Association between controlling nutritional status score and chronic kidney disease in diabetic patients: a cross-sectional study based on the National Health and Nutrition Examination Survey.

PURPOSE: This study aimed to explore the association between controlling nutritional status (CONUT) score and chronic kidney disease (CKD) in type-2 diabetes mellitus (T2DM) patients. METHODS: This was a cross-sectional study based on the National Health and Nutrition Examination Survey (NHANES). The data on demographic characteristics, physical examination, lifestyle behaviors, comorbidities, medicine use, laboratory values, and energy were extracted. Nutritional status was assessed using CONUT score, and patients were divided into normal nutrition group and malnutrition group. Association between CONUT score and CKD in T2DM patients was assessed using logistic regression analysis, and odds ratio (OR) and 95% confidence intervals (CIs) were reported. Subgroup analysis based on age, body mass index (BMI), cardiovascular disease (CVD), diabetic retinopathy, and hyperlipidemia was performed. RESULTS: A total of 4581 patients were finally included for analysis. In the adjusted model, high CONUT score was found to be associated with the high odds of CKD (OR = 1.28, 95% CI 1.05-1.56). Also, high CONUT score was associated with the high odds of CKD in T2DM patients with age ≥ 65 years, with BMI < 25 kg/m2, with BMI ≥ 25 kg/m2, without CVD, without diabetic retinopathy, with hyperlipidemia, or without hyperlipidemia (all P < 0.05). CONCLUSIONS: Malnutrition was associated with the high odds of CKD in T2DM patients, indicating that actively monitoring the nutritional status is important for the management of CKD in T2DM patients.

Multiple roles of ALK3 in osteoarthritis.

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive cartilage degradation, synovial membrane inflammation, osteophyte formation, and subchondral bone sclerosis. Pathological changes in cartilage and subchondral bone are the main processes in OA. In recent decades, many studies have demonstrated that activin-like kinase 3 (ALK3), a bone morphogenetic protein receptor, is essential for cartilage formation, osteogenesis, and postnatal skeletal development. Although the role of bone morphogenetic protein (BMP) signalling in articular cartilage and bone has been extensively studied, many new discoveries have been made in recent years around ALK3 targets in articular cartilage, subchondral bone, and the interaction between the two, broadening the original knowledge of the relationship between ALK3 and OA. In this review, we focus on the roles of ALK3 in OA, including cartilage and subchondral bone and related cells. It may be helpful to seek more efficient drugs or treatments for OA based on ALK3 signalling in future.

Symptoms, disc position, occluding pairs, and facial skeletal characteristics of older patients with temporomandibular disorders.

OBJECTIVE: To describe the proportions of different osseous diagnoses in older patients with temporomandibular disorders (TMD) and to analyze the symptoms, disc position, occluding pairs, and facial skeletal characteristics of patients with bilateral osteoarthrosis (BOA) and bilateral normal joints (BNJ). METHODS: This retrospective cross-sectional study constituted 88 older patients (age ≥60 years). The osseous diagnosis, symptoms, disc position, occluding pairs, and facial skeletal characteristics were evaluated. Variables in BOA patients and BNJ patients were compared using the t-test and chi-square test. RESULTS: Forty-eight patients had BOA, 7 had unilateral osteoarthrosis, 11 had intermediate osteoarthrosis, and 22 had BNJ. The prevalence of disc displacement without reduction (DDw/oR) in BOA patients was significantly higher than in BNJ patients. BOA patients exhibited greater ANB angle, PP-MP, U1-NPo, L1-NPo, and facial convexity angle; shorter posterior cranial base; and decreased ramus height. CONCLUSION: BOA patients with associated DDw/oR had more complaints of orofacial pain and exhibited a shorter posterior cranial base, and greater mandibular retrusion, anterior tooth protrusion, and protruded profile than BNJ patients.

The alteration of A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) in the knee joints of osteoarthritis mice.

