Pancreatic damage induced by cigarette smoke: The specific pathological effects of cigarette smoke in the rat model

In recent years, pancreatic pathologies have become common problems and their etiology and pathogenesis are generally unknown. Studies have shown that smoking may increase the risk of pancreatic disorders but very scant knowledge is available about the pathogenesis of cigarette induced pancreatic pathology. This study aimed to evaluate the oxidative stress status, biochemical, pathological and immunohistochemical findings of rats exposed to cigarette smoke, pathogenesis of smoking related pancreatic damage and usability of Alpha Lipoic Acid (ALA) for amelioration of cigarette smoking induced harmful effects on rat pancreas. Twenty eight female, Sprague Dawley rats were randomly distributed into three groups. The sham group (S) (n = 8), rats were given 0.1 ml of physiological serum by oral gavage for 8 weeks. The cigarette smoke exposed group (CSE) (n = 10), rats were exposed to successive periods of cigarette smoke for 2 hours per day per 8 weeks and given 0.1 ml of physiological serum orally during the study. The cigarette smoke exposed and ALA treated group (CSE + ALA) (n = 10), animals were exposed to cigarette smoke (2 hours per day per 8 weeks) and simultaneously treated with 100 mg per kg per day ALA orally during the study. At the end of the study, the serum samples were collected for insulin, glucagon, glucose and amylase analyses. Tissue samples were collected for biochemical, histopathological and immunohistochemical examinations. Total oxidant status (TOS), total antioxidant status (TAS) levels and oxidative stress index (OSI) were evaluated in the pancreas samples. Immunohistochemical analyses of insulin, glucagon, calcitonin gene related protein (CGRP), active caspase-3, hypoxia inducible factor-1 (Hif-1), Hif-2 and tumor necrosis factor (TNF-α) expressions of pancreas were examined. Cigarette smoke caused statistically significant increase in serum amylase and glucose but decreased insulin levels indicating both endocrine and exocrine cell damage. There were no statistically significant differences in serum glucagon levels between the groups. Histopathological examination of the pancreas exhibited generally normal tissue architecture but slightly degenerative and apoptotic cells were noticed both in the endocrine and exocrine part of the pancreas in the CSE group. Immunohistochemical analyses revealed marked increase in active caspase-3, Hif-1 and Hif-2, CGRP and TNF-α expressions with a slight increase in glucagon immunoreactivity in cells while a marked decrease was observed in insulin expression in some Langerhans islets in the CSE group. ALA ameliorated biochemical and pathological findings in the CSE + ALA group. These findings clearly demonstrated that cigarette smoke can cause damage in both endocrine and exocrine cells in rat pancreas and ALA has an ameliorative effect of cigarette induced lesions. © 2016 The Royal Society of Chemistry

Protective effects of aspirin and vitamin C against corn syrup consumption-induced cardiac damage through sirtuin-1 and HIF-1α pathway

Objective: The aim of this study was to investigate the protective effects of aspirin (AS) and vitamin C (VC) against cardiac damage induced by chronic corn syrup (CS) consumption via a mechanism involving sirtuin-1 (ST-1), hypoxia-inducible factor-1α (HIF-1α), and the caspase-3 pathway in rats. Methods: Forty male Sprague-Dawley rats (14-16 weeks) that weighed 250-300 g were randomly distributed into 5 groups, each containing 8 rats: control group, CS+AS group, CS+VC group, CS+AS+VC group, and CS group. AS (10 mg/kg/day) and VC (200 mg/kg/day) were orally given to the rats. F30 (30% fructose syrup solution) was given to the rats in drinking water for 6 weeks. The rats were sacrificed by exsanguination 24 h after the last administration. Blood samples and tissue were collected for biochemical, histopathological, and immunohistochemical examinations. Non-parametric Kruskal-Wallis test and Mann-Whitney U test used for the parameters without normal distribution and ANOVA and post-hoc LSD tests were used for parameters with a normal distribution to compare groups. Results: Uric acid, creatine kinase (CKMB), and lactate dehydrogenase (LDH) levels were increased in the CS group compared with the control group (1.45±0.39 and p=0.011; 3225.64±598.25 and p=0.004; 3906.83±1064.22 and p=0.002, respectively) and decreased in all the treatment groups. In addition, increased levels of MDA and decreased activity of CAT in the CS group (0.172±0.03 and p=0.000; 0.070±0.005 and p=0.007, respectively) were reversed with AS and VC therapy. A decrease in ST-1 activity and increases in caspase-3 and HIF-1 activities corrected by VC and AS therapy were observed. Conclusion: AS and VC, which display antioxidant and antiapoptotic activities, ameliorated cardiac damage induced by chronic fructose consumption by increasing the levels of ST-1 and decreasing the levels of HIF-1α and caspase-3. © 2016 by Turkish Society of Cardiology

