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Lin C.-H.,Taipei Medical University | Lin C.-H.,Taipei Medical University Hospital | Chang W.-P.,Metabolism | Tai D.-Y.,Wei Gong Memorial Hospital | Yang S.-H.,Taipei Medical University
Journal of Internal Medicine of Taiwan | Year: 2015

Metformin has been considered the first choice of oral antidiabetic drugs (OADs) for typo 2 diabetes melitus (T2DM) patients. It has been proposed that Metformin could reduce Vitamin B12 absorption since 1971. Vitamin B12 is one of the essential nutrients for body and human cells growth, red blood cells formation and maintains epithelium and neuron myelin function. The symptoms of Vitamin B12 deficiency Include precious anemia and nervous system disorders, such as neuropathy, spinal cord lesions, and memory disorders. We observed whether Metformin treatment for T2DM patients with adequate Vitamin B12 intake may cause serum Vitamin B12 deficiency or not. This was a cross-sectional study and recruited T2DM subjects aged from 20-85 yrs., excluded patients of vegetarians, postgastrotomy, and taking vitamin supplements more than thrice a week regularly. We collected medicaJ history and blood data, dietary information by 24 hours dietary recalls and food frequency questionnaire (FFQ). TotaJ 200 subjects were recruited in this study, Vitamin B12 Intake was 1.8 ± 1.7 μg/day by 24- hour dietary recalls, 3.7 ± 2.6 μg/day by FFQ, serum Vitamin B12 levels was 493.6 ± 318.3 pg/ml. There were strong correlations between 24 hours and FFQ (p < 0.000) in Vitamin Bl2 intake, but no correlation between dietary Vitamin B12and serum Vitamin B12 (p > 0.05). No significant correlation existed among Metformin dosage and dietary Vitamin B12, blood Vitamin B12 level. No serum Vitamin B12 deficiency existed when Metformin treatment forT2DM patients with adequate Vitamin B12 intake in a Taiwan regional teaching hospital. Source

Among women, the polycystic ovarian syndrome (PCOS) is considered a form of metabolic syndrome with reproductive abnormalities. Women with PCOS show increased sympathetic tone, visceral adiposity with enlarged adipocytes, hypoadiponectinemia, insulin resistance, glucose intolerance, increased inactive osteocalcin, and hypertension. Excess fetal exposure to androgens has been hypothesized to play a role in the pathogenesis of PCOS. Previously, we showed that neonatal exposure to the androgen testosterone (NT) programs leptin resistance in adult female mice. Here, we studied the impact of NT on lean and adipose tissues, sympathetic tone in cardiometabolic tissues, and the development of metabolic dysfunction in mice. Neonatally androgenized adult female mice (NTF) displayed masculinization of lean tissues with increased cardiac and skeletal muscle as well as kidney masses. NTF mice showed increased and dysfunctional white adipose tissue with increased sympathetic tone in both visceral and subcutaneous fat as well as increased number of enlarged and insulin-resistant adipocytes that displayed altered expression of developmental genes and hypoadiponectinemia. NTF exhibited dysfunctional brown adipose tissue with increased mass and decreased energy expenditure. They also displayed decreased undercarboxylated and active osteocalcin and were predisposed to obesity during chronic androgen excess. NTF showed increased renal sympathetic tone associated with increased blood pressure, and they developed glucose intolerance and insulin resistance. Thus, developmental exposure to testosterone in female mice programs features of cardiometabolic dysfunction, as can be observed in women with PCOS, including increased sympathetic tone, visceral adiposity, insulin resistance, prediabetes, and hypertension. Source

Frieler R.A.,University of Michigan | Berger S.,German Cancer Research Center | Schutz G.,German Cancer Research Center | Mortensen R.M.,Metabolism | Mortensen R.M.,University of Michigan
Stroke | Year: 2011

