Anti-oxidant effect of nitrite in the pancreatic islets of type 2 diabetic male rats.

Objectives: Nitrite, a nitric oxide (NO) donor, increases insulin secretion from pancreatic islets and has positive metabolic effects in type 2 diabetes (T2D). Here, we test the hypothesis of whether nitrite-induced insulin secretion is due to blunting of diabetes-induced oxidative stress in the islets.

Materials And Methods: T2D was created in male rats using a combination of streptozotocin at 25 mg/kg and a high-fat diet.

Reduced Expression Level of Protein Phosphatase PPM1E Serves to Maintain Insulin Secretion in Type 2 Diabetes.

Reversible phosphorylation is an important regulatory mechanism. Regulation of protein phosphorylation in β-cells has been extensively investigated, but less is known about protein dephosphorylation. To understand the role of protein dephosphorylation in β-cells and type 2 diabetes (T2D), we first examined mRNA expression of the type 2C family (PP2C) of protein phosphatases in islets from T2D donors.

Hydrogen sulfide potentiates the protective effects of nitrite against myocardial ischemia-reperfusion injury in type 2 diabetic rats.

Decreased heart levels of nitric oxide (NO) and hydrogen sulfide (HS) in type 2 diabetes (T2D) are associated with a higher risk of mortality following ischemia-reperfusion (IR) injury. This study aimed to determine the effects of co-administration of sodium nitrite and sodium hydrosulfide (NaSH) on IR injury in the isolated heart from rats with T2D. Two-month-old male rats were divided into 5 groups (n = 7/group): Control, T2D, T2D + nitrite, T2D + NaSH, and T2D + nitrite + NaSH.

Ribosomal biogenesis regulator DIMT1 controls β-cell protein synthesis, mitochondrial function, and insulin secretion.

We previously reported that loss of mitochondrial transcription factor B1 (TFB1M) leads to mitochondrial dysfunction and is involved in the pathogenesis of type 2 diabetes (T2D). Whether defects in ribosomal processing impact mitochondrial function and could play a pathogenetic role in β-cells and T2D is not known. To this end, we explored expression and the functional role of dimethyladenosine transferase 1 homolog (DIMT1), a homolog of TFB1M and a ribosomal RNA (rRNA) methyltransferase implicated in the control of rRNA.

Discovery of thymosin β4 as a human exerkine and growth factor.

Skeletal muscle is an endocrine organ secreting exercise-induced factors (exerkines), which play a pivotal role in interorgan cross talk. Using mass spectrometry (MS)-based proteomics, we characterized the secretome and identified thymosin β4 (TMSB4X) as the most upregulated secreted protein in the media of contracting C2C12 myotubes. TMSB4X was also acutely increased in the plasma of exercising humans irrespective of the insulin resistance condition or exercise mode.

Sodium hydrosulfide has no additive effects on nitrite-inhibited renal gluconeogenesis in type 2 diabetic rats.

Objective: Increased renal and hepatic gluconeogenesis are important sources of fasting hyperglycemia in type 2 diabetes (T2D). The inhibitory effect of co-administration of sodium nitrite and sodium hydrosulfide (NaSH) on hepatic but not renal gluconeogenesis has been reported in rats with T2D. The present study aimed to determine the effects of co-administration of sodium nitrite and NaSH on the expression of genes involved in renal gluconeogenesis in rats with T2D.

Long-term co-administration of sodium nitrite and sodium hydrosulfide inhibits hepatic gluconeogenesis in male type 2 diabetic rats: Role of PI3K-Akt-eNOS pathway.

Objective: A deficiency in hydrogen sulfide (HS) and nitric oxide (NO) contributes to the development of type 2 diabetes (T2D). An inhibitory effect on liver gluconeogenesis has been reported in rats with T2D with co-administration of sodium nitrite and sodium hydrosulfide (NaSH); the underlying mechanisms have however not yet been elucidated. The aim of this study is to determine the long-term effects of co-administering sodium nitrite and NaSH on expression of genes involved in liver gluconeogenesis in rats with T2D.

Insulin/Glucose-Responsive Cells Derived from Induced Pluripotent Stem Cells: Disease Modeling and Treatment of Diabetes.

Type 2 diabetes, characterized by dysfunction of pancreatic β-cells and insulin resistance in peripheral organs, accounts for more than 90% of all diabetes. Despite current developments of new drugs and strategies to prevent/treat diabetes, there is no ideal therapy targeting all aspects of the disease. Restoration, however, of insulin-producing β-cells, as well as insulin-responsive cells, would be a logical strategy for the treatment of diabetes.

Insulin secretion: The nitric oxide controversy.

Nitric oxide (NO) is a gas that serves as a ubiquitous signaling molecule participating in physiological activities of various organ systems. Nitric oxide is produced in the endocrine pancreas and contributes to synthesis and secretion of insulin. The potential role of NO in insulin secretion is disputable - both stimulatory and inhibitory effects have been reported.

Inorganic nitrate, a natural anti-obesity agent: A systematic review and meta-analysis of animal studies.

Evidence for potential effects of inorganic nitrate (NO) on body weight is limited to inconsistent findings of animal experiments. In this systematic review and meta-analysis, we aimed to quantify the overall effect of inorganic NO, administered via drinking water, on body weight gain in rats. We searched PubMed, Scopus, and Embase databases, and the reference lists of published papers.

Roles and Interaction of the MAPK Signaling Cascade in Aβ25-35-Induced Neurotoxicity Using an Isolated Primary Hippocampal Cell Culture System.

