Nesfatin-1 (NES-1) is a newly discovered multi-functional peptide hormone with an approximate molecular weight of 9.8 kilo Dalton and a half-life of 23.5 minutes. It was first discovered in 2006 by Oh-I and his coworkers. 1-3 NES-1 is derived from nucleobindin2 (NUCB2) precursor, which is DNA and calcium binding protein that is found in the plasma membrane and neuroplasma. NUCB2 is highly conserved in humans, rats, and mice, that shares more than 85% of homology between humans and the other mammal species and even demonstrates similarities with lower organisms. [3][4][5] The NUCB2 precursor protein is possibly posttranslationally cleaved by the enzyme prohormone-convertase into the N-terminal NES-1amino acids 1-82 (AA 1-82), NES-2 (AA 85-163) and the C-terminal NES-3 (AA 166-396). 1,6 Several biological actions for NES-1 have been identified, specifically of the middle part of it, which corresponds to AA 24-53, it has a key role in physiological effects of NES-1, particularly for an anorexic effect, whereas no biological action has been described for NES-2 and NES-3. 6,7 NUCB2 and NES-1 are expressed by the central nervous system (CNS) and peripheral tissues. In CNS, expressed prominently in the Background and objective: Nesfatin-1 is a newly described peptide, derived from nucleobindin2. Nesfatin-1 suppresses food intake and it is involved in regulating insulin secretion. The aim of this study was to compare serum levels of Nesfatin-1 in patients having type 2 diabetes and non-diabetic subjects. Methods: This cross-sectional study included 90 participants; 64 patients with type 2 diabetes mellitus (32 males and 32 females) and 26 control subjects (13 males and 13 female). Body mass index, fasting serum level of glucose, fasting serum level of insulin, and glycated hemoglobin were estimated. Homeostasis model assessment of insulin resistance was calculated. Nesfatin-1 level was measured using enzyme-linked immunesorbent assay kit. The data was analyzed using Graphpad prism 7.04 for windows. Results: Type 2 diabetes patients aged from 33-78 years and the control group aged from 32-75 years. Nesfatin-1 level in the diabetic group was significantly lower than controls. The median interquartile range (IQR) of Nesfatin-1 was 0.765 (0.4-1.173) in diabetes and 1.02 (0.775-1.458) in controls. The diabetes group has significantly higher homeostasis model assessment of insulin resistance compared with non-diabetics. Serum Nesfatin-1 was correlated negatively with body mass index, fasting serum glucose, fasting serum insulin, glycatedhemoglobin, and homeostasis assessment of insulin resistance. Conclusion: Serum Nesfatin-1 level is negatively correlated with fasting serum glucose, fasting serum insulin, and glycated hemoglobin. This association supports the role of Nesfatin-1 in increased insulin resistance in patients with type 2 diabetes.

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Cadmium (Cd) is a toxic element and a common pollutant associated with many industrial processes. 1 It is widely distributed in the environment and has high toxicity and mobility in the ecosystem. Exposure to Cd occurs mainly through the ingestion of contaminated food, water, inhalation, and tobacco smoking. Cd has a long biological half-life (>20 years) and accumulates in the body, mostly in the liver, kidney, and intestines. Also, Cd accumulates in the testes for about 1-2% of an acute dose depending on age, body nutritional status, dosage, and the time exposure to Cd. 2 Cadmium affects the cardiovascular system negatively, and it is involved in producing several acute and chronic diseases such as hypertension, atherosclerosis, and endothelial dysfunction. 3 The most common mechanisms causing hypertension associated with Cd may include the interference with the renin-angiotensin system, impaired nitric oxide, oxidative stress, altered vascular response to the Background and objective: Cadmium is a widely distributed metal in the environment that causes testicular toxicity and various tissue damage associated with hypertension. Omega-3, an essential fatty acid, has been demonstrated to be an effective antioxidant and anti-inflammatory agent. This study aimed to investigate the toxic effects of cadmium on cardiovascular and reproductive systems in male rats and examine the possible protective effects of omega-3 against cadmium-induced hypertension and testicular dysfunctions. Methods: The rats were divided into three groups. The first group served as the control, the second group received cadmium chloride in drinking water, and the third group received cadmium chloride plus omega-3 for 28 days. Blood pressure and heart rate were estimated. Blood samples were collected; sexual hormones and other biochemical parameters were evaluated. Testes and epididymis were taken for semen analysis and histopathology. Results: Significant adverse effects were seen in the studied parameters of the cardiovascular and reproductive systems after cadmium exposure, including hypertension, alteration in sperm parameters, weights of sex glands, and histological structures. In contrast, co-administration of omega-3 significantly reduced mean blood pressure, but improved sperm parameters and the histology of testis. No protective effect of omega-3 could be seen on male hormone and lipid profile parameters except high-density lipoprotein. Conclusion:Exposure to cadmium induced hypertension, impaired testicular functions, and histology. Omega-3 has protective effects on vascular and testicular functions. Therefore, supplementation with omega-3 had a protective effect against cardiovascular and reproductive toxicity induced by cadmium.