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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the last several decades, the concept of "endocrinology" has been greatly changed. One major change was due to the discovery of peptide hormones secreted by the organs that were not "classical" endocrine organs. For example, corticotropin-releasing hormone and many neuropeptides are secreted by the neurons, atrial natriuretic peptide by the heart, endothelin-1 by the vascular endothelial cells, and leptin by the adipose tissues. Now, the brain, heart, vascular tissue and adipose tissue can be considered to be endocrine organs. Cardiovascular diseases and obesity are therefore important targets of the endocrine research. Adrenomedullin is a potent vasodilator peptide consisting of 52 amino acids. It was originally discovered from a human pheochromocytoma, and belongs to the calcitonin gene-related peptide (CGRP) family. Adrenomedullin is produced and secreted by various types of cells, for example, vascular endothelial and smooth muscle cells, cardiomyocytes, fibroblasts, macrophages, neurons, glial cells, and retinal pigment epithelial cells. Such ubiquitous expression has not been observed in other neuropeptides, including neuropeptide Y and CGRP. Expression of adrenomedullin is induced by hypoxia and proinflammatory cytokines. In addition to vasodilator actions, this peptide has central inhibitory actions on water drinking and salt appetite, effects on the secretion of some hormones and cytokines, inotropic actions and effects on cell growth and apoptosis. Adrenomedullin is produced by various non-endocrine tumors, as well as endocrine tumors, and acts as a growth stimulatory factor for the tumor cells. Adrenomedullin seems to be involved in the pathophysiology of many diseases, including ischemic heart diseases, inflammatory diseases, tumors, and even eye diseases. The adrenomedullin research implies that "the neuroendocrine system" exists in much broader types of cells than previously thought, and that the endocrine research is able to contribute to the understanding of the pathophysiology of many diseases.
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PMID:Adrenomedullin from a pheochromocytoma to the eye: implications of the adrenomedullin research for endocrinology in the 21st century. 1131 31

A 31-year-old woman was admitted to our hospital because of diabetic ketoacidosis (DKA). Ultrasound sonography revealed the existence of the left adrenal tumor and endocrinological examinations established a diagnosis of pheochromocytoma. She had been healthy and there was no evidence for gestational diabetes in her personal history. Characteristic features were not found in her tumor size and the catecholamine levels as compared with typical cases of pheochromocytoma. An overwhelming secretion of catecholamine might suppress insulin secretion, as evidenced by the improvement after the resection of the tumor. However, a significant insulin resistance continued after tumor resection. Obesity and the heterozygosity of beta3-adrenergic receptor gene (Try64Arg) might play a role in insulin resistance, which resulted in DKA at least in part. Literature survey revealed four cases of DKA in the patients with pheochromocytoma including ours, three of which were Japanese. Pancreatic capacity to secrete insulin has been reported to be less than Caucasians, which might be another reason for DKA. Thus, we speculate that both suppressed insulin secretion and insulin resistance deteriorated by obesity or other factor(s) such as abnormality in beta3 adrenergic receptor probably depress beta-cell function resulting in abnormal metabolic imbalance such as DKA.
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PMID:Diabetic ketoacidosis in a case of pheochromocytoma. 1164 Sep 97

