Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to clarify the hypothalamic neuropeptides that are associated with hyperphagic feeding in Tsumura Suzuki Obese Diabetes (TSOD) mice, a model of type 2 diabetes with polygenic abnormalities. TSOD mice showed an increase in body weight and hyperleptinemia from 1 month of age and hyperphagic feeding, hyperglycemia, hyperlipidemia and hyperinsulinemia from 3 to 12 months of age compared with age-matched non-diabetic control Tsumura Suzuki Non Obesity (TSNO) mice. The mRNA level of nucleobindin-2 (NUCB2), the precursor of the anorexigenic neuropeptide nesfatin-1, was significantly decreased in the hypothalamus of TSOD mice compared with that in TSNO mice from 3 to 12 months of age. The protein level of NUCB2 was significantly decreased in the hypothalamus of TSOD mice compared with that in TSNO mice at 3 months of age. The mRNA levels of galanin, melanin-concentrating hormone, neuropeptide Y, and pro-opiomelanocortin were significantly changed in the hypothalamus in TSOD mice at several time points. Another model of type 2 diabetes, db/db mice, which is a mutant mouse that lacks a functional leptin receptor, showed hyperphagic feeding but no change in hypothalamic NUCB2 mRNA compared with non-diabetic control db/+ mice. The results suggest that the disrupted control of hypothalamic NUCB2-mediated signaling may contribute to hyperphagic feeding in TSOD mice. In addition, the mechanism for the development of hyperphagic feeding in TSOD mice is different than that in db/db mice.
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PMID:Possible involvement of hypothalamic nucleobindin-2 in hyperphagic feeding in Tsumura Suzuki obese diabetes mice. 2303 68

Primary aldosteronism characterized by the overproduction of aldosterone by the adrenal glands, is sometimes accompanied by autonomous cortisol secretion. In this study, we retrospectively analyzed 8 cases of primary aldosteronism (PA) with subclinical Cushing's syndrome (SCS). A total of 71 patients with PA underwent surgery at Jikei University Hospital from 2004 to 2013, and 8 of them were diagnosed with coexistent SCS. Four patients were male and four were female. The mean patient age was 56.9 years. One of the patients also had pheochromocytoma in the adrenal gland on the ipsilateral side. All patients had hypertension, 6 had hypokalemia, 5 had diabetes mellitus, and 3 had hyperlipidemia. All patients had autonomous cortisol secretion as shown in 1 mg- or 8 mg-dexamethasone suppression tests even though baseline cortisol levels were normal. Adrenal venous blood sampling with adrenocorticotropic hormone (ACTH) stimulation was performed on 5 patients, but the localization of PA could not be detected in 1 patient. Adrenocortical scintigraphy revealed suppression of the contra-lateral adrenal uptake in all 7 patients. Six patients including one patient who showed complete suppression of the contra-lateral adrenal uptake in adrenocortical scintigraphy, and 2 patients, whose ACTH levels were less than the detection limit, received postoperative steroid hormone replacement. In the literature, SCS co-existed in approximately 8. 6% of the patients with PA. In our study, SCS co-existed in approximately 11.3%. The degree of the autonomous secretion of cortisol varied with the patient, and some cases are accompanied by Cushing's syndrome. Therefore, it is important to analyze the autonomous cortisol secretion even in patients with PA.
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PMID:[Clinical Evaluation of Primary Aldosteronism with Subclinical Cushing's Syndrome]. 2608 19


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