BACKGROUND: Vanadium and zinc are identified as low-concentration elements in the body of living organisms with a wide range of activities. Their insulin-like activity, through regulating the metabolism of carbohydrates, lipids, and eliminating the secondary symptoms of the disease, clearly demonstrates the ability of these elements to improve diabetes.OBJECTIVES: The present study aimed to evaluate the effect of vanadium-zinc complex on the structural, functional, and oxidative stress changes in liver tissue in adult diabetic male rats.METHODS: Herein, we recruited 40 adult male rats with the same weight range. They were randomly divided into four groups of 10, namely control, diabetic, healthy mice receiving vanadium-zinc complex, diabetic mice receiving vanadium-zinc complex) and received this combination at the rate of 10 mg / kg once a day for 60 days by oral gavage. At the end of the course, following blood sampling, part of the liver tissue was removed from the body to measure oxidative stress and the rest for stereological and histological studies. The serum isolated from the animals was also used to measure liver tissue functional enzymes (aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase).RESULTS: The results of this research revealed that vanadium-zinc complex has no side effects on liver tissue in most case, but can greatly prevent structural damage to liver tissue by lowering blood glucose levels in diabetic rats and improving oxidative stress.CONCLUSIONS: Vanadium-zinc complex can be utilized with a certain mechanism in order to control blood sugar and inhibit oxidative stress. It could be regarded as an appropriate approach to preventing liver damage following chronic hyperglycemia in diabetic patients.

BACKGROUND: Flufenamic acid is a member of the fenamates and is used as an analgesic and NSAID drug. According to the ability of this drug on blocking connexin and preventing leakage of substances such as ATP from cells, it seems to be beneficial in healing diabetic wounds. OBJECTIVES: Evaluation of the effects of topical flufenamic acid as a connexin-channel blocker on skin wound healing in alloxan-induced diabetic rats. METHODS: In this study diabetics was induced in 40 male rats by IP injection of 150mg/kg of alloxan and they were divided to 4 groups. After anesthesia, 2×2 cm incision was made on the back of the rats and the skin was separated completely. Three groups were treated by 2, 5 and 10 percent concentration of flufenamic acid ointment separately, and one group was treated by Vaseline and ucerine ointment as control. Bandage and ointment were changed daily and the procedure was carried out for 21 days. The wound surface was measured on odd days. Half of the rats of each group on day five and half of them on day 21 were euthanized to get pathologic slides. RESULTS: Process of healing, fibroblast concentration, epithelialization, angiogenesis, collagen formation and wound closure in 2 percent group were better than other groups and in control, 5 and 10 percent groups had a decreasing trend respectively and had a significant difference. In the last two groups, the healing process was disrupted. CONCLUSIONS: The 2 percent concentration of drug not only did not show potent anti-inflammatory effects, but also improved the process of healing by blocking the connexin 43 and inhibition of ATP release, while in the concentration of 5 and 10 percent, anti-inflammatory effects of the drug predominated and delayed the healing process.

The relation of the glycated serum protein, fructosamine, to serum protein, albumin, and glucose concentrations was examined in healthy dogs, dogs with hypo- or hyperproteinemia, and diabetic dogs. Fructosamine was determined by use of an adaptation of an automated kit method. The reference range for fructosamine in a composite group of control dogs was found to be 1.7 to 3.38 mmol/L (mean +/- SD, 2.54 +/- 0.42 mmol/L). Fructosamine was not correlated to serum total protein, but was highly correlated to albumin in dogs with hypoalbuminemia. To normalize the data with respect to albumin, it is suggested that the lower limit of the reference range for albumin concentration (2.5 g/dl) be used for adjustment of fructosamine concentration and only in hypoalbuminemic dogs. In 6 hyperglycemic diabetic dogs, fructosamine concentration was well above the reference range. It is concluded that although fructosamine may be a potentially useful guide to assess the average blood glucose concentration over the preceding few days in dogs, further study is required to establish its value as a guide to glucose control in diabetic dogs.

This study investigated the effects of intragastric administration of apelin-13 on the secretion of critical pancreatic hormones in a cohort of three-week-old Wistar rats. The research aimed to uncover apelin’s modulatory roles in endocrine interactions dictating metabolic homeostasis during early life.

Glucagon-like peptide-1 (GLP-1) is a polypeptide that is mainly produced by intestinal L cells and is encoded by the proglucagon gene. In this study, GLP-1 localisation was investigated in the ileum of healthy and diabetic mice by immunohistochemistry and proglucagon gene expression was assayed by reverse transcription-polymerase chain reaction. This study included 18 male Balb/c mice that were divided into diabetic, sham, and control groups. Mice in the diabetic group received 100 mg/kg of streptozotocin. Immunohistochemical expression of GLP-1 was determined using the avidin–biotin–peroxidase complex technique, and proglucagon gene expression was determined by RT-PCR. Analysis of GLP-1 immunohistochemical localisation showed that GLP-1-immunopositive cells (L cells) were present between epithelial cells in the intestinal crypts. The intensity and localisation of GLP-1 immunoreactivity were similar among the mice in all the groups. Proglucagon gene expression levels were also statistically similar among the mice in all the groups. No difference was demonstrated among the mice in the diabetic, sham, or control groups with respect to proglucagon gene expression and GLP-1 localisation in the ileum, suggesting that diabetes does not affect proglucagon gene expression in the ileum.

