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

The neurovegetative state was studied by a questionnaire in 70 obese patients. In 61 of them frontal and distal thermometry with liquid crystal cholesterol thermoindicators was performed and the polarization currents of the hands were recorded. In 21.3% of the obese patients deviations in the thermoregulatory state were found. A tendency toward hypothermia of about 2 degrees C, localized predominantly in the medial frontal zone, was registered. Disturbances in the sudomotorics--hypo or hyperhydrosis--were found. The results show mixed and/or parasympathicotonic dystonia in the patients studied. Thermodiagnostics with liquid crystals and registration of the polarization currents are recommended as noninvasive methods for determination of neurovegetative disorders in obesity.
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PMID:[Autonomic disorders and thermography using liquid crystals in obesity]. 320 11

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

It is well known that cold and diet-induced thermogenesis, which is mediated in small rodents by the hypothalamic-noradrenergic fibers-brown adipose tissue axis, is impaired in genetically obese mice. To test whether these adaptive mechanisms are also impaired in obese humans, 12 young males who were otherwise healthy (6 lean and 6 obese) were examined. The obese subjects had an early-onset type of obesity with a strong family history of it as well. Deep body temperature was measured by using a deep body thermometer furnished with three thermocouples. They were respectively placed on the sternum, on the interscapular area immediately under the neck (HIS), and on the 4th intercostal space (LIS) in order to study core temperature as well as heat production where brown adipose tissue could also be present in adults. Both lean and obese subjects were kept in a thermoneutral environment (28 degrees C) until they reached a steady-state body temperature and then rapidly transferred into a cold room (6-8 degrees C) where they remained up to 60 min. Body temperature decreased in both groups, but the decrease was more marked in the obese individuals on the sternum (P less than 0.01), on HIS (P less than 0.05) and on LIS (P less than 0.05) when compared to lean individuals. In conclusion, cold-induced thermogenesis is impaired in familial early-onset human obesity and in genetically obese mice.
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PMID:Reduced cold-induced thermogenesis in familial human obesity. 395 96

The body temperatures of mature lean and obese C57BL/6J mice were measured just after feeding, during ad libitum access to food, or every 24 h throughout a 3-day fast. Obese mice had body temperatures 1.0-1.4 degrees C lower than lean mice in the postprandial state and during ad libitum feeding. During food deprivation, obese mice became more hypothermic than lean sex-matched controls. A 5 degrees C fall in body temperature was observed in mutant females in the first 24 h of starvation, about twice that seen in any other experimental group. Over the same period the temperature changes of obese males and lean females were similar and both groups had larger hypothermic responses than lean males. The present results indicate that both genotype and gender affect thermoregulation in these mice. Under normal colony room conditions (ad libitum feeding, 23 degrees C) the ob/ob mutation is expressed by lower body temperatures which along with hypoactivity and hyperphagia account for the high rates of energy storage. When food availability is limited, females of both phenotypes display an increased capacity to reduce their maintenance energy requirements by lowering body temperatures. This hypothermia may be responsible for both the increased conservation of body mass seen during starvation and the slightly greater (5%) fat stores observed in female mice.
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PMID:Fed and fasting thermoregulation in ob/ob mice. 406 46

After adrenalectomy in obese mice the rate of weight gain parallels that in lean controls and falls progressively behind that in intact ob/ob mice. Food intake was reduced to normal, but the body temperature of adrenalectomized ob/ob mice was similar to that of intact ob/ob mice and remained below that of control lean mice. After exposure to an ambient temperature of 6 degrees C the body temperature in adrenalectomized ob/ob mice fell at the same rate as in intact ob/ob mice. The increase in tail length, brain weight, spleen weight, and muscle weight after adrenalectomy in ob/ob mice could not be duplicated by reducing the weight gain of ob/ob mice to that of the adrenalectomized mice. Similarly the induction of obesity with gold thioglucose significantly increased the weight of the gastrocnemius muscle and spleen rather than lowering it to levels found in ob/ob mice. Treatment of adrenalectomized ob/ob mice with cortisone acetate, but not with deoxycorticosterone acetate (DOCA), reduced muscle weight, spleen weight, brain weight, and the growth in tail length. Both cortisone and DOCA increased food intake, liver weight, growth rate, and the weight of the adipose tissue in ob/ob mice. These effects are significantly greater than observed in comparably treated lean animals and suggest that glucocorticoids of adrenal origin play an integral role in the phenotypic expression of genetic obesity. These data also indicate that the hypothermia is not a sufficient cause of the obesity in the ob/ob mice, since hypothermia persists in the adrenalectomized mice, but when food intake falls to normal there is no progression of the obesity.
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PMID:Adrenalectomy and food restriction in the genetically obese (ob/ob) mouse. 642 Nov 74

