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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although characterized as hypothyroid, streptozotocin-diabetic rats have reduced serotonin turnover (5-hydroxyindoleacetic acid/serotonin, 5-HIAA/5-HT) in brain stem, while hypothyroid rats have increased 5-HIAA/5-HT. In the present study the two treatments were combined to determine if they affected 5-HIAA/5-HT through the same mechanism. In addition, an alternative method was used to assess 5-HT activity in thyroidectomized (TX) rats, i.e. measurement of 5-HT disappearance after inhibition of tryptophan hydroxylase with p-chlorophenylalanine (PCPA). Adult male rats were first TX (experiment 1) or given methimazole (METH; experiment 3). Two weeks later, diabetes (DB) was induced with streptozotocin in hypothyroid rats and euthyroid controls. Two weeks later, functional measurements were taken. Rats were then killed, and spinal cord and brain stem serotonin turnover (5-HIAA/5-HT), as well as plasma T3, T4 and corticosterone (CORT) concentrations were measured. TX attenuated diabetic hyperphagia and weight loss. DB alone led to moderate reductions in T3 and T4, but the hormones were barely detectable in plasma of TX and METH rats. CORT was elevated in DB but was not affected by TX. Open field activity was not affected by DB or TX. TX and METH significantly increased 5-HIAA/5-HT in both spinal cord and brain stem. TX also led to enhanced disappearance of 5-HT after PCPA. DB significantly reduced 5-HIAA/5-HT, suggesting independent effects of the treatments. However, DB-TX rats still had significantly higher 5-HIAA/5-HT than control-sham surgery rats, while DB-METH rats had 5-HIAA/5-HT indistinguishable from controls. In both cases, prior induction of primary hypothyroidism interfered with the expected diabetes-induced reduction in 5-HT turnover.
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PMID:Streptozotocin-induced decreases in serotonin turnover are prevented by thyroidectomy. 127 45

Fifty-nine patients with both clinical evidence of thyroid dysfunction and patent diabetes mellitus were investigated in our diabetology department. Patients with euthyroid goitre and iatrogenic or pituitary hypothyroidism were excluded from the study. Among the 45 diabetics with hyperthyroidism, 32 had Graves' disease and 13 had toxic adenoma; 71% were insulin-treated. Hyperthyroidism had passed unnoticed in 7 of these 32 patients because fatigue and loss of weight, which initially were the predominant or sole symptoms, are extremely frequent in uncontrolled diabetes. These symptoms, as well as polyuria, polyphagia and even sweating are common to both diseases. Considerable deterioration in the control of glycaemia was observed in 63% of the insulin-treated patients when hyperthyroidism developed, with a 17 to 212% (mean 82%) increase in insulin dosage in 53%. There was no correlation between the degree of hyperthyroidism and the loss of control. Following treatment of the hyperthyroidism, control was improved in 63%, with an 11-83% (mean 44%) decrease in insulin dosage in 59% of them. Insulin therapy could be withdrawn in only one of the 32 insulin-treated patients. Non-iatrogenic primary hypothyroidism was found in 0.2% of the diabetics investigated. This incidence was significantly higher than the calculated probability of the two diseases occurring by chance in the same patient. Eleven out of 14 patients were insulin-treated. When hypothyroidism developed, 73% of them had their insulin dosage reduced, with a high frequency of hypoglycaemic disorders: repeated "malaise" in 55% and coma in 27%. A higher proportion of vitiligo was also noted: 14% in the total patient population reported, and 18% in insulin-treated patients.
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PMID:[Effect of clinical hyperthyroidism and hypothyroidism on patent diabetes. 59 cases]. 315 40

A 61-year-old woman with profound hypothyroidism underwent surgery for a ventricular septal perforation 15 days following an acute myocardial infarction, with no preoperative thyroid replacement. Her immediate postoperative course was complicated by a low cardiac output, respiratory suppression and high output renal failure, requiring prolonged hemodynamic and respiratory support. Thyroid replacement (50 micrograms of thyronine and 100 micrograms of thyroxine daily) was given in two installments on the 2nd day after the operation. The effect of the inotropic agents increased gradually and the patient was weaned off intra-aortic balloon pumping. A large quantity of diuretics, hydration and hyperalimentation also successfully reduced her elevated BUN and serum creatinine. After full thyroid replacement, she was discharged in good health on the 40th postoperative day.
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PMID:Ventricular septal perforation following acute myocardial infarction in a patient with hypothyroidism--a case report. 323 Jul 28

