Allogeneic islet cells implant on poly-l-lactide matrix to reduce hyperglycaemia in streptozotocin-induced diabetic rat.

OBJECTIVE: To demonstrate the effects of allogeneic islet cell matrix implants for glycaemic control in rats with induced diabetes. METHOD: Sprague-Dawley rats were used as allogeneic donors of islet cells. Cells were seeded on three-dimensional proprietary poly-(l-lactide) matrices. Animals were rendered diabetic and a week later a matrix seeded with islet cells (IMI group) or a control matrix (placebo group) was implanted in the small bowel mesentery. Blood glucose levels were measured weekly for 12 weeks. After sacrifice, implant sections were Gomori stained for beta-cells and immuno-stained for insulin 3, 4, 5, and 6 months post implantation. RESULTS: 82% of seeded islet cells attached to the matrices. In the IMI group blood glucose levels were significantly reduced after implantation compared with before implantation across several time points. In the IMI group beta-cells and insulin-positive cells were identified at the implant site. CONCLUSION: The islet cell matrix implant reduced the blood glucose levels although complete normo-glycaemia was not established. The islet cell matrix implant may serve as an additional option for islet cell transplantation using 3D scaffold platforms for better survival and function of the islet cells.

The Effects of High Fat Diet on the Incidence of Obesity and Monocyte Chemoattractant Protein-1 Levels on Histological Changes in Prostate Wistar Rats.

Introduction: Benign prostatic hyperplasia (BPH) is a histopathological diagnosis characterized by the increase in stromal cells and epithelial cells of the prostate gland in the transitional zone surrounding the urethra. Obesity is the risk factor of BPH. The most frequent cause of obesity is a high-fat diet (HFD). Obesity and HFD lead to pro-inflammatory conditions. One of the pathomechanisms for the occurrence of BPH is a low-degree inflammatory factor, one of which is the level of monocyte chemoattractant protein-1/MCP-1. This study aims to determine the influence of HFD on the incidence of obesity and inflammatory factors (monocyte chemoattractant protein-1/MCP-1 levels) on the histopathological picture of the prostate. Methods: Experimental research was performed on male Wistar rats with each of the 6 rats given normal fat (ND) and HFD intake and terminated at 8 weeks and 6 rats given each ND and HFD were terminated at 16 weeks. The determination of obesity was determined based on Lee's criteria which were categorized as obese if the Lee index >0.3 and non-obese if ≤0.3. Examination of circulating MCP-1 was carried out by the ELISA method and determination of prostatic hyperplasia was done by calculating the percentage of prostate glands that had a large per-field cystic dilatation on light microscopy examination. All data are analyzed statistically with the Fisher Exact Test and Spearman Correlation Test. Results: Of the 12 rats that were given ND, none of them became obese according to Lee's criteria, on the other hand, of the 12 rats that were given HFD 8 became obese (66.7%, p = 0.001). Serum MCP-1 levels and the percentage of prostate glands that had cystic dilatation were significantly higher in mice receiving HFD than ND; both at week-8 (MCP-1; 18.87 vs 15.66) and (prostate gland experiencing cystic dilatation; 63.46% vs 47.24%) and week-16 (MCP-1; 21.27 vs 21.27) and (prostate gland experiencing cystic dilatation; 67.79% vs 56.39%). Spearman correlation analysis showed that only circulating MCP-1 levels were significantly correlated (p < 0.05) to the percentage of the prostate gland that had cystic dilatation; especially in week 16 (r = 0.713 and p < 0.001). At 8 weeks, it was not statistically significant (r = 0.406 and p = 0.095). Conclusion: High fat intake has been shown to increase the risk of obesity, but obesity does not increase inflammatory status and the incidence of prostate glands with cystic dilatation. On the other hand, high-fat intake increases inflammatory status which in turn causes prostate glands to develop cystic dilatation.

High-fat diet increases the level of circulating Monocyte Chemoattractant Protein-1 in Wistar rats, independent of obesity.

