbes played an indispensable role in naringenin-induced beige fat browning and naringenin-exerted anti-obesity effects. Our study suggests that naringenin activated beige adipose thermogenesis and browning by gut microbe-SCFA-host interactions, which increase energy expenditure and prevent HFD-induced obesity.

miR-181c protects CsA-induced renal damage and fibrosis through inhibiting EMT.

Cyclosporine A (CsA), a widely used immunosuppressive drug in organ transplantation and autoimmune disorders, frequently induces renal damage and fibrosis. Recent evidence has implicated epithelial-mesenchymal transition (EMT) in CsA-induced nephrotoxicity. Microarray analysis disclosed miR-181c as the microRNA most dramatically repressed by CsA. Downregulation of miR-181c expression at the transcriptional level by CsA is dependent on the transcription factor Nrf2. miR-181c mimics or inhibitors attenuate or aggravate CsA-induced EMT gene changes, respectively. Importantly, in Nrf2-/- mice, CsA-induced renal damage, fibrosis, and EMT gene changes are restored by miR-181c mimics. Mechanistically, we identified Notch2 as a potential target of miR-181c. Collectively, our data support the notion that miR-181c may serve as an important factor for protecting renal tissues from CsA-induced nephrotoxicity.