To investigate the possible effect of N-acetylcysteine (NAC) treatment on rat diabetes-induced liver damage and immune reactivity of asprosin hormone in the liver. Twenty-eight Wistar albino male rats were used in the study. They were separated into 4 groups as Control (n=7), Diabetes (n=7), Diabetes+NAC (n=7), and NAC (n=7). The rats in all groups were dissected after the treatment, and liver tissues were taken for pathological examination. Tissue sections were stained with immunohistochemistry for detecting asprosin immunoreactivity, hematoxylin-eosin and picrosirius red staining were performed to determine the changes in the tissues.In the microscopical examination of hematoxylin-eosin-stained sections normal histological hepatic tissues were seen in the Control and NAC groups. Pathological examination of liver tissue from diabetic rats showed marked dissociation, fibrosis, degeneration, inflammation, necrosis, Kupffer cells activation, bile duct proliferation, and congestion. A significant decrease in these lesions was observed in the DM+NAC group. Immunohistochemical studies showed that asprosin immunoreactivity was increased in the DM group in a significant manner. Asprosin expression was observed to be significantly reduced in the DM+NAC group in comparison to the DM group.Our findings show that NAC administration reduces liver damage in diabetic rats and can be used to reduce/eliminate the negative effects of diabetes in rat liver tissue..

This study was conducted with the purpose of investigating the distribution of the Activating Transcription Factor 6 (ATF6) and the Nerve Growth Factor (NGF) in the duodenum tissue of diabetic and non-diabetic rats. Eighteen female Sprague dawley rats were randomly divided into three groups as thecontrol, sham and diabetes groups. Routine histological and immunohistochemical methods were appliedon the duodenum tissues collected at the end of the study.Results: It was determined that the villus length measurements showed a statistically significant differencebetween the control and diabetes groups. There was NGF immunoreactivity which was moderate anddiffuse cytoplasmic in the villus intestinalis and muscularis layer in all groups, weak in the crypts andglands in the control and sham groups and moderate and diffuse cytoplasmic in the diabetes group. ATF6immunoreactivity was determined moderate in the villus intestinalis, crypts, glands and muscularis layerin the control and sham groups and strong diffuse cytoplasmic in the diabetes group. It wasdetermined that both NGF and ATF6 immunoreactivity increased in the duodenum tissue of the rats onwhich diabetes was induced experimentally.

Although benfotiamine has various beneficial anti-diabetic effects, the detailed mechanisms underlying the impact of this compound on the insulin signaling pathway are still unclear. In the present study, we evaluated the effects of benfotiamine on the hepatic insulin signaling pathway in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are a type 2 diabetes mellitus model. OLETF rats treated with benfotiamine showed decreased body weight gain and reduced adipose tissue weight. In addition, blood glucose levels were lower in OLETF rats treated with benfotiamine. Following treatment with benfotiamine, the levels of Akt phosphorylation (S473/T308) in the OLETF groups increased significantly compared to the OLETF control group so that they were almost identical to the levels observed in the control group. Moreover, benfotiamine restored the phosphorylation levels of both glycogen synthase kinase (GSK)-3¥�/¥�(S21, S9) and glycogen synthase (GS; S641) in OLETF rats to nearly the same levels observed in the control group. Overall, these results suggest that benfotiamine can potentially attenuate type 2 diabetes mellitus in OLETF rats by restoring insulin sensitivity through upregulation of Akt phosphorylation and activation of two downstream signaling molecules, GSK-3¥�/¥� and GS, thereby reducing blood glucose levels through glycogen synthesis.

Carnosine is a dipeptide (β-alanyl-L-histidine) found in mammalian brain, eye, olfactory bulb and skeletal muscle at high concentrations. Its biological functions include antioxidant and anti-glycation activities. The objectives of this study were to investigate anti-diabetic effects of carnosine as determined by blood glucose levels, glucose tolerance test (GTT), glycosylated emoglobin, and serum biochemical and lipid levels in streptozotocin-induced diabetic mice. There were five experimental groups including normal (ICR mice), control (saline), and three groups of carnosine at doses of 6, 30, and 150 mg/kg b.w.. Carnosine was orally administered to the diabetic mice everyday for 12 weeks. There was no significant difference in body weight changes in carnosine-treated groups compared to the control. The treatments of carnosine at the dose of 6 mg/kg significantly decreased the blood glucose level compared with the control at 2 and 4 weeks. The treatments of carnosine at the doses of 6 and 30 mg/kg significantly decreased the blood glucose levels in GTT and glycosylated hemoglobin compared with the control. Carnosine significantly increased total proteins compared with the control. Carnosine at the dose of 6 mg/kg significantly decreased total cholesterol and triglyceride in the serum compared to the control. These results suggest that carnosine at a low level has a hypoglycermic effect resulting from reduction of blood glucose and that a carnosine-containing diet or drug may give a benefit for controlling diabetes mellitus in humans.