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

Polydipsia, polyuria, polyphagia, and glucosuria followed the administration of streptozotocin to 6 nonpregnant and 15 pregnant monkeys (Macaca mulatta) in the first trimester of pregnancy. The diabetogenic action of the drug was also reflected in an induced but variable deterioration in maternal intravenous glucose tolerance and a marked attenuation of maternal plasma insulin responsiveness to intravenous glycemic stimuli. The products of conception were examined in 29 pregnancies. The neonates and the placentas of the streptozotocin-treated pregnant animals were significantly heavier than average for the period of gestation, polyhydramnios was consistently present, and there was an increase in the incidence of third trimester stillbirths. The fetal and maternal plasma glucose, insulin, and growth hormone concentrations were examined after the intravascular administration of glucose or a solution of mixed amino acids to the fetus in the third trimester. The neonatal plasma responses to similar insulinogenic stimuli were also examined.Fetal and neonatal base line plasma insulin concentrations were significantly elevated compared to those of the controls. The administration of intravascular glucose to the fetus, mother, or neonate was associated with a prompt 2-to 5-fold increase in fetal or neonatal plasma insulin concentrations. These findings contrast to the unresponsiveness of the pancreatic islet tissue we reported in normal subhuman primate pregnancy. The intravascular infusion of a relatively low concentration of mixed amino acids (2 mg/min) to the conceptii from the streptozotocin-treated pregnancies was associated with an elevation in fetal and neonatal plasma insulin levels, whereas normal monkey fetuses and neonates required a 10-fold greater concentration of amino acids in the infusate for similar responses. The induced hyperaminoacidemia or hyperglycemia did not consistently alter plasma growth hormone concentrations in the conceptii from normal or streptozotocin-treated pregnancies. These data provide evidence that maternal glucose intolerance during pregnancy is associated with enhanced fetal and neonatal pancreatic islet cell responsiveness to glucose and mixed amino acids. Although the specific mechanism(s) that alters both the sensitivity and responsiveness of the normal pancreatic fetal islet to insulinogenic stimuli remains unclear, the data do indicate that insulin-dependent maternal hyperglycemia and hyperaminoacidemia, separately or in combination could contribute to the fetal hyperinsulinemia of pregnancies complicated by diabetes mellitus. Moreover, the overall experiences with these streptozotocin-treated animals suggest that a subhuman primate model may be available to examine directly the antenatal pathophysiology of abnormal carbohydrate metabolism.
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PMID:Subhuman primate pregnancy complicated by streptozotocin-induced diabetes mellitus. 425 54

Ten women with low estriol excretion received hyperalimentation prior to induction of labor. Six received an amino acid mixture (5% Aminofusin) and 25% dextrose, two received the amino acid mixture, and two received 25% dextrose. Amniotic fluid obtained before and after hyperalimentation was assayed for fetal surfactant production, thyroid, pituitary, and carbohydrate regulating hormones. In the combined amino acid/dextrose infusion group the amniotic fluid palmitic acid levels increased significantly post infusion; rT3 also increased significantly but T3 and T4 showed no significant change. The pituitary hormones growth hormone, prolactin, and ACTH showed no significant change, but beta-endorphin-like activity was significantly elevated. No thyroid-stimulating hormone was detected in any of the samples. All the carbohydrate regulating hormones, insulin, cortisol, and cAMP, showed significant increases but cGMP showed a significant decrease. The amino acid and dextrose only groups gave similar results. Seven of the infants showed some degree of intrauterine growth retardation but no neonatal complications attributable to the hyperalimentation.
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PMID:Amniotic fluid endocrine changes during maternal hyperalimentation. 608 68

Progressive left hemiparesis followed by face and trunk cutaneous vasodilation and hyperphagia developed in a 28-year-old man. He began eating five to six meals a day and gained 16 kg in 60 days. Computed tomography disclosed a neoplastic lesion involving the midline via the hypothalamus and reaching the contralateral lenticular nucleus. Findings from endocrine studies, including thyroid-stimulating hormone, growth hormone, prolactin, and cortisol serum levels, were normal. Hyperphagia and consequent obesity were associated with bilateral destruction of the ventromedial hypothalamic area; cutaneous vasodilation was related to involvement of the preoptic area.
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PMID:Hyperphagia and obesity. Relationship to medial hypothalamic lesions. 626 71

We studied insulin-like growth factors (IGF) I and II, prolactin, and the insulin response to arginine in 19 children with craniopharyngioma and documented growth hormone deficiency. Patients were divided into three groups according to their growth rate during the first postoperative year. Seven patients with excessive growth (Group A) had hyperinsulinism, normal IGF values, elevated basal prolactin levels, and a delayed thyrotropin response to thyrotropin-releasing hormone, which was compatible with hypothalamic lesions. In the six patients with normal growth (Group B), the insulin level was low; all other hormone values were similar to those of Group A. In the six patients with decreased growth (Group C), levels of IGF I, insulin, prolactin, and thyrotropin were low, indicating the presence of severe pituitary damage and explaining the failure to grow. Patients in all groups had low or undetectable basal levels of growth hormone. We conclude that in Group B, normal IGF permitted normal growth, and prolactin hypersecretion may have been responsible for normal IGF I values. Excessive growth in Group A may have been caused by hyperinsulinism associated with hyperphagia and obesity of hypothalamic origin.
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PMID:Insulin-like growth factors I and II, prolactin, and insulin in 19 growth hormone-deficient children with excessive, normal, or decreased longitudinal growth after operation for craniopharyngioma. 635 37