The A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family is gradually being recognized as an important family of mediators that, along with the matrix metalloproteinases (MMPs), control the degradation process in osteoarthritis (OA). The objective of this study was to uncover the detailed alterations of ADAMTS1, ADAMTS2, and ADAMTS5 in the knee joint of OA mice. The OA model was established by anterior cruciate ligament transection (ACLT) on the knee joints of C57BL/6 J mice. The mice showed representative phenotypes of ACLT-induced OA, including obvious deterioration of the cartilage, reductions in the collagen and proteoglycan components in the cartilage matrix of OA mice, and increased inflammation and osteoclast activity. By qPCR, the gene expression levels of Adamts1, -2, and -5 were the top-ranked among Adamts1-5 in cartilage/chondrocytes, osteogenic tissue/osteoblasts, and cortical bone/osteocytes. Moreover, the protein expression levels of ADAMTS1, -2, and -5 were all increased in articular cartilage, the growth plate, and subchondral bone of the knee joint. The results suggest the important roles of ADAMTS1, -2, and -5 in OA disease, which will be helpful in further research on degenerative changes in OA.

Ginsenoside Rg1 ameliorates diabetic cardiomyopathy by inhibiting endoplasmic reticulum stress-induced apoptosis in a streptozotocin-induced diabetes rat model.

Ginsenoside Rg1 has been demonstrated to have cardiovascular protective effects. However, whether the cardioprotective effects of ginsenoside Rg1 are mediated by endoplasmic reticulum (ER) stress-induced apoptosis remain unclear. In this study, among 80 male Wistar rats, 15 rats were randomly selected as controls; the remaining 65 rats received a diet rich in fat and sugar content for 4 weeks, followed by intraperitoneal injection of streptozotocin (STZ, 40 mg/kg) to establish a diabetes model. Seven days after STZ injection, 10 rats were randomly selected as diabetic model (DM) controls, 45 eligible diabetic rats were randomized to three treatment groups and administered ginsenoside Rg1 in a dosage of 10, 15 or 20 mg/kg/day, respectively. After 12 weeks of treatment, rats were killed and serum samples obtained to determine cardiac troponin (cTn)-I. Myocardial tissues were harvested for morphological analysis to detect myocardial cell apoptosis, and to analyse protein expression of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and Caspase-12. Treatment with ginsenoside Rg1 (10-20 mg/kg) significantly reduced serum cTnI levels compared with DM control group (all P < 0.01). Ginsenoside Rg1 (15 and 20 mg/kg) significantly reduced the percentage of apoptotic myocardial cells and improved the parameters of cardiac function. Haematoxylin and eosin and Masson staining indicated that ginsenoside Rg1 could attenuate myocardial lesions and myocardial collagen volume fraction. Additionally, ginsenoside Rg1 significantly reduced GRP78, CHOP, and cleaved Caspase-12 protein expression in a dose-dependent manner. These findings suggest that ginsenoside Rg1 appeared to ameliorate diabetic cardiomyopathy by inhibiting ER stress-induced apoptosis in diabetic rats.

Ginsenoside Rg1 ameliorates oxidative stress and myocardial apoptosis in streptozotocin-induced diabetic rats.

We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneally for 12 weeks. Myocardial injury indices and oxidative stress markers were determined. Changes in cardiac ultrastructure were evaluated with transmission electron microscopy. Myocardial apoptosis was assessed via terminal deoxynucleotidyl transferase (TDT)-mediated DNA nick-end labeling (TUNEL) and immunohistochemistry. Ginsenoside Rg1 was associated with a significant dose-dependent reduction in serum levels of creatinine kinase MB and cardiac troponin I, and lessened ultrastructural disorders in diabetic myocardium, relative to the untreated diabetic model rats. Also, compared with the untreated diabetic rats, significant reductions in serum and myocardial levels of malondialdehyde were noted in the ginsenoside Rg1-treated groups, and increased levels of the antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) were detected. TUNEL staining indicated reduced myocardial apoptosis in ginsenoside Rg1-treated rats, which may be associated with reduced levels of caspase-3 (CASP3) and increased levels of B-cell lymphoma-extra-large (Bcl-xL) in the diabetic myocardium. Ginsenoside Rg1 treatment of diabetic rats was associated with reduced oxidative stress and attenuated myocardial apoptosis, suggesting that ginsenoside Rg1 may be of potential preventative and therapeutic value for cardiovascular injury in diabetic patients.