Increased renal ANP synthesis, but decreased or unchanged cardiac ANP synthesis in water-deprived and salt-restricted rats

Increased renal ANP synthesis, but decreased or unchanged cardiac ANP synthesis in water-deprived and salt-restricted rats.BackgroundExperiments were performed to examine the effect of water deprivation and salt restriction on ANP synthesis in the kidneys and hearts of normal rats.MethodsA 4-day water deprivation (WD) and 7-day salt restriction (SR; 0.01% NaCl) were performed in 12 and 14 rats, respectively. Atrial natriuretic peptide (ANP) mRNA expression in the kidney was assessed with reverse transcription-polymerase chain reaction coupled with Southern blot hybridization, while the ANP mRNA in the hearts was measured by Northern blot hybridization. ANP and angiotensin II concentrations in the extracted plasma were measured by radioimmunoassay. The molecular form of renal ANP-like protein was characterized by reverse phase—high-performance liquid chromatography (RP-HPLC).ResultsRenal outer and inner medullary ANP mRNA showed a respective 11-fold and ninefold increase in WD rats, and an eightfold and fivefold increase in SR rats as compared to corresponding control groups. Inversely, cardiac atrial ANP mRNA and plasma ANP were decreased in WD rats, whereas they did not change in the SR group. Plasma angiotensin II concentration increased in conjunction with the decrease of urine sodium excretion in both groups. RP-HPLC analysis revealed a 45% extraction of ANP in the WD rat kidneys, whereas only 3% ANP in the control kidneys migrated in a molecular form similar to cardiac atrial proANP.ConclusionsOur results demonstrate that water deprivation and salt restriction markedly enhance renal ANP mRNA, whereas water deprivation suppresses cardiac atrial ANP mRNA and plasma ANP concentrations. The current study indicates that renal ANP and cardiac atrial ANP appear to be two distinct systems regulated by different mechanisms and possibly exhibiting different intra-renal paracrine and systemic endocrine functions

Pioglitazone retrieves hepatic antioxidant DNA repair in a mice model of high fat diet

<p>Abstract</p> <p>Background</p> <p>Pioglitazone was reported to improve hepatic steatosis and necroinflammation in human studies. To investigate whether the hepato-protective effect of pioglitazone was associated with an improvement of antioxidant defense mechanism, oxidative DNA damage and repair activity were determined in a high fat diet model. Male C57BL/6 mice were respectively fed with a 30% fat diet, the same diet with pioglitazone 100 mg/kg/day, or a chow diet as control for 8 weeks. Tissue oxidative stress was indicated by malondialdehyde concentration. Oxidative DNA damage was detected by immunohistochemical 8-oxoG staining. Enzymatic antioxidant defense was detected by the real-time PCR of superoxide dismutase (<it>Sod1, Sod2</it>) and DNA glycosylase (<it>Ogg1, MutY</it>). Oxidative DNA repair was detected by immunohistochemical staining and western blotting of OGG1 expression.</p> <p>Results</p> <p>Our results show that hepatic steatosis was induced by a high-fat diet and improved by adding pioglitazone. Malondialdehyde concentration and 8-oxoG staining were strongly increased in the high-fat diet group, but attenuated by pioglitazone. Gene expressions of antioxidant defense mechanism: <it>Sod1, Sod2, Ogg1 </it>and <it>MutY </it>significantly decreased in the high-fat diet group but reversed by pioglitazone co-administration.</p> <p>Conclusion</p> <p>The attenuation of hepatic oxidative DNA damage by pioglitazone in a high-fat diet may be mediated by up-regulation of the antioxidant defense mechanism and oxidative DNA repair activity. The diminution of oxidative damage may explain the clinical benefit of pioglitazone treatment in patients with non-alcoholic fatty liver disease.</p

Dietary patterns, dietary biomarkers, and kidney disease in patients with type 2 diabetes: a repeated-measure study in Taiwan

