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

The endocrinological and biochemical mechanisms controlling energy expenditure in brown adipose tissue at the cellular as well as at the total tissue levels are briefly reviewed. Thermogenesis in brown adipose tissue is principally controlled by the activity of hormone-sensitive lipases that represent the 'flux-generating' step in the stimulus-calorigenesis sequence. Long chain fatty acids are the physiological messengers regulating mitochondrial respiration. Agents stimulating brown adipocyte lipolysis (catecholamines, glucagon, methylxanthines) also stimulate respiration, and conversely, agents inhibiting lipolysis (adrenergic antagonists, insulin, prostaglandins) also inhibit respiration. This indicates that lipolysis and respiration are functionally coupled in brown adipose tissue. On the other hand, brown adipose tissue thermogenic capacity increases during cold acclimation or adaptation to hyperphagia. Brown adipocyte proliferation and differentiation from precursor cells (interstitial cells and brown preadipocytes) represent the fundamental phenomena explaining the increase capacity of cold acclimated and/or hyperphagic animals for responding calorigenically to catecholamines. Physiological situations associated with a stimulation of energy expenditure and a negative energy balance (cold acclimation, exercise training, caffeine consumption) generally induce a stimulation of adipocyte proliferation in brown adipose tissue that is accompanied by a simultaneous inhibition of cell proliferation in white adipose tissue. The physiological significance of these metabolic adaptations is to modulate the capacity of homeothermic animals for energy expenditure in accordance with energy requirements.
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PMID:Regulation of energy expenditure in brown adipose tissue. 299 14

The rapid growth (0.8 +/- 0.3 g/day) of a transplantable insulinoma, which also contained substance P (2.9 +/- 2.3 pmol/g) and gastrin-releasing peptide (3.2 +/- 2.1 pmol/g), resulted in the development of hyperphagia, hyperinsulinaemia and hypoglycaemia in rats (n = 8). After a 14-day growth period, the insulinoma-bearing rats showed an increase (49%; p less than 0.01) in the weight of the small intestine but no significant change in stomach weight compared with control animals. The content (pmol/organ) of somatostatin, substance P, neurokinin A and vasoactive intestinal peptide in the stomachs of the tumour rats was unchanged. A depletion in the content (53% p less than 0.01) and concentration (57%; p less than 0.01) of gastrin-releasing peptide, however, suggested either hypersecretion, possibly mediated through hypoglycaemia-induced vagal stimulation, or inhibition of synthesis. The concentration and content of glucagon-like immunoreactivity (enteroglucagon) in the small intestine of the insulinoma rats increased markedly (47%; p less than 0.01 and 120%; p less than 0.01). This increase is consistent with a proposed role of this peptide as a factor trophic to the intestinal mucosa. No significant changes in the concentrations of somatostatin, substance P, neurokinin A, vasoactive intestinal peptide and gastrin-releasing peptide in the small intestine were observed. However, the increase in gut weight resulted in a greater content of vasoactive intestinal peptide (40%; p less than 0.01) and substance P (37%; p less than 0.05) in the insulinoma rats.
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PMID:Effects of a transplantable insulinoma upon regulatory peptide concentrations in the gastrointestinal tract of the rat. 301 8

The growth of gastrointestinal mucosa can be related to ingestion and digestion of diet, with fasting producing mucosal hypoplasia and hyperphagia producing mucosal hyperplasia. Experiments were designed to determine whether induction of polyamine metabolism following ingestion of a meal was related to mucosal growth. Activity of the enzyme ornithine decarboxylase (ODC) in both jejunum and ileum but not in duodenum was dependent on the presence of food in the gut; ODC activity was more than 200-fold greater in mucosa of fed rats than in fasted rats. Inhibition of ODC with difluoromethylornithine lead to mucosal atrophy in ileum but not in duodenum. Refeeding of fasted rats resulted in significant induction of ODC in duodenal, ileal, and colonic, but not fundic, mucosa. In addition, two hormones, epidermal growth factor and glucagon, were effective inducers of ileal ODC activity. Direct evidence for hormonal involvement in the postprandial rise in mucosal ODC activity was provided by experiments in rats that had undergone ileal bypass surgery. After refeeding of fasted rats mucosal ODC activity was induced in both ileum left in continuity and in the bypassed segment. Refeeding of elemental diets demonstrated that ingestion of carbohydrate alone was sufficient for maximal enzyme induction. Mixed amino acids or glyceryl trioleate were no more effective inducers than nonnutritive solutions of cellulose or saccharin. These data demonstrate that hormones which are released during ingestion and digestion of a meal are the stimuli for induction of mucosal polyamine metabolism, suggesting that food-induced mucosal growth is hormonally mediated.
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PMID:Hormonal regulation of postprandial induction of gastrointestinal ornithine decarboxylase activity. 309 78