Background and Purpose-Mineralocorticoid receptor (MR) antagonists have protective effects in rodent models of ischemic stroke, but the cell type-specific actions of these drugs are unknown. In the present study, we examined the contribution of myeloid cell MR during focal cerebral ischemia using myeloid-specific MR knockout mice. Methods-Myeloid-specific MR knockout mice were subjected to transient (90 minutes) middle cerebral artery occlusion followed by 24 hours reperfusion (n=5 to 7 per group). Ischemic cerebral infarcts were identified by hematoxylin and eosin staining and quantified with image analysis software. Immunohistochemical localization of microglia and macrophages was performed using Iba1 staining, and the expression of inflammatory markers was measured after 24 hours of reperfusion by quantitative reverse transcription-polymerase chain reaction. Results-Myeloid-specific MR knockout resulted in a 65% reduction in infarct volume (P=0.005) after middle cerebral artery occlusion. This was accompanied by a significant reduction in activated microglia and macrophages in the ischemic core. Furthermore, myeloid-specific MR knockout suppressed classically activated M1 macrophage markers tumor necrosis factor-α, interleukin-1β, monocyte chemoattractant protein-1, macrophage inflammatory protein-1α, and interleukin-6 at the same time as partially preserving the induction of alternatively activated, M2, markers Arg1, and Ym1. Conclusions-These data demonstrate that myeloid MR activation exacerbates stroke and identify myeloid MR as a critical target for MR antagonists. Furthermore, these data indicate that MR activation has an important role in controlling immune cell function during the inflammatory response to stroke. © 2010 American Heart Association, Inc. Source

Objective: To report the case of a patient with a pheochromocytoma and apical left ventricular dysfunction that resolved after surgical resection of the pheochromocytoma, to review the effects of catecholamines on myocyte function and the concept that takotsubo cardiomyopathy (TC) is caused by excess catecholamines, and to illustrate the difficulty in the management of an acute coronary syndrome (ACS) during a hypertensive crisis attributable to a pheochromocytoma.Methods: We present the clinical history, physical findings, laboratory results, and imaging studies in a 60-year-old man with an ACS, TC, and an incidentaloma later diagnosed to be a pheochromocytoma. The association with TC and the pertinent literature are reviewed.Results: A 60-year-old man was suspected of having myocardial ischemia on the basis of symptoms of paroxysmal chest pain extending to the left shoulder, diaphoresis, ST-segment elevation on an electrocardiogram, and elevated serial levels of cardiac enzymes. Coronary angiography did not reveal substantial coronary artery obstruction but detected ballooning of the apical, anterior, and inferior cardiac walls, consistent with TC. He had a history of labile hypertension and palpitations of 3 months' duration. An adrenal mass detected on a prior computed tomographic scan and increased 24-hour urine catecholamine levels were consistent with a pheochromocytoma. Treatment with phenoxybenzamine was initiated, and he underwent a right adrenalectomy, which confirmed that the tumor was a pheochromocytoma and dramatically improved the patient's condition.Conclusion: Pheochromocytomas manifest with labile blood pressures and should be considered in the differential diagnosis of ACS. This case also supports the concept that TC is caused by excess catecholamines. Copyright © 2012 AACE. Source

Jia G.,Metabolism | Jia G.,Diabetes Cardiovascular Center | Jia G.,University of Missouri | Aroor A.R.,Metabolism | And 3 more authors.
CardioRenal Medicine | Year: 2014

Vascular disease is the leading cause of morbidity and mortality in the Western world, and vascular function is determined by structural and functional properties of the arterial vascular wall. Cardiorenal metabolic syndrome such as obesity, diabetes, hypertension, kidney disease, and aging are conditions that predispose to arterial stiffening, which is a pathological alteration of the vascular wall and ultimately results in target organ damage in heart and kidney. In this review, we provide new insights on the interactions between arterial stiffness, vascular resistance and pulse wave velocity as well as final end-organ damage in heart and kidney. Better understanding of the mechanisms of arterial functional and hemodynamic alteration may help in developing more refined therapeutic strategies aimed to reduce cardiovascular and chronic kidney diseases. © 2014 S. Karger AG, Basel. Source

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