Western dietary patterns have been linked with kidney disease. This study investigated the association between Chinese dietary patterns and kidney disease in a Taiwanese population with type 2 diabetes and evaluated dietary fatty acid patterns, a kidney-related dietary biomarker.We recruited 838 patients with type 2 diabetes and used their dietary and renal data obtained from three repeated measures in 2008, 2009 and 2010. Diet was assessed using food-frequency questionnaires, and factor analysis was performed to identify dietary patterns. Albuminuria was defined by having an albumin-to-creatinine ratio >=30 mg/g and kidney dysfunction by estimated glomerular filtration rat

Congenital and Environmental Factors Associated with Adipocyte Dysregulation as Defects of Insulin Resistance

The metabolic syndrome refers to insulin resistance and its associated cluster of related cardiovascular metabolic risk factors including type 2 diabetes, hypertension, dyslipidemia and central obesity. Although many hypotheses and facts have been proposed to explain the interaction between genetic and environmental causes of this syndrome, the primary etiology of the metabolic syndrome is adipose tissue dysregulation. Firstly, the thrifty genotype and phenotype hypothesis may explain the endemic increase in type 2 diabetes and cardiovascular disease in developing countries and may elucidate congenital susceptibility to and environmental triggering of the metabolic syndrome. Secondly, overnutrition leads to fatty acid (FA) accumulation in adipocytes and to an overflow to ectopic fat storage organs. This causes functional changes in adipocytes shifting the intra-cellular metabolic pathway toward insulin resistance. Thirdly, obese subjects exhibit increased fat cell size and over-secretion of biologic adipocytokines. Fourthly, failure to adequately develop adipose tissue mass, as seen in lipodystrophy cases, causes severe insulin resistance and diabetes. Lastly, similarly to human type 2 diabetes, Psammonys obesus, a desert rat which feeds mainly on low-calorie vegetation, develops the metabolic syndrome when given a diet of calorie-rich food. The above evidence indicates that adipocyte dysregulation and secretion of FA as well as certain molecules from overloaded adipocytes-adipokines contribute to the pathogenesis of impaired insulin secretion and insulin resistance, endothelial dysfunction, a pro-inflammatory state and promote progression of atherosclerosis. The metabolic syndrome is a modern disease resulting in adipocyte dysmetabolism which originates from the paradox of slow human evolution combined with rapid environmental changes

Emphysematous Cystitis, A Rare Complication of Urinary Tract Infection in a Male Diabetic Patient: A Case Report

Emphysematous cystitis is a rare complication of urinary tract infection, characterized by spontaneous gas formation in the urinary bladder due to bacterial fermentation. Approximately 50 to 80% of patients with this disease are diabetic, and there is a higher incidence in females. We report a case of emphysematous cystitis in a diabetic male who was admitted under the impressions of hypoglycemia, acute bronchitis, and chronic renal failure. Treatment of the emphysematous cystitis consisted of adequate urinary drainage, empirical antibiotic therapy, and strict blood sugar control. The patient recovered satisfactorily after 9 days of hospitalization

Subacute Thyroiditis Following Influenza Vaccine (Vaxigrip®) in A Young Female

Subacute thyroiditis (SAT), also called de Quervain thyroiditis or granulomatous thyroiditis, is a self- limiting, possibly viral, and inflammatory thyroid disorder that is usually associated with thyroid pain and systemic symptoms. This report details a case of SAT possibly associated with influenza vaccine (Vaxigrip®) in a young female. The diagnosis, therapeutic management and outcome are discussed

The association of pioglitazone and urinary tract disease in type 2 diabetic Taiwanese: bladder cancer and chronic kidney disease.