Obese children display constant hyperinsulinism and, frequently, hyperphagia. In animals, lesions of the hypothalamic system affect simultaneously the circadian rhythm of insulin secretion and of food intake. In this study, circadian metabolic rhythm was examined in obese and non-obese children, by two different protocols. (1) Oral glucose tolerance tests (OGTT) were carried out at 9 a.m. and 3 p.m. on 2 consecutive days. (2) Circadian variations of plasma glucose and insulin were determined. After OGTT, in the control children there was a significant drop in the insulin/glucose ratio in the afternoon, whereas in the obese group this ratio remained high, with no significant change during the day. Differences were also observed in free fatty acid, growth hormone, and cortisol responses. The control children showed a circadian rhythm for blood glucose levels which was not present in obesity. These preliminary data suggest impairment of metabolic rhythms in obese children; they should stimulate further studies on the hypothalamic system in obesity.
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PMID:Circadian metabolic rhythms in obese children. 704 63

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

Protein and calorie malnutrition often starts before initiation of dialysis, and reflects the anorexia and the catabolic state of chronic renal failure. In the face of inadequate dialysis, which perpetuates the uremic state, malnutrition often worsens. Several studies, though not all, suggest that optimal dialysis improves nutritional status of dialysis patients. Such optimal dialysis now must include the use of biocompatible membranes to deliver Kt/V > 1.4 (urea reduction ratio > 65%). Additional interventions can include the use of enteral or intravenous hyperalimentation, and recombinant growth factors such as growth hormone or insulin-like growth factor-1. Importantly, studies to document the improvement in the morbidity and mortality of patients with these interventions are still needed and require large multicenter trials.
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PMID:Interventions to treat malnutrition in dialysis patients: the role of the dose of dialysis, intradialytic parenteral nutrition, and growth hormone. 761 Dec 60

It is well known that serum IGF-I concentrations are regulated endocrinologically since IGF-I has a growth-promoting action as a mediator of growth hormone. However, recent reports suggest that nutritional states influence serum IGF-I concentration because IGF-I shows anabolic effects like insulin. The aim of this study was to clarify the influences of maternal nutritional states or metabolism on the IGF-I concentrations in normal and abnormal pregnancy. In normal pregnant women, a significant positive correlation was indicated between serum IGF-I concentrations and maternal weight gain during pregnancy or serum triglyceride levels, and a significant negative correlation was observed between serum IGF-I concentrations and serum total protein levels. In the cases complicated with hyperemesis or hyperthyroidism during early gestation, a marked reduction of maternal body weight was observed, and serum IGF-I concentration was extremely low compared with that in normal pregnant women, but serum IGF-I levels gradually increased as the maternal body weight recovered after treatment by intravenous hyperalimentation or an anti-thyroid drug. In cases of severe toxemia of pregnancy, maternal weight gain and serum triglyceride levels were markedly increased, but serum IGF-I levels were significantly lower compared with those in normal pregnant women in the same gestational age. In severe toxemia of pregnancy, there was no significant correlation between serum IGF-I levels and maternal weight gain or serum triglyceride levels, and these results may be influenced by such abnormalities as water retention, hemoconcentration, severe hypoproteinemia and severe negative nitrogen balance not found in normal pregnancy. In conclusion, it is considered that IGF-I concentration is regulated not only by endocrinological factors, but also by metabolic factors in maternal circulation during pregnancy, and the measurement of maternal IGF-I concentration seems to be a useful parameter to evaluate the maternal nutritional states.
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PMID:[Maternal nutritional states and serum insulin-like growth factor-I (IGF-I) concentrations in normal and abnormal pregnancy]. 795 9

Neuropeptide Y (NPY) is a 36 amino acid peptide belonging to the pancreatic polypeptide family of neuroendocrine hormones. It is the most abundant peptide yet discovered in the mammalian brain and is widely expressed by neurons in the central and peripheral nervous systems as well as adrenal medullary cells. Recently, a large number of studies have focussed on the potential roles played by NPY within the hypothalamus and pituitary with respect to the control of food intake and energy homeostasis. It is now clear that NPY is a potent stimulator of food intake in models of hyperphagia, that hypothalamic NPY also regulates sympathetic neural activity and it appears that NPY may also influence the glucocorticoid, growth hormone and thyroid hormone axes. Taken together, current data suggest that hypothalamic and pituitary NPY-expressing cells represent an important and critical site of integration of peripheral hormonal signals with regulation of energy homeostasis.
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PMID:Neuropeptide Y: a central regulator of energy homeostasis. 813 18

We describe 5 children, 4 girls, aged 4-14 years with evolving hypothalamic-pituitary dysfunction. They had presenting features, isolated or combined, of polyuria and polydipsia (n = 3), weight gain and hyperphagia (n = 3), and growth failure (n = 1). During periods of 1-5 years per child, the following abnormalities developed: diabetes insipidus (n = 5), osmoreceptor dysfunction (hypernatraemia with absent thirst) (n = 3), hyperprolactinaemia (n = 3), growth hormone (GH) deficiency (n = 4, of whom 3 had normal linear growth), ACTH deficiency (n = 2), TSH deficiency (n = 2) and precocious puberty (n = 1, female). In 2 patients, high-resolution CT scans and MRI showed structural lesions of the hypothalamus 1.5 and 3.5 years after presentation. These were inaccessible and not biopsied. Scans in the remainder were normal. In conclusion, weight gain, impaired thirst, and hyperprolactinaemia were early features of evolving hypothalamic-pituitary dysfunction, and occurred with diabetes insipidus, accompanied by progressive anterior pituitary deficiencies. Pituitary hormone replacement with clinical and neuroradiological surveillance is important in any child with symptoms suggestive of an evolving hypothalamic lesion.
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PMID:Idiopathic hypothalamus-pituitary dysfunction: review of five cases. 840 39


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