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

A chromophobic pituitary adenoma induced on BD IX-rats has been grafted on animals of the same strain. The transplanted tumour takes in 90-100%; it grows at a slow rate (in 7 months after grafting a weight of 7-20 g is attained). Tumour-bearing animals display gigantism and hypertrophy of adrenals; moreover, in 33% of cases, diabetes is observed. With non-diabetic animals, splenomegaly and marked leukocytosis are observed; immature white and red cells are present in the peripheral blood. Spontaneous regression of the tumour never occurs. After surgical removal, tumour regrowth and the formation of metastases are observed. Diabetes is characterised by pronounced hyperglycaemia, glucosuria, polyphagia and polydipsia. Histochemically, insulin cannot be detected in pancreas. Splenomegaly is never observed in diabetic animals. Transplanted adenoma frequently tends to stop growing. No recurrence is observable after extirpation. Spontaneous regression of the tumour sometimes occurs. Gigantism, hypertrophy of adrenals and diabetes are considered as consequences of growth hormone- and ACTH-secretion of the transplanted adenoma. At present the tumour is running in the 8th passage. It did not change its characteristics over a period of 5 years.
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PMID:Transplantable, STH-producing and diabetogenic pituitary adenoma of the BD IX-strain of rats. 17 13

Obese Zucker rats were either pair-fed to their lean litter-mates or fed ad lib, to determine the effect of hyperphagia on serum hormone levels and tissue metabolism as indicated by enzyme activities and in vitro metabolite flux. Hyperphagia was shown to be non-essential for the elevation in serum insulin and suppression in serum growth hormone and prolactin in the genetically obese rat. It was also shown that the increased liver cell lipogenic rate was not dependent on hyperphagia in the obese rat and that adipose cell lipogenesis was not significantly altered in the pair-fed obese rat. The utilization of alanine for glucose synthesis in vitro was similar for both lean and obese rats, but its utilization for fatty acid synthesis was higher in the obese rat. Data is presented which suggest that the inhibitory effect of glucagon on liver lipogenesis is blunted in the obese rat.
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PMID:Serum hormone levels and tissue metabolism in pair-fed lean and obese Zucker rats. 19 81

Two girls, one with septo-optic dysplasia and the other with posttraumatic brain damage, had the unusual combination of human growth hormone, thyrotropin, adrenocorticotrophic hormone, and vasopressin deficiencies that were associated with sexual precocity in one patient and early sexual maturation in the second patient, and of adult follicle-stimulating hormone and luteinizing hormone concentrations. At autopsy, the first patient had optic nerve aplasia, a normal pituitary gland, and some disorganization of myelinated fibers in the hypothalamus. The second patient had a normal thyrotropin and prolactin response to thyrotropin-releasing hormone, plus hyperphagia, deranged thirst mechanism, and temperature instability. These findings suggest that the lesion may be a defective hypothalamic regulation of pituitary hormone secretion. Congenital or traumatic hypothalamic-pituitary lesions may not affect all releasing factors or trophic hormones in a similar fashion.
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PMID:Sexual precocity with hypothalamic hypopituitarism. 22 32

The authors report a girl with acute lymphoblastic leukaemia presenting hypothalamic syndrome characterized by meningeal leukaemia, hyperphagia and obesity. Insulin and growth hormone secretion, studied with arginine and insulin stimulation tests, showed a high peak of serum insulin and no response of growth hormone. Insulin and growth hormone responses to these tests reverted to normal after intrathecal methotrexate.
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PMID:Insulin and growth hormone secretion in a leukaemic girl with hypothalamic syndrome. 26 33

The renewal of the digestive mucosa is the most efficient process assuming the maintenance of the gastrointestinal barrier. The mucous and absorptive cells, born in the proliferative zone, are migrating to the surface and they extrude duirng meals, living 4 to 6 days. Hyperphagia, pregnancy, lactation and intestinal resection induce a hypertrophic state. Fasting, ageing, germ free status provoke a hypoplasia. The ulcerogenic and antimitotic drugs decrease the proliferative activity. The gastrointestinal cell renewal is controlled by hormonal, vitaminic and nervous agents. Gastrin and growth hormone are the major trophic factors, secretom amd cprtocpsteroids act as antitrophic agents. The vitamins A, D and B12, and the nervous transmittors participate in the feed back control assuming a steady state between proliferation and extrusion. Chalones and immunologic factors are probably the most important but unknown inhibitors. The pathological events concerned with abnormal renewal are peptic ulcer, atrophic gastritis, intestinal villous atrophy and digestive cancer.
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PMID:[Regulation of cell renewal in the gastrointestinal mucosa (author's transl)]. 32 43