OBJECTIVE: Although studies have shown an association between pioglitazone and bladder cancer, the associated factors have not been identified. The aim of this study was to investigate the factors that may link pioglitazone to bladder cancer. MATERIALS AND METHODS: In total, 34,970 study subjects were identified from the National Health Insurance Research Database in 2003 with follow-up from 2005 to 2009. The demographic characteristics of patients who had used and had never used pioglitazone, including age, sex, diabetes duration, urinary tract disease, nephropathy, bladder cancer, and cumulative dose and duration of pioglitazone therapy, were analyzed using the χ2 test. Cox proportional hazard regression models were used to determine the independent effects of pioglitazone on bladder cancer and newly developed chronic kidney disease. RESULTS: Among 3,497 ever users and 31,473 never users of pioglitazone, the respective incident cases of bladder cancer were 12 (0.4%) and 72 (0.2%), and for newly developed chronic kidney disease 245 (8.1%) and 663 (2.3%), respectively. Ever use of pioglitazone [1.59(1.32-1.91)], cumulative dose of pioglitazone <10,500 mg [1.69 (1.37-2.01)] and >10,500 mg [1.34 (1.04-1.73)], and duration of therapy <12 months [1.68 (1.36-2.08)] and >12 months [1.39 (1.09-1.76)] were associated with the development of chronic kidney disease. CONCLUSIONS: There was no association of pioglitazone use with bladder cancer development, however, there was an association with an increased risk of newly developed chronic kidney disease

A Case of Acquired Generalized Lipodystrophy with Cerebellar Degeneration and Type 2 Diabetes Mellitus

Acquired generalized lipodystrophy (AGL) is a rare disorder of adipose tissue characterized by loss of fat from large regions of the body, occurring after birth. Its etiology remains unknown. Most AGL patients have had fasting and/or postprandial hyperinsulinemia, diabetes mellitus, hypertriglyceridemia, and fatty liver. We describe the case of a 30-year-old woman with a progressively unsteady gait and a generalized loss of body fat beginning at the age of 7. Cerebellar degeneration was revealed by imaging study, and the patient was eventually bedridden at the age of 15, due to progressive ataxia. She developed diabetes at the age of 25 without the presence of any evidence of ketoacidosis. The glutamic acid decarboxylase antibody was negative, C-peptide level 3.6 ng/ml, HbA1c 13%, triglyceride 412 mg/dl, total cholesterol 196 mg/dl, high-density lipoprotein-cholesterol 28 mg/dl, adiponectin 0.76 μg/ml, and resistin was 22.8 ng/ml at the initial state of diabetes. AGL accompanied by type 2 diabetes and cerebellar degeneration was diagnosed on the basis of the clinical features and metabolic derangements

Severe Hypoglycemia as a Predictor of End-Stage Renal Disease in Type 2 Diabetes: A National Cohort Study

Aims: This study investigated whether there is a link between severe hypoglycemia and progression into end-stage renal disease (ESRD) in patients with type 2 diabetes. Methods: Tapping into Taiwan&#8217;s Health Insurance Research Database, we identified all type 2 diabetes patients between 1996 and 2013 and identified those diagnosed with a severe hypoglycemia episode during an emergency department visit and those who were not. Controls were then matched 1:1 for age, sex, index year, and medication. Results: We identified 468,421 type 2 diabetes patients diagnosed as having severe hypoglycemia in an emergency department visit. Compared with controls, these patients with SH had a higher risk of all-cause mortality (Hazard Ratio (HR), 1.76; 95% confidence interval, 1.61&#8315;1.94) and progressed into ESRD within a shorter period of time. Results were similar after controlling for competing risk. Conclusion: Severe hypoglycemia is significantly associated with worsening renal dysfunction in patients with type 2 diabetes and hastened progression into ESRD

Acute Brachial Artery Thrombosis: A Rare Complication of Diabetic Ketoacidosis

Diabetes mellitus is a worldwide disease that leads to several acute complications including diabetic ketoacidosis, hyperosmolar hyperglycemia, and hypoglycemia. In addition, diabetes causes many chronic complications that lead to debilitation and diminished quality of life. Diabetic ketoacidosis is one of the serious acute complications; however, it is usually preceded by infection, acute myocardial infarction, stroke, or other dire events. Rarely does it accompany acute arterial thrombosis. Here, we report on a female patient who suffered from diabetic ketoacidosis combined with acute brachial artery thrombosis. After emergency treatment, including insulin therapy and surgical thrombectomy, the brachial artery was rescued and her prognosis was good