A case of acromegaly in the presence of coincidental liver cirrhosis

Context: Acromegaly is a rare and serious syndrome and commonly associated with pituitary neoplasm. Classic cause of acromegaly in adults is the tumors of the somatotrophs that secrete growth hormone. Cirrhosis is the end stage of chronic liver disease and commonly a cause of death. It is characterized by diffuse hepatic fibrosis resulting in altered construction of the lobular parenchyma with widespread connective tissue scptae, circumscribed regenerative nodules of hepatocytcs and anastomoses between vascular channels linking portal and central vessels. Objective: To report the simultaneous cases of acromegaly and cirrhosis. Case report: A 62-year old, male patient came to the hospital complaining of severe abdominal swelling. Laboratory and imaging findings were compatible with the presence of hepatitis B virus related cirrhosis together with acromegaly. In this case, he had high GH level but lower IGF-1 level because of hepatic failure which can impair IGF-1 production by the liver. Definitive diagnosis was made by pituitary MR and a 1 cm in diameter tumor was detected. Conclusion: This paper showed that cirrhosis can result in a low IGF-I level in patients with acromegaly. There is no previous report available of the in the presence of coincidental combination of acromegaly and cirrhosis in a patient

Leptin receptor gene polymorphism may affect subclinical atherosclerosis in patients with acromegaly

Background: Acromegaly is associated with increased morbidity and mortality related to cardiovascular diseases. Leptin (LEP) and Leptin Receptor (LEPR) gene polymorphisms can increase cardiovascular risks. The aim of this study was to investigate association between the frequencies of LEP and LEPR gene polymorphisms and subclinical atherosclerosis in acromegalic patients. Methods: Forty-four acromegalic patients and 30 controls were admitted to study. The polymorphisms were identified by using polymerase chain reaction from peripheral blood samples. The levels of systolic and diastolic blood pressure, BMI, fasting plasma glucose, fasting insulin, IGF-I, GH, IGFBP3, leptin, triglyceride, carotid Intima Media Thickness (cIMT) and HDL and LDL cholesterol concentrations were evaluated. Results: There was statistically significant difference between the LEPR genotypes of acromegalic patients (GG 11.4%, GA 52.3%, and AA 36.4%) and controls (GG 33.3%, GA 50%, and AA 16.7%) although their LEP genotype distribution was similar. In addition, the prevalence of the LEPR gene G and A alleles was significantly different between patients and controls. No significant difference was found among the G(-2548) A leptin genotypes of groups in terms of the clinical parameters. cIMT significantly increased homozygote LEPR GG genotype group compared to AA subjects in patients. But the other parameters were not different between LEPR genotypes groups of patients and controls. Conclusion: It can be said that the LEPR gene polymorphism may affect cIMT in patients. The reason is that LEPR GG genotype carriers may have more risk than other genotypes in the development of subclinical atherosclerosis in acromegaly. © 2016, Avicenna Journal of Medical Biotechnology. All rights reserved

The association between central adiposity and autonomic dysfunction in obesity

Objective: To determine the relationship between central adiposity parameters and autonomic nervous system (ANS) dysfunction. Subjects and Methods: The study included 114 obese individuals without any cardiovascular risk factors. Weight (in kg), height (in m), and waist circumference (WC; in cm) were measured and body mass index was calculated. Echocardiographic examination was performed to measure left ventricular mass and epicardial fat thickness (EFT). All the participants underwent an exercise test and electrophysiological evaluation using electromyography. Heart rate recovery (HRR) at 1-5 min, R-R interval variation at rest and during hyperventilation, and sympathetic skin response were measured. Pearson's correlation analysis was used. Multiple linear regression analysis was used to identify the factors associated with autonomic dysfunction. Results: The HRR at 1-5 min was negatively correlated with WC and age (WC-HRR1: r = -0.32; WC-HRR2: r = -0.31; WC-HRR3: r = -0.26; WC-HRR4: r = -0.23; WC-HRR5: r = -0.21; age-HRR2: r = -0.32; age-HRR3: r = -0.28; age-HRR4: r = -0.41; age-HRR5: r = -0.42). Age was the only independent predictor of reduced HRR at 1-5 min. In addition, WC predicted a reduced HRR at 3 min. There were no significant associations between central obesity and electrophysiological parameters. EFT was not associated with ANS dysfunction. Conclusion: In this study, central adiposity and aging were associated with ANS dysfunction in obese individuals. The WC could be a marker of ANS dysfunction in obese individuals without any cardiovascular risk factors. The HRR assessment at a later decay phase could be more valuable for evaluating ANS function than during early recovery. © 2016 S. Karger AG, Basel