Intravenous hyperalimentation allows complete nutrition and anabolism in patients who cannot be fed by the oral route. However, several complications have been reported, e.g. septicaemia and hyperglycaemina. In 51 intensive-care patients receiving hyperalimentation, 18% were found to be hyperglycaemic in spite of insulin administration. Hyperglycaemia was frequently associated with stress. In 8 patients undergoing major surgery, which was chosen as a stress model, decreased insulin and increased glucagon, growth hormone and cortisone levels were observed. These findings could explain stress-induced glucose intolerance. In a further experiment, 8 intensive-care patients were given alternative intravenous feedings with either 600g of a mixture of glucose, fructose and xylitol in a ration of 1:2:1 or 600g glucose per day. During both regimens insulin administration was required in 4 patients, but the insulin dosage was lower with the mixture. Plasma glucose during glucose infusion was 205+/-25mg/100ml(M+/-SEM) and the sum of plasma glucose, fructose and xylitol during infusion of the mixture was 176+/-33mg/100ml, the difference being of borderline significance (p less than 0.05). The advantages and disadvantages of infusable substrates are summarized on the basis of the available literature and it is concluded that, in general, glucose is preferable. However, if hyperglycaemia is difficult to control, partial replacement of glucose by glucose substitutes or fat emulsions may be advantageous. A routine infusion programme for central venous feeding is suggested. Causes and prevention of side-effects are reviewed. In many patients receiving central venous nutrition less hazardous and less expensive methods could be used such as nasogastric tube feeding, elemental diet or peripheral venous nutrition.
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PMID:[Parenteral hyperalimentation (author's transl)]. 40 48

In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.
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PMID:Feeding behavior in monkeys with and without lesions of the hypothalamus. 81 9

Destruction of the ventromedial hypothalamic nuclei (VMN) in the weanling rat without injury to the median eminence results in a series of somatic, endocrine, and metabolic changes that are characterized by normal food and water intake but decreased linear growth, normal body weight but increased carcass fat and reduced carcass protein, lean body mass, and water. The endocrine alterations comprise hyperinsulinemia in the face of normoglycemia, hypertriglyceridemia and hypercholesterolemia and reduced growth hormone levels. The metabolic changes include greater oxidation of glucose and incorporation into lipid and reduced palmitate oxidation but increased incorporation into lipid. Weanling rats with VMN lesions are normophagic in absolute terms, relative to body weight and per metabolic unit, but their nocturnal feeding and weight gain cycles are disrupted and their locomotor activity is reduced. The VMN are involved in the long-term control of feeding - as in the mature rat - as shown by intragastric preloading studies and dietary density manipulation, glucose preference tests and intraperitoneal injections with glucose. Hyperinsulinemia and hypertriglyceridemia are present four days after the VMN operation in the presence of subnormal food intake and plasma glucose levels. Manipulations of the fat content of the diet revealed that the hyperlipidemia is of both endogenous and exogenous origin and that lipoprotein lipase is increased; a 48-hour fast reduced the hyperlipidemia to control levels, however. This suggests that weanling VMN rat tissue may have an impaired ability to take up circulating lipid. An increased incorporation of glycerol into lipid may be due to induction of glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed glycerokinase by hyperinsulinemia. Adipose tissue of weanling VMN rats showed neither depressed lipolysis nor diminished lipolytic activity per milligram of tissue protein. Glucose oxidation and incorporation into adipose tissue is increased in several tissues in vitro and there is enhanced glucose disappearance from plasma and incorporation into tissue lipids in vivo. These changes develop within a short time after lesion production and persist at least partially up to six months: glucose utilization in liver increases already four hours after the operation whereas it takes 72 hours to commence in adipose tissue. Insulin resistance is not apparent either in vivo or in vitro. The decreased growth hormone levels are not critical to the metabolic changes, nor is the hyperinsulinemia totally necessary. The metabolic changes also appear on several different types of diet and persist with fasting. The latter does not reduce insulin sensitivity of VMN rat tissues, wheras it does so in normal rats. Mature rats developed the same metabolic changes even in the absence of hyperphagia. The metabolic alterations can be blocked by pharmacologic doses of glucocorticoids, but are enhanced by the administration of estrogen...
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PMID:Origin of endocrine-metabolic changes in the weanling rat ventromedial syndrome. 95 Jun 80

The effects of bilateral lesions of the ventral noradrenergic bundle (VNA) were studied in male rats. In contrast to data reported by others, hyperphagia and obesity were not observed following VNA lesions. Indeed, except for a depression during the first three postoperative days, food intake (FI) of the VNA lesioned animals (VNAL) was normal. Interestingly, the body weight (BW) of the VNAL was significantly reduced compared to the controls, and a pair feeding study indicated that this depression of BW was not due to their FI. Computation of FI per metabolic size showed that the VNAL actually had a significantly increased FI compared to the controls. After a two day fast the VNAL lost more metabolic size than controls and upon refeeding they defended their pre-fast BW. The VNAL rats showed normal body composition and circulating glucose, insulin and prolactin. They had reduced free fatty acids, triglycerides, growth hormone and body length. The data suggest that the mesencephalon influences BW set point, some metabolites and possibly overall metabolism.
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PMID:Mesencephalic lesions resulting in normophagia, reduced weight and altered metabolism. 99 50

The regulation of energy metabolism in obesity may differ from normal condition in several respects. The synthesis of lipids may be enhanced due to a greater production of insulin, estrogens and cortisol and to a lack of dehydroepiandrosterone. Lipolysis is reduced in obese subjects by a decreased secretion of catecholamines, growth hormone, adipsin and cachectin. Inadequate intake of food and stress modify the T3/rT3 ratio. Oxidative phosphorylation and the production of ATP is modified, thermogenesis decreases due to a reduced synthesis of thermogenin. A decreased activity of substrate cycles and of the Na-K ATPase, is expected. Most of these disorders are normalized in post-obese patients. Many common drugs interfere with energy metabolism, namely those used in psychiatry and all hormones and their antagonists mentioned above and used for a long time. Obesity should not be considered as a simple result of overeating and lack of physical activity.
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PMID:[Energy metabolism in obesity]. 158 28


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