Alzheimer's disease (AD) is characterized with increased formation of amyloid-β (Aβ) in the brain. Aβ peptide toxicity is associated with disturbances of several intracellular signaling pathways such as mitogen activated protein kinases (MAPKs). The aim of this study was to investigate the role of MAPKs and their interactions in Aβ-induced neurotoxicity using isolated hippocampal neurons from the rat.

Protective effect of intermediate doses of hydrogen sulfide against myocardial ischemia-reperfusion injury in obese type 2 diabetic rats.

Objective: Subjects with type 2 diabetes (T2D) have lower circulating hydrogen sulfide (HS) levels following myocardial ischemia and a higher risk of mortality. The aim of this study was to determine the dose-dependent favorable effects of sodium hydrosulfide (NaSH) on myocardial ischemia-reperfusion (IR) injury in rats with T2D.

Methods: T2D was induced using a high-fat diet (HFD) and low-dose of streptozotocin.

Dose-Dependent Effects of Long-Term Administration of Hydrogen Sulfide on Myocardial Ischemia-Reperfusion Injury in Male Wistar Rats: Modulation of RKIP, NF-κB, and Oxidative Stress.

Decreased circulating levels of hydrogen sulfide (HS) are associated with higher mortality following myocardial ischemia. This study aimed at determining the long-term dose-dependent effects of sodium hydrosulfide (NaSH) administration on myocardial ischemia-reperfusion (IR) injury. Male rats were divided into control and NaSH groups that were treated for 9 weeks with daily intraperitoneal injections of normal saline or NaSH (0.

Data Extraction from Graphs Using Adobe Photoshop: Applications for Meta-Analyses.

Graphs, an effective form of data presentation, are used for summarizing complex information and making them easier to understand. Extracting numerical data from graphs, which is commonly required in systematic reviews and meta-analyses, is however a challenging issue. Since this kind of results presentation is common, ignorance of such data may result in publication bias when conducting meta-analyses.

Regulation of carbohydrate metabolism by nitric oxide and hydrogen sulfide: Implications in diabetes.

Nitric oxide (NO) and hydrogen sulfide (HS) are two gasotransmitters that are produced in the human body and have a key role in many of the physiological activities of the various organ systems. Decreased NO bioavailability and deficiency of HS are involved in the pathophysiology of type 2 diabetes and its complications. Restoration of NO levels have favorable metabolic effects in diabetes.

Hydrogen sulfide potentiates the favorable metabolic effects of inorganic nitrite in type 2 diabetic rats.

Objective: Decreased nitric oxide (NO) bioavailability and hydrogen sulfide (HS) deficiency have been linked with the pathophysiology of type 2 diabetes (T2D). Restoration of NO levels by nitrite have been associated with favorable metabolic effects in T2D. Moreover, HS can potentiate the effects of NO in the cardiovascular system.

Altered gene expression of hydrogen sulfide-producing enzymes in the liver and muscles tissues of hyperthyroid rats.

Thyroid hormones have a role in the regulation of hydrogen sulfide (H S) biosynthesis. In this study, we determined the effects of hyperthyroidism on H S levels in various tissues and messenger RNA (mRNA) expression of cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST) in the liver and muscles of the rat. Sixteen male Wistar rats were divided into the hyperthyroid and the control groups.

Effects of Hydrogen Sulfide on Carbohydrate Metabolism in Obese Type 2 Diabetic Rats.

Hydrogen sulfide (H₂S) is involved in the pathophysiology of type 2 diabetes. Inhibition and stimulation of H₂S synthesis has been suggested to be a potential therapeutic approach for type 2 diabetes. The aim of this study was therefore to determine the effects of long-term sodium hydrosulfide (NaSH) administration as a H₂S releasing agent on carbohydrate metabolism in type 2 diabetic rats.

Effects of long-term oral nitrate administration on adiposity in normal adult female rats.

Introduction: Nitric oxide (NO) deficiency is associated with obesity. Nitrate could act as a substrate for production of NO and is a novel therapeutic agent in obesity. This study aims at determining effects of long-term nitrate administration on obesity indices in normal adult female rats.

Effects of long-term nitrate supplementation on carbohydrate metabolism, lipid profiles, oxidative stress, and inflammation in male obese type 2 diabetic rats.

Purpose: Supplementation with inorganic nitrate to boost the nitrate-nitrite-nitric oxide (NO) pathway, may act as a potential therapeutic agent in diabetes. The aim of this study was to determine the effects of nitrate on carbohydrate metabolism, lipid profiles, oxidative stress, and inflammation in obese type 2 diabetic rats.

Methods: Male Wistar rats were divided into 4 groups: Control, control + nitrate, diabetes, and diabetes + nitrate.

Regulation of vascular tone homeostasis by NO and HS: Implications in hypertension.

Nitric oxide (NO) and hydrogen sulfide (HS) are two gasotransmitters that are produced in the vasculature and contribute to the regulation of vascular tone. NO and HS are synthesized in both vascular smooth muscle and endothelial cells; NO functions primarily through the sGC/cGMP pathway, and HS mainly through activation of the ATP-dependent potassium channels; both leading to relaxation of vascular smooth muscle cells. A deficit in the NO/HS homeostasis is involved in the pathogenesis of various cardiovascular diseases, especially hypertension.

A practical guide for induction of type-2 diabetes in rat: Incorporating a high-fat diet and streptozotocin.

Prevalence of diabetes, a serious public health problem is rapidly increasing worldwide. Type-2 diabetes is the common form of diabetes characterized by insulin resistance and abnormalities in insulin production. Despite the current development of therapeutic agents, there is no effective treatment without side effects; it is therefore necessary to find new prevention strategies and better treatments.