A 61-year-old male, while recovering from a Whipple's procedure for pancreatic carcinoma, was treated for 13 days with an insulin infusion pump for diabetes exacerbated by enteral hyperalimentation. Treatment with continuous subcutaneous insulin infusion resulted in improved blood glucose control. Associated with this improvement was a reduction in plasma cholesterol, triglyceride and free fatty acid levels. Plasma epinephrine, norepinephrine, glucagon and cortisol concentrations were also lowered although growth hormone levels remained unchanged. It is concluded that enhanced metabolic control during hyperalimentation results in a decrease in counter-regulatory hormone levels and an improvement in the catabolic state in this patient. These preliminary observations provide evidence for maintaining euglycemia in diabetic patients while receiving nutritional support.
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PMID:Continuous subcutaneous insulin infusion (CSII) reduces counter-regulatory hormone concentrations in a patient receiving enteral hyperalimentation. 310 71

Laboratory rodents can be induced to overeat voluntarily when exposed to a choice of highly palatable human foods so-called "cafeteria diet". The hyperphagia of these animals is associated with marked increases in energy expenditure and reduced levels of energetic efficiency. Increases in Diet-Induced-Thermogenesis (DIT) in response to overfeeding have been demonstrated in several species including man. The studies with the cafeteria-fed rats confirm the large potential for DIT in young animals. In older (26-week-old rats) a dramatic decline in the capacity for DIT is observed. Increases in energy expenditure resulting from hyperphagia appear to be mediated by the sympathetic nervous system, which causes activation of heat production in brown adipose tissue (BAT). The high thermogenic potential of BAT is due to the physiological uncoupling of oxidative phosphorylation in the inner mitochondrial membrane. This activity is enhanced by overfeeding, which causes hypertrophy. DIT and BAT are controlled by hormonal action: noradrenaline appears to be the primary activator of BAT and insulin may be required for DIT and may even activate thermogenesis. Other hormones such as glucagon, thyroid, melatonin, TSH, endorphins and sex hormones are also implicated in one way or another in the regulation of energy balance and the control of thermogenesis.
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PMID:The role of brown fat in diet-induced thermogenesis. 346 Sep 73

The effects of intraperitoneal injections of pancreatic glucagon and bombesin on meal size were tested in female rats in the dynamic phase of ventromedial hypothalamic (VMH) hyperphagia. Both pancreatic glucagon (100-2500 micrograms/kg) and bombesin (4-16 micrograms/kg) inhibited meal size in a dose-related manner. Percent inhibitions of meal size in VMH-lesioned and control rats did not differ significantly. These results suggest that the VMH is not necessary for peripheral administration of either pancreatic glucagon or bombesin to elicit postprandial satiety.
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PMID:Pancreatic glucagon and bombesin inhibit meal size in ventromedial hypothalamus-lesioned rats. 353 24

A 30% body surface area, open-flame, full-thickness burn of adult rats induced a 4-day period of anorexia that was followed by hyperphagia beginning on postburn day 10. The hyperphagic burned rats also exhibited increased resting energy expenditure and no gain in body weight, suggesting hypermetabolism. Plasma levels of immunoreactive insulin and albumin were decreased in both groups of burned rats; immunoreactive pancreatic glucagon concentrations were elevated only in the anorectic burned rats. Plasma levels of epinephrine were elevated in the hyperphagic burned rats. In the brain, dopamine metabolism appeared to be increased in the corpus striatum, nucleus accumbens, and amygdala of anorectic burned rats; norepinephrine levels were elevated in the hypothalamus and nucleus accumbens of the hyperphagic-hypermetabolic rats. These data indicate that this animal model of major burn trauma exhibits anorexia, hyperphagia, catabolism, and hypermetabolism. Furthermore, elevated dopamine metabolism appears to be associated with the anorexia, while the hyperphagia-hypermetabolism may be mediated by norepinephrine.
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PMID:Burn-induced alterations in feeding, energy expenditure, and brain amine neurotransmitters in rats. 357 6

