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Query: UMLS:C0028754 (
obesity
)
124,988
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
While insomnia is a familiar management problem for most doctors, disorders of hypersomnolence are much less familiar. The evolution of sleep monitoring at a major South African teaching hospital is described and the classification of sleep disorders reviewed. Analysis of the first 5 years' experience revealed that 27 of 46 patients had sleep apnoea (all obstructive, but 13 with a central component), while 3 had narcolepsy. Contributing causes of sleep apnoea included
obesity
(25 patients), tonsillar enlargement (3),
acromegaly
(3), rheumatoid cervical spondylosis (1), Hunter's syndrome (1) and haemangioma of the throat (1). Death from sleep apnoea occurred in 3 cases. Treatment of specific causes was effective in abolishing sleep apnoea, although attempts at weight loss were effective in a minority only. Nasal continuous positive airway pressure was effective in achieving symptomatic relief. Sleep monitoring was found to be valuable, provided all-night study facilities are available, and provided that patients who simply snore are excluded by prior clinical evaluation.
...
PMID:The diagnosis and management of respiratory sleep disorders--the first 5 years at Groote Schuur Hospital. 225 27
Androgens arise from either adrenal or ovarian secretion or by peripheral conversion of secreted precursors. The adrenals and ovaries normally contribute about equally to testosterone and AD production. DHAS is the major adrenal 17-KS. Testosterone is the major circulating form of androgen. More than 96% of plasma testosterone is bound to SHBG; the free testosterone seems to be the bioavailable fraction. Hyperandrogenism must be considered in any girl with premature or excessive development of public hair or acne, menstrual irregularity (whether it be oligo-amenorrhea or dysfunctional uterine bleeding), or
obesity
. The most common cause of premature public hair development (pubarche) is premature adrenarche. The most common cause of hyperandrogenism presenting in a teenage girl is polycystic ovary syndrome. However, the differential diagnosis includes "exaggerated adrenarche," late-onset congenital adrenal hyperplasia, virilizing tumors, Cushing's syndrome, hyperprolactinemia,
acromegaly
, and abnormalities of androgen action or of metabolism. The plasma free testosterone is a more sensitive indicator of hyperandrogenism than is the total testosterone concentration. The pattern of response of plasma free testosterone, DHAS, and cortisol to dex-suppression testing is diagnostic of the source of androgen excess. Most hyperandrogenic adolescents will be found to have PCOS. The treatment is chosen according to particular symptoms, such as menstrual irregularity, hirsutism, or
obesity
.
...
PMID:Hyperandrogenism in peripubertal girls. 225 43
Human growth hormone releasing hormone (GHRH) was originally extracted from two pancreatic tumours in patients with
acromegaly
, and is now known to consist of a 44 residue amidated peptide or its C-terminal-shortened derivatives. The sequence of rat GHRH has also been determined; this 43 residue peptide shows approximately 70% homology with human GHRH, and is located mainly in the arcuate nucleus of the hypothalamus. Pulsatile GH release in the rat is principally a consequence of the pulsatile release of hypothalamic GHRH, although this appears to be associated with a transient suppression of somatostatin release. Exogenous GHRH specifically increases circulating GH in many species, and in the long term may increase growth. In normal man, several analogues of GHRH have been shown to be safe, sensitive and specific stimuli to GH release; although there may be a variable prolactin response, this is usually of small magnitude. Continuous infusion of GHRH leads to a decrement in responsiveness, due at least in part to changes in hypothalamic somatostatin. The GH response to GHRH is also modulated by
obesity
, blood sugar, free fatty acids, and GH itself. Many children with 'GH deficiency' (idiopathic, radiation-induced, or secondary to hypothalamopituitary tumours) respond to intravenous GHRH with an acute rise in serum GH. Early studies also indicate that long-term therapy with subcutaneous GHRH may increase growth velocity in some of these children. It is concluded that analogues of GHRH are useful in the investigation of the hypothalamopituitary axis, and may be important in the therapy of short stature.
...
PMID:Growth hormone releasing hormone. 242 96
As previously shown, in essential hypertension postprandial plasma insulin concentrations are elevated. In order to determine a relationship of high blood pressure and plasma insulin levels in
acromegaly
and in
obesity
59 subjects with normal glucose tolerance were studied. They were divided into three groups: (I) patients with
acromegaly
: 7 normotensives and 8 hypertensives, (II) 12 obese normotensives and 12 obese hypertensives and (III) 10 non-obese hypertensives, and 10 healthy subjects. Blood glucose and plasma insulin concentrations were measured in a fasting state and after an oral glucose load of 75 g. The fasting insulin concentrations in all the acromegalics and in all the obese patients were higher than those in healthy subjects. The insulin response to the glucose load was significantly enhanced in all the three groups of hypertensive patients compared with those of matched normotensive controls. The results indicate that insulin may play a role in the regulation of blood pressure in essential hypertension, and in such hyperinsulinaemic disorders as
acromegaly
and
obesity
.
