The relationship between dietary inflammatory index and osteoporosis among chronic kidney disease population.

Dietary inflammation index (DII) is an epidemiological survey tool to evaluate dietary inflammation potential. Osteoporosis, whose development is deeply affected by inflammation, may be also affected by dietary inflammatory patterns. However, the relationship between DII and osteoporosis is unclear for chronic kidney disease (CKD) population. Our study involved 526 CKD patients from the US National Health and Nutrition Examination Survey (NHANES). DII levels were stratified into four quantile groups. Multivariable regression models were used to examine the association between DII and osteoporosis. Restricted cubic splines and subgroup analysis were additionally adopted. Results showed that the overall prevalence of osteoporosis among CKD patients was 25.3%. After fully adjusted, OR (95% confidence interval) for Q4 group compared with Q3 (reference group) in total and female population were 2.09 (1.05, 4.23) and 2.80 (1.14, 7.08), respectively. Subgroup analysis indicated that these results had no interaction with age, gender, body mass index (BMI), renal function, urinary protein, calcium, phosphorus and total 25-hydroxyvitamin D. DII was negatively correlated with lumbar spine bone mineral density (BMD) in CKD population (P < 0.05). Therefore, in CKD patients, higher DII was associated with higher osteoporosis risk and lower BMD of lumber spine, especially in female. Anti-inflammatory diet patterns may be a protective intervention for some CKD-related osteoporosis.

Lower expression of Hsa_circRNA_102682 in diabetic hyperhomocysteinemia negatively related to creatinemia is associated with TGF-ß and CTGF.

BACKGROUND: Diabetic nephropathy is a kidney disease caused by long-term hyperglycemia. Hsa_circRNA_102682 is related to the pathogenesis of preeclampsia. Preeclampsia is related to hypertension and proteinuria, and diabetic nephropathy is mainly manifested by hypertension and proteinuria. The main pathological change in diabetic nephropathy is glomerular fibrosis. METHODS: This study used serum samples of patients treated at Li Huili Eastern Hospital, Ningbo, China, from July 10, 2018 to February 15, 2019. We included 73 patients with diabetes and divided them into a normal-homocysteine group and a high-homocysteine group. We selected used quantitative reverse transcriptase-polymerase chain reaction to measure Hsa_circRNA_102682 concentration in the serum. Serum transforming growth factor-beta and connective tissue growth factor levels were tested using ELISA. The Pearson correlation test was used to assess the correlations between Hsa_circRNA_102682, transforming growth factor-beta, connective tissue growth factor, homocysteine, and creatinine. RESULT: Hsa_circRNA_102682 was significantly lower in diabetic patients with high levels of homocysteine than in those with normal levels of homocysteine, whereas transforming growth factor-beta and connective tissue growth factor levels were higher in diabetic patients with hyperhomocysteinemia. Hsa_circRNA_102682 was negatively correlated with the levels of transforming growth factor-beta, connective tissue growth factor, homocysteine, and creatinine. Transforming growth factor-beta and connective tissue growth factor were both positively correlated with homocysteine and creatinine. CONCLUSION: Low Hsa_circRNA_102682 was associated with high levels of transforming growth factor-beta and connective tissue growth factor as well as homocysteine and creatinine. These results suggest that Hsa_circRNA_102682 might be related to the pathogenesis of hyperhomocysteinemia in diabetic nephropathy.

Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus.

Ferroptosis is a novel form of nonapoptotic regulated cell death (RCD). It features iron-dependent lipid peroxide accumulation accompanied by inadequate redox enzymes, especially glutathione peroxidase 4 (GPX4). RAS-selective lethal 3 (RSL3), erastin, and ferroptosis inducing 56 (FIN56) induce ferroptosis via different manners targeting GPX4 function. Acyl-CoA synthetase long-chain family 4 (ACSL4), lysophosphatidylcholine acyltransferase 3 (LPCAT3), and lipoxygenases (LOXs) participate in the production of lipid peroxides. Heat shock protein family B member 1 (HSPB1) and nuclear receptor coactivator 4 (NCOA4) regulate iron homeostasis preventing ferroptosis caused by the high concentration of intracellular iron. Ferroptosis is ubiquitous in our body as it exists in both physiologic and pathogenic processes. It is involved in glucose-stimulated insulin secretion (GSIS) impairment and arsenic-induced pancreatic damage in the pathogenesis of diabetes. Moreover, iron and the iron-sulfur (Fe-S) cluster influence each other, causing mitochondrial iron accumulation, more reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, failure in biosynthesis of insulin, and ferroptosis in ß-cells. In addition, ferroptosis also engages in the pathogenesis of diabetic complications such as myocardial ischemia and diabetic cardiomyopathy (DCM). In this review, we summarize the mechanism of ferroptosis and especially its association with type 2 diabetes mellitus (T2DM).

Mitochondrial dysfunction and pancreatic islet ß-cell failure (Review).

Pancreatic ß-cells are the only source of insulin in humans. Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in ß-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Previous studies have demonstrated that GSIS is negatively regulated by various factors in the mitochondria, including tRNALeu mutations, high p58 expression, reduced nicotinamide nucleotide transhydrogenase activity, abnormal levels of uncoupling proteins and reduced expression levels of transcription factors A, B1 and B2. Additionally, oxidative stress damages mitochondria and impairs antioxidant defense mechanisms, leading to the increased production of reactive oxygen species, which induces ß-cell dysfunction. Inflammation in islets can also damage ß-cell physiology. Inflammatory cytokines trigger the release of cytochrome c from the mitochondria via the NF-κB pathway. The present review examined the potential factors underlying mitochondrial dysfunction and their association with islet ß-cell failure, which may offer novel insights regarding future strategies for the preservation of mitochondrial function and enhancement of antioxidant activity for individuals with diabetes mellitus.