SummaryMicroglia‐mediated neuroinflammation plays a dual role in various brain diseases due to distinct microglial phenotypes, including deleterious M1 and neuroprotective M2. There is growing evidence that the peroxisome proliferator‐activated receptor γ (PPARγ) agonist rosiglitazone prevents lipopolysaccharide (LPS)‐induced microglial activation. Here, we observed that antagonizing PPARγ promoted LPS‐stimulated changes in polarization from the M1 to the M2 phenotype in primary microglia. PPARγ antagonist T0070907 increased the expression of M2 markers, including CD206, IL‐4, IGF‐1, TGF‐β1, TGF‐β2, TGF‐β3, G‐CSF, and GM‐CSF, and reduced the expression of M1 markers, such as CD86, Cox‐2, iNOS, IL‐1β, IL‐6, TNF‐α, IFN‐γ, and CCL2, thereby inhibiting NFκB–IKKβ activation. Moreover, antagonizing PPARγ promoted microglial autophagy, as indicated by the downregulation of P62 and the upregulation of Beclin1, Atg5, and LC3‐II/LC3‐I, thereby enhancing the formation of autophagosomes and their degradation by lysosomes in microglia. Furthermore, we found that an increase in LKB1–STRAD–MO25 complex formation enhances autophagy. The LKB1 inhibitor radicicol or knocking down LKB1 prevented autophagy improvement and the M1‐to‐M2 phenotype shift by T0070907. Simultaneously, we found that knocking down PPARγ in BV2 microglial cells also activated LKB1–AMPK signaling and inhibited NFκB–IKKβ activation, which are similar to the effects of antagonizing PPARγ. Taken together, our findings demonstrate that antagonizing PPARγ promotes the M1‐to‐M2 phenotypic shift in LPS‐induced microglia, which might be due to improved autophagy via the activation of the LKB1–AMPK signaling pathway.

There is increasing interest in the association between depression and the development of metabolic diseases. Rosiglitazone, a therapeutic drug used to treat type 2 diabetes mellitus, has shown neuroprotective effects in patients with stroke and Alzheimer’s disease. The present study was performed to evaluate the possible roles of rosiglitazone in in vivo (unpredictable chronic mild stress-induced depressive mouse model) and in vitro (corticosterone-induced cellular model) depressive models. The results showed that rosiglitazone reversed depressive behaviors in mice, as indicated by the forced swimming test and open field test. Rosiglitazone was also found to inhibit the inflammatory response, decrease corticosterone levels, and promote astrocyte proliferation and neuronal axon plasticity in the prefrontal cortex of mice. This series of in vivo and in vitro experiments showed that autophagy among neurons was inhibited in depressive models and that rosiglitazone promoted autophagy by upregulating LKB1, which exerted neuroprotective effects. Rosiglitazone was also found to activate the Akt/CREB pathway by increasing IGF-1R expression and IGF-1 protein levels, thereby playing an anti-apoptotic role in astrocytes. Rosiglitazone’s autophagy promotion and neuroprotective effects were found to be reversed by the PPARγ antagonist T0070907 in primary neurons and by PPARγ knockdown in an N2a cell line. In conclusion, we found that rosiglitazone protects both neurons and astrocytes in in vivo and in vitro depressive models, thereby playing an anti-depressive role. These findings suggest that PPARγ could be a new target in the development of anti-depressive drugs.

Periostin, an extracellular matrix protein, is widely expressed in a variety of tissues and cells. It has many biological functions and is related to many diseases: for example, it promotes cell proliferation and differentiation in osteoblasts, which are closely related to osteoporosis, and mediates cell senescence and apoptosis in chondrocytes, which are involved in osteoarthritis. Furthermore, it also plays an important role in mediating inflammation and reconstruction during bronchial asthma, as well as in promoting bone development, reconstruction, repair, and strength. Therefore, periostin has been explored as a potential biomarker for various diseases. Recently, periostin has also been found to be expressed in intervertebral disc cells as a component of the intervertebral extracellular matrix, and to play a crucial role in the maintenance and degeneration of intervertebral discs. This article reviews the biological role of periostin in bone marrow-derived mesenchymal stem cells, osteoblasts, osteoclasts, chondrocytes, and annulus fibrosus and nucleus pulposus cells, which are closely related to spinal degenerative diseases. The study of its pathophysiological effects is of great significance for the diagnosis and treatment of spinal degeneration, although additional studies are needed.

Purpose: Several previous reports have highlighted the association between adiposity and risk of metabolic syndrome (MetS). Although it is necessary to identify which adiposity indices are best suited to identify MetS, no such study has been completed in diabetic patients. The aim of this study was to evaluate the ability of eight anthropometric indices to identify MetS in diabetic, middle-aged and elderly Chinese patients. Patients and Methods: A cross-sectional study was conducted in 906 type 2 diabetic patients in Guangxi. Results: The highest odds ratios for the identification of MetS were identified with CUN-BAE (OR = 28.306). The largest areas under the curve (AUCs) were observed for WHtR and BRI in men aged 40-59; CUN-BAE in men aged 60 and over; WHtR, BRI, and TyG in women aged 40-59; and BMI for women aged 60 and over. The weakest indicator for the screening of MetS in type 2 diabetes was the ABSI. Conclusion:The most effective anthropometric indicator for the identification of MetS varied across sex and age subgroups.

This study aimed to investigate the association between mean platelet volume (MPV) and metabolic syndrome (MetS) in patients with type 2 diabetes mellitus (T2DM). Data for 1240 patients with T2DM admitted to the Department of Endocrinology at the First Affiliated Hospital of Guangxi Medical University between January 1, 2017 and June 1, 2020 were collected retrospectively via electronic medical records, including demographic information, complete blood count, lipid profile, and glucose metabolism indexes. MetS was defined according to the Chinese Diabetes Society. Among the 1240 patients enrolled, 873 (70.40%) had MetS. MPV was significantly higher in patients with MetS ( P < .001). For individual MetS components, MPV was significantly higher in the presence of abdominal obesity ( P = .013) and hypertriglyceridemia ( P = .026), but did not differ in the presence of elevated blood pressure ( P = .330) or low high-density lipoprotein cholesterol ( P = .790). Moreover, MPV was independently associated with MetS after adjustment for sex, smoking, alcohol drinking, white blood cell count, fasting C-peptide, and body mass index (odds ratio 1.174, 95% confidence interval 1.059–1.302). The odds ratio for MetS in the highest tertile, compared with the lowest MPV tertile, was 1.724 (95% confidence interval 1.199–2.479, P for trend = .003) after multiple adjustment. In stratified analyses, the positive correlation of MPV with MetS was significant only in patients who were older, male, or overweight, or who had poor glycemic control. In conclusion, high MPV was positively associated with the presence of MetS in patients with T2DM, particularly older, male, or overweight patients, or those with poor glycemic control.