A 54-year-old woman, with no previously documented thyroid disease, treated with amiodarone (200 mg/day, five days a week for 33 months) for paroxysmal tachyarrhythmia complicating mitral stenosis, suddenly developed extremely severe thyrotoxicosis. After therapeutic failures with carbimazole and propylthyrouracil (PTU) associated with beta-blockers, she was transferred to intensive care for plasma exchange (PE). Two PE were performed, temporarily aggravating the cardiovascular status of the patient, with no secondary improvement. The quantity of T3 removed was very small, about 1,000 ng per exchange. On the 14th day PTU had to be discontinued (toxic thrombopenia) and only symptomatic treatment was maintained (assisted ventilation, digitalis, hyperalimentation). In the 4th month, while the patient had a high total serum iodine, hypothyroidism developed due to partial block of the organification of the iodine with high TSH and fixation; this state also lasted 4 months. Spontaneous recovery was observed after 8 months. In addition a severe peripheral neuropathy was observed during the hyperthyroid phase confirmed by electromyography, distinct from the signs of thyrotoxic myopathy. This gradually regressed over 7 months and may be attributed to amiodarone therapy. The association of these two successive types of thyroid disorder due to amiodarone is an exceptionally rare phenomenon. Severe thyrotoxicosis generally requires long-term symptomatic therapy, its natural course being towards spontaneous regression. PE are ineffective on the circulating hormonal levels and were dangerous because of the underlying cardiac disease. The development of hypothyroidism at the 4th month is explained by the persistent iodine overload, and therefore prolonged surveillance after withdrawal of therapy is advised. The neurological complication of amiodarone was quite distinct from the hyperthyroid myopathy.
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PMID:[Thyrotoxicosis, then hypothyroidism caused by iodine overload (amiodarone) associated with neuropathy. Failure of plasma exchange]. 630 50

A 26-year-old woman had hyperphagia, obesity, aggressive behavior, visual hallucinations, reversal of wake-sleep patterns, hypothermia, hypothyroidism, and amenorrhea. She died of pancreatitis, probably secondary to hypothermia. Autopsy revealed a low-grade astrocytoma in the third ventricle and medial anterior and mid hypothalamus, primarily on the right. Although she exhibited thyroid and ovarian hypofunction, the patient had intact median eminence and pituitary function, suggesting end-organ failure, possibly of an autoimmune nature.
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PMID:Hypothalamic astrocytoma. Syndrome of hyperphagia, obesity, and disturbances of behavior and endocrine and autonomic function. 657 19

Because of the development in parenteral nutrition, the replacement of thyroid hormones in hypothyroid or athyroid patients under intravenous hyperalimentation has become a new problem to be considered. We tried parenteral replacement of the hormones, intravenously or by enema, in three such patients. Two patients, 54 y-o and 64 y-o females, who underwent laryngo-esophago-thyroidectomy for cervical esophageal cancer or thyroid cancer, had replacement with intravenous l-thyroxine with an initial dose of 100 micrograms/day for 9 and 22 days, respectively. Another patient, a 56 y-o female with dysphagia due to local recurrence of cervical esophageal cancer after laryngo-esophago-thyroidectomy, was given 100 mg of desiccated thyroid by enema for 8 days followed by intravenous l-thyroxine for 104 days. Serum levels of thyroxine, triiodothyronine and TSH before l-thyroxine treatment indicated severe hypothyroidism in all cases. During the first 7 days of the intravenous therapy, serum thyroxine and triiodothyronine levels increased by 0.87 +/- 0.14 microgram/dl/day and 6.7 +/- 4.7 ng/dl/day, respectively, while serum TSH levels decreased by 7.8 +/- 6.4 microU/ml/day. Plasma T4 levels reached the normal level within 7 days, and plasma T3 levels within 11 days, while it took 14 days for plasma TSH levels to decrease to the normal level. The maintenance dose checked by the normal TSH levels in a patient undergoing a long term therapy was 75 micrograms/day or 1.83 micrograms/kg of body weight/day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parenteral replacement of thyroid hormones]. 674 69

Obese-hyperglycemic mice show hyperphagia and hypothyroidism. The reduced body temperature can be normalized by injection of thyroxin. Limiting food intake to normal non-obese levels reduces blood sugar level, insulin content of the blood and body weight. However, reduction of all these parameters together until normal level occurs only when combining thyroxin injection with restricted diet. Weight of epididymal fat pad, nuclear volume of Leydig cells and volumes of islets of Langerhans normalize too during the combined treatment. It is argued that in adult obese mice hyperphagia and hypothyroidism are two separate factors which cannot be completely compensated for one by another. At least some symptoms in the obese-hyperglycemic syndrome could be attributed to hypothalamic disturbances caused by a reduced thyroidal activity at a very early age after birth.
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PMID:The role of hyperphagia and hypothyroidism in the development of the obese-hyperglycemic syndrome in mice (ob/ob). 694 82