Interaction apelin, procalcitonin and fetuin-a levels with thicness of carotis intima media in acromegalic patients

Akromegali, kardiyovasküler mortalitenin arttığı bir hastalık olup, artmış metabolik bozukluklar erken kardiyovasküler komplikasyonlara sebep olmaktadır. Araştırmalar aterosklerozun erken tespiti ve bu konuda kullanılacak yeni yöntemler üzerinde yoğunlaşmaktadır. Apelin, adipoz dokudan derive bir peptiddir. Plazma düzeylerinin, obezitede hiperinsülinemi ile birlikte arttığı rapor edilmiştir. Fetuin-a, hepatositler tarafından üretilen bir plazma glikoproteini olup, en önemli sistemik kalsifikasyon inhibitörüdür. Yapılan çalışmalarda, koroner kalsifikasyonun patogenezinde rol oynadığı gösterilmiştir. Aterosklerozun patogenezinde inflamasyonun önemi bilinmektedir. İnflamasyonda rol oynayan prokalsitonin (PKT) gibi sistemik belirteçlerin aterosklerozda yükseldiği ve hastalık aktivitesini gösterdiği saptanmıştır. Karotis intima media kalınlık ölçümü (KİMK), hem endotel disfonksiyonunu, hem de erken dönem yaygın aterosklerozu gösteren bir tekniktir. Bu çalışmanın amacı; akromegali hastalarında apelin, PKT ve fetuin-a düzeylerinin ateroskleroza etkisini araştırmaktır. Çalışmaya 37 hasta ve 30 kontrol alındı. Grupların boy-kilo ölçümleri, beden kitle indeksleri, tansiyonları kaydedildi. AKŞ, lipit profili, GH, IGF-1, IGFBP3, TSH, insülin değerleri ölçüldü. Her iki gruba KİMK ölçümü yapıldı. Elisa yöntemiyle apelin, PKT ve fetuin-a çalışılması için kan alındı. Akromegali hastalarında apelin, PKT ve fetuin-a düzeylerini istatistiksel olarak anlamlı yüksek saptadık. Bizim çalışmamız akromegalide fetuin-a'yı inceleyen ilk çalışmaydı ve hastalarda çok yüksek saptandı. Hasta ve kontrollerin KİMK ölçümleri arasında fark saptanmadı. Korelasyon analizinde KİMK ölçümleri ile apelin, fetuin-a ve PKT düzeyleri arasında bağlantı gözlenmedi.Acromegaly is associated with increased risk of cardiovascular mortality. Numerous studies have been focused on new methods that can detect aterosclerosis at early stages. Apelin is a peptide that is derived from adipose tissue. Reports are available about higher plasma levels in obesity with hyperinsulinemia. Fetuin-a is a plasma glycoprotein that is produced by hepatocytes and it is the most important systemic calcification inhibitor. Studies showed that it plays a role in the pathogenesis of coronary calcification. The importance of inflammation is known in the pathogenesis of atherosclerosis. Systemic markers of inflammation like procalcitonin (PCT) increases in atherosclerosis and correlates with disease activity. Measurement of carotis intima media thickness (CIMT) is a technique that shows both endothelial dysfunction and early changes of extensive atherosclerosis. The aim of this study was to investigate the effect of apelin, PCT and fetuin-a levels on atherosclerotic process in acromegalic patients. In this study 37 acromegalic patients and 30 controls were included to the study. Height, weight, body mass index and blood pressure of the groups were noted. Fasting blood glucose, lipid profile, GH, IGF-1, IGFBP3, TSH, insulin levels were measured. CIMT was measured in both groups. Apelin, PCT and fetuin-a levels were measured by Elisa method. We observed significantly higher apelin, PCT and fetuin-a levels in acromegalic patients. Our study was the first study that evaluates fetuin-a levels in acromegalic patients and we found high levels of fetuin-a in acromegalic patients. CIMT of patients and controls were similar. There was no correlation between CIMT and apelin, fetuin-a and PCT levels

Preventive effect of agomelatine in lipopolysaccharide-induced pancreatic pathology