Electrolytic lesions of the ventromedial hypothalamus including nucl. hypothalamicus inferior caused the cockerels to become hyperphagic. The plasma insulin level of the control birds was low before feeding and it increased after feeding, while that of the hyperphagic birds was higher before feeding and increased even more after feeding. Under the fasting condition on the 19th day, the insulin secretion of the hyperphagic birds remained at a high level, and there was a high correlation between the insulin value and the food consumption. Hyperactivity of insulin secretion in the hypothalamic hyperphagic birds was inhibited by administration of diazoxide and their insulin levels declined to a level similar to that of the controls. As a result the hyperphagia was interrupted and the daily food consumption declined to the same level as the controls. Therefore, the hyperinsulinemia seemed to be necessary for maintaining the hypothalamic hyperphagia in chickens. The role of glucagon in this phenomenon is also discussed.
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PMID:Hyperinsulinemia and its role in maintaining the hypothalamic hyperphagia in chickens. 634 54

Intravenous hyperalimentation (IVH) needs 24 hour infusion everyday without an interruption. Insulin and glucagon are not physiologically secreted. Metabolic rhythm in the body is changed. Protein synthesis and nitrogen balance may be disturbed. For improvement of the metabolic disturbance in IVH, intermittent intraportal hyperalimentation was investigated. Eight Beagles weighed about 10 kg and mongrel dogs weighed 18 kg were used. Glucose and amino acids were given 12.0 g/kg and 2.5 g/kg, respectively. Those were infused into the portal vein for 10 hours every day. During the next 14 hours infusion was not performed at all. Fat was intravenously given 1.5 g/kg as emulsion every day. The levels of insulin and glucagon in the portal vein and the uptake rate of glucose and amino acids in the liver were investigated during administration of the nutrients. After 30 days the dogs were sacrificed and pathological examination was performed. Insulin and glucagon levels were almost physiologically changed. The uptake rate of amino acids into the liver was a high level of 52%. In spite of low level of 162 in non-protein calorie to nitrogen ratio, nitrogen balance remained in 106 +/- 23 mg/kg/day. The body weight increased by 3.6% on the average (p less than 0.01) and the serum protein levels significantly increased (p less than 0.01). In one out of 8 dogs, minute thrombosis and slight sclerosis of the portal vein were found. The liver showed no histological changes. In conclusion, the intermittent portal hyperalimentation seems to be a possible and excellent method of nutrition.
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PMID:[Experimental studies on intermittent intraportal hyperalimentation]. 641 42

We studied a patient with lung cancer, who exhibited severe systemic derangements of metabolism causing cachexia preceding the appearance of a large bulky tumor. The data described herein left no doubt that lung cancer growing in the patient acted as a powerful hypoglycemic factor, setting in motion widespread metabolic disorders. Inappropriate secretion of insulin may be involved in the manifestation of hypoglycemia. However, no ectopic secretion of insulin, glucagon, ACTH and aldosterone appeared to be associated with the carcinoma in the patient. From the present and previous observations, it is stressed that progressive energy loss from the patient occurs by virtue of a combination of severe anorexia and the establishment of a systemic energy-losing cycle dependent on an interplay of glycolysis in the cancer cells and stimulated gluconeogenesis in the host tissues, which in turn results in derangements of protein, lipid and electrolyte metabolism. Attempts to ameliorate the patient's distress and counterbalance the effect of the tumor by parenteral hyperalimentation were not satisfactory and resulted in only a temporary improvement. This study also demonstrated that marked granulocytosis was the result of production of an excess granulopoietic colony stimulating activity by the cancer cells.
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PMID:Hypoglycemia, hypopotassemia and hyperleukocytosis associated with squamous cell carcinoma of the lung. 697 22


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