...
PMID:High blood pressure and hyperinsulinaemia in acromegaly and in obesity. 266 41
Of 22 patients investigated for sleep disorders, habitual snoring and/or daytime hypersomnolence, 12(10 men) had obstructive sleep apnea syndrome (OSAS). 3 OSAS were mild, 5 moderate and 4 severe. The leading symptoms were daytime hypersomnolence and habitual snoring. As risk factors we found retro-micrognathia in 2 patients, macroglossia secondary to
acromegaly
in 1, alcohol abuse in 7 and
obesity
in 6. Conservative measures improved the disorder subjectively in 6 patients. One patient had a relapse 6 months after uvulopalatopharyngoplasty. 4 patients were successfully treated by nasal CPAP. Other diagnoses were idiopathic alveolar hypoventilation (2), Cheyne-Stokes breathing secondary to low cardiac output (1), monosymptomatic narcolepsy (2), sleep disturbances secondary to depression (2), chronic benzodiazepine abuse (1) and chronic bronchitis without nocturnal hypoxemia (1). History, clinical observation and oxymetry make diagnosis possible in most cases of OSAS severe enough to require treatment. Polysomnography is time-consuming and should be reserved for selected cases.
...
PMID:[Sleep-apnea syndrome. Elucidation, therapy and course]. 305 35
Type 2 diabetes is a familial disease and studies of both Caucasian and Japanese families have raised the possibility that a major susceptibility gene is involved. The majority of patients have both beta cell dysfunction and impaired insulin sensitivity but studies of relatives of Type 2 diabetic patients suggest that beta cell dysfunction is an early feature of the disease. Impaired insulin sensitivity, from
acromegaly
, Cushing's disease or steroid therapy, induces diabetes only in a small proportion of the population, and they may be those who have an inherited cell defect. We postulate that a single beta cell defect gene, on its own, may be insufficient to cause overt diabetes and would lead to life-long glucose intolerance unless associated with other defects such as impaired insulin sensitivity. The nature of such a postulated beta cell defect is uncertain. Whilst it has been reported to be specific to glucose, and not to non-glucose stimuli, this feature may be secondary to hyperglycaemia. The occurrence of islet amyloid in 70-90% of Type 2 diabetic patients, and rarely in the normal population, raises the possibility that amyloid deposition causing disruption of the islet is a factor which might affect beta cell function. Amyloid formation may be a primary abnormality or could be secondary to beta cell dysfunction induced by hyperglycaemia. A major susceptibility gene might predispose a proportion, perhaps 10-15%, of a Caucasian population towards diabetes. The subsequent development of diabetes in a particular patient is likely to depend on many factors including other genetic factors, a sedentary life style and
obesity
. In different populations different genetic influences may operate, including abnormalities of insulin receptor genes and glucose transporter genes, which may allow a beta cell abnormality to become expressed clinically.
...
PMID:Pathogenesis of NIDDM--a disease of deficient insulin secretion. 307 95
The responses of plasma growth hormone-releasing hormone (GHRH) and growth hormone (GH) to oral administration of L-dopa were studied in normal subjects and patients with various endocrine and metabolic diseases to clarify the pathophysiological role of the GHRH-GH axis. In normal subjects, the plasma GHRH concentration was increased from the basal value of 9.8 +/- 1.4 pg/ml (mean +/- SE) to 34.8 +/- 3.1 pg/ml at 30 approximately 90 min after oral administration of 500 mg L-dopa, followed by a rise of GH release (plasma GH level from less than 1 ng/ml to 21.7 +/- 4.7 ng/ml) in most cases, indicating that L-dopa stimulates GH secretion via hypothalamic GHRH. On L-dopa administration, no apparent increases in both plasma GHRH and GH concentrations were observed in patients with hypothalamic hypopituitarism, whereas GHRH administration induced almost normal GH response. In patients with
acromegaly
, the plasma levels of GHRH remained stationary after the L-dopa administration and did not correlate with plasma GH levels. In subjects with simple
obesity
, the responses of plasma GHRH (peak 13.2 +/- 1.2 pg/ml) and GH (peak 4.3 +/- 1.7 ng/ml) to L-dopa were significantly lower than those in normal subjects (p less than 0.01). In patients with primary hypothyroidism, peak levels of plasma GHRH (12.6 +/- 1.3 pg/ml) and GH (2.4 +/- 0.6 ng/ml) were significantly lower than those in normal subjects (p less than 0.01). In patients with non-insulin dependent diabetes mellitus (NIDDM), the responses of GHRH and GH were divided into 2 groups; in the responder the peak values of GHRH and GH were 19.4 +/- 8.6 pg/ml and 12.2 +/- 1.4 ng/ml and in the low or non responder 14.7 +/- 1.5 pg/ml and 2.0 +/- 0.6 ng/ml, respectively. Between both groups, there was a significant difference in the values of fasting blood sugar and HbA1 and mean suffering period. These findings suggest that GH secretion evoked by the L-dopa administration is induced by GHRH released from the hypothalamus, and impairment of GH secretion associated with simple
obesity
, primary hypothyroidism, or NIDDM may be in part attributed to insufficiency of GHRH release from the hypothalamus, and indicate that L-dopa test is clinically useful for evaluating the ability of intrinsic GHRH release in such diseased states.