The aim of this study was to examine pancreatic lesions and the possible prophylactic effects of agomelatine (AGO) in lipopolysaccharide (LPS)-induced sepsis in rats. Twenty-four female, 1-year-old Wistar albino rats were divided into three groups: group I (control), group II (study group; 5 mg/kg LPS i.p., single dose), and group III (treatment group; LPS + AGO, single dose p.o., 20 mg/kg AGO + 5 mg/kg LPS, 30 minutes after AGO treatment). The rats were sacrificed six hours after LPS administration. At the necropsy, blood and pancreatic tissue samples were collected for biochemical, pathological, and immunohistochemical analyses. The results showed that LPS caused an increase in serum amylase and lipase levels and a decrease in glucose levels. Histopathological analysis revealed infiltration of numerous neutrophils in pancreatic interstitial tissue and in vessels. In addition, slight vacuoles indicating degenerative changes were observed in endocrine and exocrine pancreatic tissues. Increased caspase-8, haptoglobin (Hp), IL-4, and IL-10 and decreased SIRT-1 expression was observed in both endocrine and exocrine parts of the pancreas in the LPS group. AGO ameliorated the biochemical, histopathological, and immunohistochemical findings. The present study results revealed that LPS-induced pancreatic damage to both endocrine and exocrine cells. In contrast, AGO had ameliorative effects on both biochemical and pathological findings in rats. © 2020, © 2020 Informa UK Limited, trading as Taylor & Francis Group

The ameliorative effect of gallic acid on pancreas lesions induced by 2.45 GHz electromagnetic radiation (Wi-Fi) in young rats

The aim of this study was to investigate the effects of electromagnetic radiation (EMR) on the pancreas tissue of young rats and the ameliorative effect of Gallic acid (GA). Six-week-old, 48 male rats were equally divided into four groups: Sham group, EMR group (2.45 GHz), EMR (2.45 GHz)+GA group (30 mg/kg/daily) orally and GA group (30 mg/kg/daily). After 30 days, serum and pancreatic tissue samples were harvested for biochemical, histopathological and immunohistochemical analysis. Serum amylase, lipase, glucose, and tissue malondialdehyde, total oxidant status and oxidative stress index were increased, whereas total antioxidant status decreased in the EMR group. The histopathological examination of the pancreases indicated slight degenerative changes in some pancreatic endocrine and exocrine cells and slight inflammatory cell infiltrations in the EMR group. At the immunohistochemical examination, marked increase was observed in calcitonin gene related protein and Prostaglandin E2 expressions in pancreatic cells in this group. There were no changes in interleukin-6 expirations. GA ameliorated biochemical and pathological findings in the EMR+GA group. These findings clearly demonstrate that EMR can cause degenerative changes in both endocrine and exocrine pancreas cells in rats during the developmental period and GA has an ameliorative effect. (C) 2017 The Egyptian Society of Radiation Sciences and Applications. Production and hosting by Elsevier B.V

Effects of caffeine and lycopene in experimentally induced diabetes mellitus

Objectives: Diabetes mellitus (DM) is a global epidemic with increasing prevalence. The disease is chronic in nature, and patients must use antidiabetic drugs or insulin during their lifespan. Because of the difficulty of using injectable insulin preparations, patients and practitioners prefer to use oral antidiabetic drugs for prophylaxis and treatment. There are, however, numerous adverse effects of antidiabetic drugs and rapidly increasing attention is being paid to new nutraceutical drugs with fewer adverse effects. The purpose of this study was to evaluate the effects of caffeine and lycopene on streptozotocin (STZ)-induced DM in rats. Methods: Caffeine and lycopene were administered to the study groups by oral gavages for 1 month whereafter experimental diabetes was induced in 90 rats in 6 groups. Results: There were no pathological effects of lycopene and caffeine on the pancreas. Marked vacuolization and degeneration were observed in STZ-treated groups. Caffeine and lycopene decreased the pathological findings and lowered the blood and urine glucose levels in the rats with STZ-induced DM, whereas these compounds increased serum insulin levels. Conclusions: This study showed that caffeine and lycopene provided protective effects against experimentally induced DM. The protective effects of lycopene were observed to be much greater than those of caffeine. © 2016 Wolters Kluwer Health, Inc. All rights reserved

Tuberculosis with adrenal insufficiency mimicking malignancy in FDG-PET images

Addison’s disease may result from adrenal tuberculosis (TB), malignancy, idiopathic adrenal atrophy, blastomycosis or histoplasmosis. Thus, adrenal masses are often characterized by fluorine-18 fluoro-2-deoxy-D-glucose positron emission tomography (18F FDG-PET), which identifies tumors by their increased glucose metabolism. However, a large number of clinical conditions lead to false positives in PET, often related to inflammation or infection. Herein, we present a patient with adrenal insufficiency associated with bilateral masses and a history of TB. We identified elevated FDG uptake in both adrenal glands that could not be differentiated from primary bilateral adrenal lymphoma or other malignancies. Following adrenalectomy, a final diagnosis of adrenal TB was made. This uncommon case emphasizes that benign adrenal lesions can have increased FDG uptake leading to false-positive results. © 2016, Nobelmedicus. All rights reserved