Metabolic Markers Associated with Progression of Type 2 Diabetes Induced by High-Fat Diet and Single Low Dose Streptozotocin in Rats.

Science is still searching for readily available, cost-effective biomarkers to assess metabolic disorders occurring before the onset and during the development of type-2 diabetes (T2DM). The aim of the present study was to induce T2DM in rats through a high-fat diet, followed by a single administration of low dose streptozotocin (STZ), and make an assessment of the development of the disease. The rats were divided into two groups-experimental and control-and were monitored for a period of 10 days. Changes in anthropometric parameters, glucose, insulin, lipids, uric acid, advanced oxidation protein products (AOPP), as well as the histological changes in the liver and pancreas, were recorded. To assess insulin resistance, we used the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and beta cell function (HOMA-ß) and visceral obesity-adiposity index (AI). The data demonstrate that the increasing values of glucose, HOMA-IR, AI, total cholesterol, triacylglycerols, low- and very-low-density lipoproteins are important markers of the pre-diabetic state. The stable hyperglycemia and increased levels of TC, TG, VLDL, LDL, uric acid and AOPP in experimental rats strongly suggest the development of T2DM. HOMA-IR, HOMA-ß, AI, and uric acid are reliable criteria for T2DM in rats.

Immune surveillance mechanisms of the skin against the stealth infection strategy of Pseudomonas aeruginosa-review.

The present review aims to provide insight into the complex interactions between the host and Pseudomonas aeruginosa-an opportunistic microbial agent causing skin infections. Heat, humidity and skin pH are among the factors beneficial for the development of this Gram-negative agent. To cause infection, Pseudomonas aeruginosa should first overcome the primary mechanisms of defense including the cell elements and humoral factors of the skin, as well as non-specific responses-phagocytosis, inflammation, acute phase response. All they are analysed with emphasis on the fact that their detailed understanding would help revealing their potential and allow for their efficient control. The microorganism, being more alterable and more flexible than the host, uses stealth strategies and modes of life. The review goes over the arsenal of virulence factors, used by Pseudomonas aeruginosa to attack the host defense mechanisms. The bacterial pathogenic strategies for invasion, resulting in collapse of skin defense are analysed. Several novel therapeutic approached to Pseudomonas aeruginosa skin infections are briefly reviewed.

High-fat feeding and Staphylococcus intermedius infection impair beta cell function and insulin sensitivity in mongrel dogs.

As obesity is a state of low-grade inflammation, we aimed to investigate the combined effect of high-fat diet and bacterial infection on beta-cell function and insulin sensitivity in dogs. We used 20 healthy, male, mongrel dogs randomly divided into four groups: control group-healthy, non-obese dogs; infected group-non-obese dogs with experimentally induced infection (Staphylococcus intermedius); obese group-obese dogs (after 90 day high-fat diet) and obese-infected group-obese dogs with experimentally induced infection (Staphylococcus intermedius). To evaluate insulin sensitivity and beta-cell function an intravenous glucose tolerance test (IVGTT) was performed. Plasma insulin increased in all group after glucose infusion. The lowest values were found in obese-infected group. Blood glucose also increased on 3 min after glucose infusion and then gradually decreased. In obese-infected group glucose concentration on 30 min was still significantly higher than initial levels, while in other groups glucose concentration returned to the initial values. The lowest rate of glucose elimination was found in infected group. In dogs of obese group and obese-infected group AUC(ins 0-60 min) was lower compared to controls. AUC(glucose 0-60 min) values were lowest in infected group, while in obese-infected group values were the highest. Levels of I/G in dogs of obese-infected group were significantly lower compared to controls and infected group. In conclusion, these results reveal that infection in obese dogs leads to impaired glucose tolerance, which is result of impairment in both insulin secretion and insulin sensitivity.

The effect of general anesthesia and abdominal surgery upon plasma thromboxane B concentrations in horses.

OBJECTIVE: To compare the effect of anesthesia alone with anesthesia and abdominal surgery on plasma thromboxane B(2) concentrations in horses. STUDY DESIGN: Non-randomized experimental study. ANIMALS: Six male mixed-bred horses (5-12 years, 350 +/- 18 kg). METHODS: All horses were anesthetized for 2.5 hours using halothane, and a month later abdominal surgery was performed using the same anesthetic technique with a similar duration. The schedule of anesthesia included pre-medication with diazepam (0.1 mg kg(-1) IM), followed by xylazine (2.2 mg kg(-1) IV), and 10 minutes later anesthesia was induced with ketamine hydrochloride (2.2 mg kg(-1) IV). After orotracheal intubation, anesthesia was maintained with halothane. Blood samples for the determination of thromboxane B(2) (TXB(2)) were obtained before, at induction, at 60 minutes after halothane was first inspired, and at recovery from anesthesia as well as at the corresponding stages of the experimental abdominal surgery (before induction, prior to laparotomy, enterectomy, enteroanastomosis, abdominal wall closure). RESULTS: Baseline value for the anesthesia group was 76 +/- 12 pg mL(-1) and increased (p < 0.001) after 1 hour of anesthesia to 265 +/- 40 pg mL(-1). With surgery, the corresponding value was 285 +/- 21 pg mL(-1) (hour 1, p < 0.001) and 210 +/- 28 pg mL(-1) (hour 2, p < 0.001), respectively. These were not different from anesthesia alone. CONCLUSION: The increased concentrations of thromboxane B(2) between 1 and 2.5 hours of halothane anesthesia and during the corresponding stages of the surgical intervention suggested that the anesthetic technique caused a significant increase in thromboxane B(2) and that surgery did not appear to contribute to this response.