...
PMID:[Effect of oral administration of L-dopa on the plasma levels of growth hormone-releasing hormone (GHRH) in normal subjects and patients with various endocrine and metabolic diseases]. 312 83
The epidemiologic link between
obesity
and hypertension is more clearly emerging to be one between insulin resistance and hypertension. Relative insulin resistance occurs not only in obese hypertensive patients but also in non-obese lean essential hypertensive patients. Although insulin has complex actions on the circulation, plausible mechanisms by which insulin might raise blood pressure include renal sodium retention and stimulation of the sympathetic nervous system. However, the evidence that insulin can actually raise blood pressure in the long-term is lacking. Since hypertension does not develop in all obese or insulin-resistant subjects, the relationship must be modulated by other genetic or environmental factors.
Obesity
, diminished physical conditioning, aging, and diabetes are ubiquitous contributors to relative insulin resistance and all are associated with a tendency for blood pressure to rise. Conditions and agents associated with acquired insulin resistance and secondary forms of hypertension include pregnancy, oral contraceptives,
acromegaly
, and glucocorticoids. Although type 2 non-insulin-dependent diabetes is a state of increased insulin resistance, hypertension is partly sustained by secondary renal mechanisms. Future research should identify the genetic and environmental determinants of insulin resistance in hypertension and utilize these in therapy.
...
PMID:The enigma of insulin resistance and hypertension. Insulin resistance, blood pressure, and the circulation. 327 70
Obstructive sleep apnea syndrome (OSAS) is a complex disorder characterized by a sleep-related collapse of the upper airway. The most likely candidate for the common pathway linking various abnormalities casually associated with OSAS (such as adenotonsillar hypertrophy,
obesity
, retro- or micrognathia,
acromegaly
, or more subtle structural anomalies) is an abnormally small upper airway lumen. Symptoms of OSAS that appear during sleep include snoring, abnormal motor activity, disturbed nocturnal sleep, a sensation of choking, heartburn, nocturia, nocturnal enuresis, and heavy sweating. Daytime waking symptoms are dominated by often profound sleepiness, which may secondarily be associated with automatic behavior, retrograde amnesia, hypnagogic hallucinations, personality changes, sexual difficulties, and headaches. Careful evaluation, both sleeping and waking, are essential to select appropriate treatment. Treatments include nasal continuous positive airway pressure, tracheostomy, weight loss, uvulopalatopharyngoplasty, mandibular advancement, and so forth.
...
PMID:Obstructive sleep apnea syndrome. A review. 333 20
Insulin binding to receptors on erythrocytes was studied in patients with
acromegaly
(n = 27) and in control subjects without any endocrine pathology, diabetes or
obesity
(n = 13). According to fasting serum concentration of growth hormone (GH), acromegalics were divided into two groups: A) GH less than 10 ng/ml (n = 16) and B) GH above 20 ng/ml (n = 11), in which patients were further divided into subgroups with regard to the presence or absence of diabetes. Insulin binding was decreased both in active and inactive acromegalics when compared with controls. A greater decrease was seen in active
acromegaly
coupled with diabetes. This was not the case of inactive hyperglycaemic acromegalics, where a compensatory increase in the affinity of "empty" receptors might account for a lack of a greater decrease in insulin binding.
...
PMID:Insulin binding to erythrocyte receptors in acromegalic patients in relation to the activity of acromegaly and to concomitant diabetes mellitus. 354 60
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