The effects of a high fat diet on the development of diabetes mellitus, insulin resistance and secretion have been widely investigated. We investigated the effects of a high fat diet on the pancreas and skeletal muscle of normal rats to explore diet-induced insulin resistance mechanisms. Forty-four male Wistar rats were divided into six groups: a control group fed standard chow, a group fed a 45% fat diet and a group fed a 60% fat diet for 3 weeks to measure acute effects; an additional three groups were fed the same diet regimens for 8 weeks to measure chronic effects. The morphological effects of the two high fat diets were examined by light microscopy. Insulin in pancreatic islets was detected using immunohistochemistry. The homeostasis model assessment of insulin resistance index and insulin staining intensity in islets increased significantly with acute administration of high fat diets, whereas staining intensity decreased with chronic administration of the 45% fat diet. Islet areas increased significantly with chronic administration. High fat diet administration led to islet degeneration, interlobular adipocyte accumulation and vacuolization in the pancreatic tissue, as well as degeneration and lipid droplet accumulation in the skeletal muscle tissue. Vacuolization in the pancreas and lipid droplets in skeletal muscle tissue increased significantly with chronic high fat diet administration. We suggest that the glucolipotoxic effects of high fat diet administration depend on the ratio of saturated to unsaturated fatty acid content in the diet and to the total fat content of the diet.

Impairment of cardiac function causes renal damage. Renal failure after heart failure is attributed to hemodynamic derangement including reduced renal perfusion and increased venous pressure. One mechanism involves apoptosis and is defined as cardiorenal syndrome type 1. Erythropoietin (EPO) is a cytokine that induces erythropoiesis under hypoxic conditions. Hypoxia inducible factor 1 alpha (HIF-1α) plays a regulatory role in cellular response to hypoxia. Protective effects of EPO on heart, kidney and nervous system are unrelated to red blood cell production. We investigated early changes in and effects of EPO on renal tissues of rats with myocardial infarction by morphology and immunohistochemistry. Coronary artery ligation was used to induce myocardial infarction in Wistar rats. Group 1 comprised sham operated rats; groups 2, 3 and 4 included rats after coronary artery ligation that were sacrificed 6 h after ligation and that were treated with saline, 5,000 U/kg EPO or 10,000 U/kg EPO, respectively; group 5 included rats sacrificed 1 h after ligation. Group 2 showed increased renal tubule damage. Significantly less tubule damage was observed in EPO treated groups. EPO and EPO receptor (EPO-R) immunostaining intensities increased slightly for group 5 and became more intense for group 2. EPO and EPO-R immunostaining was observed in the interstitial area, glomerular cells and tubule epithelial cells of EPO treated groups. HIF-1α immunostaining was observed in collecting tubules in the medulla only in group 2. Caspase-3 immunostaining is an indicator of apoptosis. Caspase-3 staining intensity decreased in renal medulla of EPO treated groups. EPO treatment may exert a protective effect on the renal tissues of patients with cardiorenal syndrome.

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Aim: Cardiac hepatopathy arises due to heart failure and influences has effects on heart recovery after myocardial infarction (MI).The aim of this study was to investigate the protective effect of Erythropoietin (EPO) on liver tissue exposed to ischemia due to MI. Material and Methods: Experimental MI was established by left anterior descending coronary artery ligation (CAL) and EPO or saline was injected immediately after CAL to five groups of rats, which groups are Control, Saline, EPO 5000, EPO 10000, CAL+1h. CAL+1h group was sacrificed one hour after CAL without any treatment. Other groups were sacrificed six hours after the operation. Liver tissues were examined histopathologically by Hematoxylin Eosin (HE) staining and electron microscopy. Results: Degenerative changes in liver tissue such as vacuolization, sinusoidal dilatation, hepatocyte pyknosis, Kuppfer cell activation were observed. Vacuolization, and sinusoidal dilatation increased in the Saline group compared to the control group (p=0.010 for both). Degenerated hepatocytes with pyknotic nuclei as well as activated Kuppfer cells were decreased in the EPO 10000 group compared to the Saline group (p=0.009), and activated Kupfer cells were decreased compared to the Saline and CAL+1h groups (p=0.035 and p=0.019, respectively). Conclusion: EPO protected liver tissue from histopathological damages regardless of dose, when given at the time of MI. EPO, when given immediately after MI, protected liver tissue from histopathological damage regardless of dose. Considering the mutual interaction of liver and heart, applying EPO to MI patients at first sight may prevent post-MI liver damage and contribute to the recovery of the heart.

Akut miyokard infarktüsü olan hastalarda koroner trombüs, kan akımının azalmasına neden olur. Amacımız, üç olguda trombüs analizi yaparak, trombüsün neden olduğu koroner oklüzyon mekanizmalarının anlaşılmasına katkıda bulunmaktı. Olgulara koroner anjiyografi ile ST elevasyon tipi miyokard infarktüsü tanısı konuldu. Trombüslerde histopatolojik inceleme ve PTX3 (Pentraksin 3, bir akut faz proteini) ve CD68 (monosit ve makrofajlardan salınan bir sitokin) ile immünohistokimyasal boyama yapıldı. Ayrıca troponin ve PTX3 kan düzeyleri ölçüldü. PTX3 immün boyama skoru, tüm vakalarda yüksekti ve kan düzeyleri ile uyumlu değildi. PTX3 kan düzeyi normal olan vakada boyanma yoğunluğunun fazla olmasının, PTX3'ün hızlı lokal salınımı sonucu olabileceği düşünüldü. En yüksek PTX3 kan düzeyi olan vakada, bu artışı sağlayabilecek başka bir inflamatuar hastalık vardı. PTX3 ve CD68 immün boyamalarının, koroner trombüsün histopatolojik değerlendirilmesinde bir belirteç olarak kullanılabileceğini düşünüyoruz.