Energy exists as organic molecules and heat in living organisms. In adult mammals, body weight and fat content remain unchanged if energy intake is strictly equivalent to energy expenditure. In other words, regulation of body weight requires energy of foods to be entirely dissipated as heat. Imbalance between ingested energy and thermogenesis induces obesity or thinness. Alterations of food intake or energy expenditure represent the two causes of body weight disturbance. It is accepted that individuals differ in food efficiency i.e. ability to metabolize foods and store fat or totally burn nutrients. Mechanisms of food efficiency and futile cycles are presented. I started my research work analysing thermogenic mechanism in brown adipose tissue. Actually, in addition to white adipose tissue which is the major type of adipose tissue, mammals own another type of adipose tissue referred to as brown adipose tissue. This later tissue is an activatable thermogenic organ which oxidizes fatty acids and releases heat in blood stream. Brown fat is activated during exposure to the cold (in rodents), at birth, and during arousal in hibernators. My initial work helped to characterize a mitochondrial protein named uncoupling protein or UCP which is responsible for activation of fatty acid oxidation and heat production in brown adipocytes. Actually, in most cells, fifty per cent of oxidation energy is recovered as ATP in mitochondria through the process of coupling of respiration to ADP phosphorylation. In contrast to mitochondria of most tissues, brown adipocyte mitochondria can escape the obligatorily coupling of respiration and waste almost ninety per cent of respiration energy as thermogenesis. UCP characterization and its molecular cloning as well as antibodies obtention were used to better understand cellular thermogenesis. Brown adipocytes were identified in babies and adult patients with pheochromocytoma. More recently, research on the brown fat UCP helped us to identify UCP2, a UCP homolog present in most human and animal tissues. A family of UCPs exist in animals and plants. These UCPs may function as mitochondrial uncouplers. However, the ancient function of the UCPs may be rather associated to adaptation to oxygen and control of free radicals than to thermogenesis. Further studies of UCPs will improve the knowledge of mitochondrial metabolism and substrate oxidation. In other respects, analysis of molecular mechanisms controlling respiration uncoupling may contribute to new strategies of treatment of metabolic disorders such as obesity.
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PMID:[To burn or to store]. 1273 25

Adrenal disorders causing hypertension can be related to the dysfunction of either the adrenal cortex or the adrenal medulla. These disorders, including congenital adrenal hyperplasia (CAH), owing to 11B-hydroxylase deficiency and to 17alpha-hydroxylase deficiency; apparent mineralocorticoid excess; familial hyperaldosteronism type I; primary aldosteronism; Cushing's syndrome; and familial glucocorticoid resistance, primarily affect the adrenal cortex and cause low-renin hypertension. The classic disorder of the adrenal medulla resulting in hypertension is pheochromocytoma, although hypertension in obesity might also be associated with catecholamine secretion. In this review, we discuss these etiologies and the most recent advances in our knowledge of their pathophysiology, diagnosis, and treatment.
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PMID:Hypertension and adrenal disorders. 1459 71

Adrenomedullin (AM) is a potent vasodilating peptide originally isolated from human pheochromocytoma cells. This report concerns the expression and secretion of AM from adipose tissue. Northern blot analysis demonstrated marked expression of AM mRNA in mouse adipose tissue. Expression levels in adipose tissues were 2.5-3.2 times higher than in the kidney. AM mRNA level in mature adipocytes was 7.3 times higher than in the stroma-vascular fraction of adipose tissue. In mature adipocyte culture, time-dependent increase of AM peptide concentration in the culture medium was detected. AM expression was also detected in human subcutaneous adipose tissue. Adipose AM expression significantly increased in obesity mouse model, high-fat diet fed mice and ob/ob mice. These results suggest that adipose tissue, especially mature adipocytes, is major source of AM in the body, and that adipocyte-derived AM plays a pathophysiological role in obesity.
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PMID:Expression of the adrenomedullin gene in adipose tissue. 1615 19

A retrospective study was done in 66 children (0.21% of all admitted children) below the age of 18 years with persistent hypertension diagnosed at the Department of Pediatrics, Faculty of Medicine Siriraj Hospital from Jan 1999 to Dec 2003. Male to female ratio was 1.4:1 with 54.5% aged between 6-12 years old and 9.1% aged less than 1 year. Hypertension was found to be severe (BP more than the 99th percentile for age, sex and height) in 79.1% but most (78.6%) of the patients did not have symptoms related to hypertension. Chronic headaches were found in 10%, hypertensive encephalopathy in 8.6%, epistaxis in 1.4% and visual disturbance in 1.4%. The most common cause of hypertension was renal parenchymal diseases (62.7%) mainly lupus nephritis (26.9%), idiopathic nephrotic syndrome (16.4%) and chronic renal failure (16.4%). Other causes of hypertension included renovascular diseases (7.5%), drug-induced (7.5%), essential (7.5%), tumors (4.5%), coarctation of aorta (3.0%), bronchopulmonary dysplasia (3.0%), and pheochromocytoma (1.5%). Obesity and overweight (body mass index, BMI more than 25) was found in only 10 patients (15.1%). The proportion of children with BMI more than 25 was not different between essential and secondary hypertension (p = 0.15). Left ventricular hypertrophy was noted in 7.5%, hypertensive retinopathy in 3.0%, and hypertensive encephalopathy in 9.0%. One-third of the patients had normal BP within 1 month and another 47.0% had normal BP within 6 months of diagnosis. One-fifth of the patients also needed surgical intervention for specific underlying diseases. The authors suggest that since a large number of children with hypertension have secondary hypertension, intensive investigation and prompt management should be done in all. Obesity and overweight is not reliable in the differentiation between primary and secondary hypertension. Short term outcome of hypertension is good with medications and surgery in selected cases but long term outcome is still unknown.
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PMID:Persistent hypertension in Thai children: etiologies and outcome. 1704 51