INTRODUCTION: Low-grade chronic inflammation has emerged as a key pathogenic link between high-fat diet (HFD)-induced obesity and the increased risk of chronic diseases. Evidence has shown that HFDs may induce inflammation in the central nervous system and peripheral tissues. Monocyte Chemoattractant Protein-1 (MCP-1) is a product of various cells that is known to be an inflammatory marker. This study investigated whether a HFD could induce obesity and increase the level of MCP-1 in Wistar rats. METHODS: The Wistar rats were randomized into two groups: normal diet (ND) and HFD (n = 12 per group). Both groups were fed for 8 and 16 weeks, thus dividing the rats into 4 arms: ND8, ND16, HFD8, and HFD16 (n = 6 per sub-group). Obesity in rats was measured using the Lee index. Blood samples were taken to measure the level of MCP-1. RESULTS: Our results showed that obesity did not occur in the group with a normal diet (ND8 and ND16). However, in the HFD group (HFD8 and HFD16), 4 of the 6 rats became obese. However, MCP-1 was significantly higher among non-obese rats in the HFD group compared with the ND group (p < 0.001). CONCLUSION: HFDs have been shown to increase the risk of obesity. In addition, increases in circulating MCP-1 were significantly different between Wistar rats given a HFD compared with the ND group.

High uric acid level increases the risk of acute kidney injury in acute coronary syndrome patients.

BACKGROUND: Both clinical and experimental evidence have been published over the past few decades supporting the existence of a close relationship between the elevated levels of serum uric acid with cardiovascular events and acute kidney injury (AKI). This study aimed to determine the effect of serum uric acid levels on the incidence of AKI in acute coronary syndrome (ACS) patients. METHODS: A retrospective cohort study with a cross sectional design was performed. The research was conducted at Dr. Wahidin Sudirohusodo Hospital from October 2019 to December 2019. Nonrandom sampling was employed in the medical records. All patients who met the inclusion criteria were at > 18 years old and diagnosed with ACS with AKI. The demographic data of age, sex and serum uric acid levels were recorded. The data obtained were analyzed using the SPSS (Statistical Package for Social Sciences). RESULTS: There were 158 subjects of ACS patients with AKI and 135 without AKI. There was a significant correlation between high uric acid levels with the incidence of AKI in ACS (p<0.001). Patients with high serum uric acid levels were 9.5 times at risk of developing AKI compared to those with normal serum uric acid levels. CONCLUSION: High uric acid level is one of the risk factors for AKI in ACS and indicates 9.5 times at risk of developing AKI compared to normal serum uric acid level. Therefore, it is necessary to monitor serum uric acid level and kidney function in ACS patients.

Albumin excretion rate among patients with diabetic retinopathy.

BACKGROUND: Chronic microvascular complications consist of diabetic nephropathy (DN), diabetic retinopathy (DR), and diabetic neuropathy. Diabetic nephropathy is assessed through albuminuria, and diabetic retinopathy is assessed through fundoscopy. Several studies have assessed the albuminuria in diabetic retinopathy but have found inconclusive results. This study aims to investigate the albumin excretion rate in patients with diabetic retinopathy. METHODS: A cross sectional design was applied in this study. The diagnosis of type 2 diabetes mellitus was determined based on the anamnesis and laboratory examinations. The study was conducted at Dr. Wahidin Sudirohusodo Hospital and Hasanuddin University Hospital in Makassar during November 2018 until April 2019. The stages of diabetic retinopathy were based on funduscopic examinations. In addition, the blood pressure, BMI, albumin excretion rate, lipid profile, and HbA1C were also examined. Chi Square and Kappa tests were performed in the statistical analysis. RESULTS: 120 subjects with type 2 diabetes mellitus were observed. Of the total subjects, the number of females within the age of 36-79 years made up the biggest fraction. There was a significant relation between hypertension comorbidity with the albumin excretion rate and grading diabetic retinopathy where the A3 and proliferative diabetic retinopathy (PDR) percentages were higher in the hypertension group at 68.8% and 54.5%. There was also a significant correlation between incidence of albuminuria with diabetic retinopathy. Particularly, proliferative diabetic retinopathy (PDR) remained associated with albuminuria, while non-proliferative diabetic retinopathy (NPDR) was related to non-albuminuria. CONCLUSION: Albuminuria incidence confirms association with diabetic retinopathy grading.