Recent evidence indicates that the paraventricular nucleus of the hypothalamus (PVN) contains both neurons that produce thyrotropic releasing hormone (TRH) and neurons that are destroyed or disconnected by the knife cuts that produce hypothalamic hyperphagia and obesity. This, and other evidence, suggested linkage between thyroid regulation and appetite control. As predicted, hyperthyroidism potentiated and hypothyroidism tempered the weight gains of knife cut rats. However, these effects were due entirely to increased and decreased, respectively, linear growth, not to differences in the degree of obesity. Enhanced linear growth and elevated growth hormone levels are a minor component of the enhanced weight gain of hypothalamically knife cut rats. Most of the weight gain is due to fat deposition. Only the enhanced linear growth and growth hormone aspect appear to possibly be mediated via the thyroid. In addition, obesifying knife cuts did not reduce goiterogenesis in PTU treated rats, as would be expected if the elaboration of TRH were blocked by obesifying knife cuts. Thus, neither TRH nor thyroxine is involved in the etiology of hypothalamic obesity.
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PMID:Hypothalamic knife cut obesity in hyper or hypothyroid rats. 740 1

We report a new syndrome that we call "recurrent optic neuromyelitis with endocrinopathies" in eight Antillean women from Martinique and Guadeloupe Ocular involvement was either monocular or binocular, whereas myelopathy was acute or subacute. In seven patients, myelopathic symptoms recurred, and in six patients, visual problems recurred. Spinal cord involvement was a consistent band-like pseudo-syringomyelic dissociated sensory loss. All eight patients had endocrinopathies consisting of amenorrhea, galactorrhea, diabetes insipidus, hypothyroidism, or hyperphagia. Spinal cord MRI revealed cavitation-like images. Various immunosuppressant treatments had little effect on the uniformly deteriorating course, ending in blindness and paraplegia. Six patients died within 5 years of onset, and an autopsy in one patient showed multiple demyelinizing lesions of the spinal cord with thickened blood vessels walls without evidence of inflammation. These cases appear to constitute a syndrome distinct from MS and from classic Devic's syndrome, not only because of the association with endocrinopathies but because of the stereotypy of the recurrences, the absence of MRI lesions in the cerebral white matter, and the unusual image of cavitation of the spinal cord. The syndrome is also distinct from HTLV-I-associated paraparesis, which is endemic in the West Indies.
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PMID:Recurrent optic neuromyelitis with endocrinopathies: a new syndrome. 937 56

The present study was undertaken to study the effects of chronic treatment with lisinopril on the cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosteroneacetate (DOCA) hypertensive rats. Injection of STZ produced severe glycosuria (> 2%), hyperglycemia, hypoinsulnaemia, polydypsia, polyphagia and loss of body weight. It also produced hypothyroidism, hypercholesterolaemia, hypertriglyceridaemia, hypertension, bradycardia and decreased left ventricular developed pressure (LVDP). Elevation in serum creatinine level and increased activity of liver enzymes were also found in STZ treated animals. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in non-diabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment of STZ-diabetic rats with DOCA did not aggravate cardiac depression or hyperglycaemia. Treatment of rats with lisinopril (1 mg kg-1, p.o. daily for six weeks), in diabetic and diabetic hypertensive animals prevented STZ induced loss of body weight and hypertension, bradycardia and hypothyroidism. It also prevented STZ induced hyperglycemia and hypoinsulinaemia in both diabetic and diabetic hypertensive animals. There was a reduction in cholesterol, triglyceride, and LDL levels; the ratio between total cholesterol to HDL and LDL to HDL and an improvement in LVDP at higher filling pressure in diabetic as well as diabetic hypertensive animals. Treatment with lisinopril also prevented hypertrophy and elevated levels of serum creatinine, SGOT and SGPT in diabetic animals. In conclusion, the present data suggests that STZ-DOCA model may not be considered as the ideal model for the study of cardiovascular complications of combined treatment hypertension and diabetes. However, the present investigation presents a number of beneficial effects of lisinopril treatment in diabetic with or without hypertensive rats and it may be considered as one of the drugs of choice in treatment of hypertension when it is associated with diabetes mellitus.
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PMID:Effects of chronic treatment with lisinopril on cardiovascular complications in streptozotocin diabetic and DOCA hypertensive rats. 907 44


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