Resistant hypertension is defined as failure to achieve goal blood pressure despite adherence to 3 different antihypertensive medications, one of which must be a diuretic. True resistant hypertension must be distinguished by apparent resistant hypertension, of which an important cause is medication nonadherence, which can be recognized through a variety of monitoring strategies and may be improved through better patient education. A thorough history and examination should focus on evaluating for associated factors such as medication and illicit drug use, alcoholism, obesity, and obstructive sleep apnea. Further evaluation to differentiate apparent resistant hypertension from true resistant hypertension should include consideration of ambulatory blood pressure monitoring to rule out white coat hypertension. Routine laboratory work will reveal chronic kidney disease, which is the most common associated factor in resistant hypertension. Secondary or identifiable causes of resistant hypertension include primary aldosteronism, renovascular disease, and pheochromocytoma. Diagnostic evaluation for identifiable causes should be tailored for each patient and guided by signs and symptoms, as well as risks and benefits.
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PMID:Clinical characteristics of resistant hypertension: the importance of compliance and the role of diagnostic evaluation in delineating pathogenesis. 1721 49

Resistant hypertension is defined as blood pressure that remains uncontrolled despite using at least three antihypertensive medications in effective doses, ideally including a diuretic. Stricter blood pressure goals, higher obesity rates, older age, and increased use of certain exogenous substances are related to an increasing prevalence of resistant hypertension. The evaluation of patients with resistant hypertension focuses on identifying contributing factors and secondary causes of hypertension including hyperaldosteronism, obstructive sleep apnea, renal artery stenosis, and pheochromocytoma. Hyperaldosteronism is now recognized as the most common secondary cause and all patients with resistant hypertension should be screened with a plasma aldosterone-renin ratio even if the serum potassium level is normal. Treatment includes reversal of contributing factors, appropriate treatment of secondary causes, and use of effective multidrug regimens. Recent studies indicate that the addition of spironolactone to standard treatment regimens induces significant blood pressure reduction in patients with resistant hypertension.
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PMID:Resistant hypertension and aldosteronism. 1817 80

Resistant hypertension is defined as blood pressure (BP) that remains uncontrolled in spite of the use of >/=3 antihypertensive medications. Stricter BP goals, higher obesity rates, older age, and increased use of exogenous BP-elevating substances are related to an increasing prevalence of resistant hypertension. The evaluation of patients with resistant hypertension is focused on identifying contributing and secondary causes of hypertension, including hyperaldosteronism, obstructive sleep apnea, chronic kidney disease, renal artery stenosis, and pheochromocytoma. Hyperaldosteronism is now recognized as the most common cause of resistant hypertension, and all patients with resistant hypertension should be screened with a plasma aldosterone/renin ratio even if the serum potassium level is normal. Treatment includes removal of contributing factors, appropriate management of secondary causes, and use of effective multidrug regimens. Recent studies indicate that the addition of spironolactone to standard treatment induces significant BP reduction in most patients with resistant hypertension.
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PMID:Mechanisms and treatment of resistant hypertension. 1832 68

The high prevalence of obesity is associated with diverse health problems, including endocrine disorders. Laparoscopic adrenalectomy has become the preferred approach for removal of the adrenal gland, but several authors still debate the role of laparoscopic adrenalectomy in pheochromocytoma. We describe a case of a morbidly obese man (weight, 142 kg; body mass index, 40.2 kg/m(2)) who underwent elective laparoscopic adrenalectomy for a large right pheochromocytoma without incidences.
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PMID:Laparoscopic adrenalectomy for a large pheochromocytoma in a morbidly obese patient. 1894 9


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