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

This study was designed to sequence the earliest metabolic abnormalities associated with the development of obesity in the obese hyperglycemic mouse (C57BL/6J ob/ob). In situ lipogenesis was measured with 3H2O in fetuses at day 19 of gestation and in 5-, 10-, 15-, and 35-day-old mice. Preobese 15-day-old animals were identified on the basis of rectal hypothermia. The earliest increased accumulation of fatty acids was observed in the carcass of 15-day-old preobese animals (ob/ob) compared to their lean littermates (+/?) and known lean controls (+/+). The increased carcass lipogenesis in these animals was accompanied by an increase in plasma insulin concentration. Weaned 35-day-old obese animals showed a significant increase in hepatic and subcutaneous adipose tissue lipogenesis, plasma insulin, and glucose values when compared to their littermates (+/?). The results indicate that increased carcass lipogenesis, hyperinsulinemia, and hypothermia appear between days 10 and 15 and that these abnormalities precede the hyperglycemia and increased hepatic lipogenesis observed in the mature ob/ob mice.
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PMID:Early development of lipogenesis in genetically obese (ob/ob) mice. 699 15

The functional integrity of the peripheral sympathetic nervous system and adrenal medulla was assessed in homozygous, lean and obese, 7--8 month old male Zucker rats by the changes in plasma catecholamines during cold and immobilization stresses. Five of eight obese, but no lean rats died during a 24 hr cold stress (4--7 degrees C) from hypothermia. While both lean and obese rats had decreased rectal temperatures after 4 hr of cold stress, the obese had lower temperatures, relatively less of an increase of plasma norepinephrine (NE) and epinephrine (E) than the lean rats, and were unable to consistently maintain their temperatures even during intravenous NE infusions. Obese rats had lower rectal temperatures and higher plasma NE and dopamine levels at 21--22 degrees C ambient temperature, a relative failure to increase plasma NE and E levels after 1 hr of immobilization, but normal or supranormal plasma catecholamine levels after decapitation compared to the lean rats. These results suggest that the obese Zucker rat has abnormalities of both peripheral sympatho-adrenal function and thermoregulation, which may play roles in the development and/or maintenance of many of the physiological and metabolic defects in this animal model of genetic obesity.
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PMID:Abnormal sympatho- adrenal function and plasma catecholamines in obese Zucker rats. 740 13

We report the case of a 9-year-old girl with multiple problems due to hypothalamic dysfunction of obscure origin: apnoeic spells, behavioural problems, developmental delay, hypodipsia with bouts of hypernatraemia, episodes of spontaneous hypothermia, obesity, petit-mal seizures, non-progressive precocious puberty, absence of respiratory response to CO2 and probably insensitivity of hyposensitivity to pain. She also had hyperprolactinaemia and decreased human growth hormone secretion. Hypothyroidism of central origin and hyposecretion of cortisol were also present. Multiple brain CT-scans failed to reveal any tumour or other anatomical abnormality. Her clinical course was improved initially by treatment with clomipramine, but she died suddenly, and the autopsy failed to disclose any anatomical lesion. We compare this case with three similar previously reported cases.
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PMID:Hypothalamic dysfunction in a child: a distinct syndrome? Report of a case and review of the literature. 768 46

A case of hypothalamic dysfunction in a girl with a twelve-year follow-up is reported. Onset occurred at the age of three with severe obesity, hypothermia, hypersomnia, and lethargy. Somatotropic, gonadotropic, and thyrotropic hormones were low, whereas prolactin was increased. Imaging techniques failed to disclose any lesion of the hypothalamus or pituitary. Clomipramine improved the vegetative disorders. The literature on clinical and hormonal disorders of hypothalamic dysfunction is reviewed.
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PMID:[Hypothalamic syndromes. Review of clinical and endocrinal semiology]. 823


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