Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of training to various rhythms of intermittent total starvation (ITS) or intermittent protein starvation (IPS) on the plasma glucose and the plasma insulin levels were studied in the growing chicken. Both types of feeding improved the glucose tolerance in spite of a decrease in the insulin response. After an oral glucose load, plasma free fatty acids showed opposite variations to plasma insulin and plasma glucose. The insulin released in response to a test meal was unchanged. In the ITS 1-1 group (1 day fasting-1 day feeding cycles), low glycemia-low insulinemia were observed during the fasting period of the cycle and high glycemia-hyperinsulinemia during the repletion period in response to the "adaptive hyperphagia." In the IPS 1-1 group (1 day feeding with the protein free diet-1 day feeding with the balanced diet cycles), glycemia was sustained at a high level during both periods of the cycle and insulinemia was depressed by feeding with the protein-free diet and highly stimulated by refeeding with the balanced diet. Therefore, in the chicken, intermittent feeding increases the insulin sensitivity of target tissues and modifies the B-cell sensitivity to glucose. The highest decrease in B-cell sensitivity to glucose was obtained with the protein free diet which further emphasizes the glucose-amino acid synergism previously observed for insulin release.
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PMID:Effect of intermittent feeding on glucose-insulin relationship in the chicken. 43 Feb 64

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

A patient with liver dysfunction following small-bowel bypass for obesity was treated successfully with intravenous hyperalimentation. The hepatic steatosis and dysfunction were most likely caused by the preferential absorption of carbohydrate in the remaining small bowel, with resulting relative protein starvation. Routine use of high-protein, low-carbohydrate diets postoperatively until weight stabilization has occurred may prevent this complication.
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PMID:Liver dysfunction following small-bowel bypass for obesity. Nonoperative treatment of fatty metamorphosis with parenteral hyperalimentation. 81 54

In abuse dwarfism the behavioral signs include some or all of the following: (1) a history of unusual eating and drinking behavior, reversible on change of domicile, such as eating from a garbage can and drinking from a toilet bowl, stealing food, alleged picky eating and rejecting food at the table, polydipsia and polyphagia, possibly alternating with vomiting and possibly also with self-starvation; (2) a history of such behavioral symptoms as enuresis, encopresis, social apathy or inertia, defiant aggressiveness, sudden tantrums, crying spasms, insomnia, eccentric sleeping and waking schedule, pain agnosia, and self-injury, all occurring only in the growth-retarding environment; (3) retarded motor development, with improvement on removal of the child from the domiclle of abuse; (4) retarded intellectual growht, reversible on change of domicile by as much as 30 to 50 IQ points; and (5) a history of pathologic family relationships, including unusual cruelty and neglect, either somatic or psychic or both.
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PMID:The syndrome of abuse dwarfism (psychosocial dwarfism or reversible hyposomatotropism). 85 51

Obesity is one of the most common prosperity diseases. As a consequence of this disease there is a decrease in the expectation of life. Obesity is bascially caused by overeating. The low-caloric reducing diets are differentiated into a low-fat and high-carbohydrate form, and into a carbohydrate-free and high-fat diet. The metabolic advantages and the disadvantages of these two forms of low-caloric diets are discussed with respect to starvation metabolism. It is assumed that without ketoacidosis, at least 100-140 g glucose per day are required to meet the energetic demands of the central nervous system. Since the conversion rate of protein to glucose is about 2:1, during a carbohydrate-free diet about 200-260 g of protein per day would be necessary to meet the glucose requirements of the organism. As such a high-protein supply with food is almost impossible, ketogenesis in the liver must take place as a sort of "glucose-sparing mechanism". Only under these conditions, the otherwise extreme nitrogen catabolism can be avoided during an almost carbohydrate-free diet. However, using a fat-free (600 kcal) diet it is possible to furnish the glucose requirements of the central nervous system by the food supply. Therefore, a compensatory ketoacidosis is not required. Additionally, the fat-free diet does not contain cholesterol. In this way, the hypercholesterinemia which is a common feature in obesity is favourably influenced by the absence of foods of animal origin. Therefore, within a short period a marked decrease in serum cholesterol concentration results by the high-carbohydrate diet. The same is true for the concentration of free fatty acids and serum triglycerides. It is concluded that the high-carbohydrate low-caloric diet is suited best for reduction of body weight.
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PMID:[Nutrition physiological aspects in the treatment of obesity]. 125 23

Brown adipose tissue (BAT) is characterized by the existence of a unique mitochondrial protein (uncoupling protein or UCP) that uncouples oxidative phosphorylation and thus allows heat production. Its role in thermogenesis has been emphasized in recent years in response to cold stress (nonshivering thermogenesis, NST) as well as to hyperphagia (diet-induced thermogenesis, DIT). The present work was a first attempt to determine whether varying nutritional conditions could affect UCP gene expression. Total RNA was isolated from interscapular BAT and hybridized with a cDNA probe for UCP. Changes in UCP mRNA level were studied in rats fasted and refed for various periods at 23 or 28 degrees C. A 2 d fast at 23 degrees C reduced UCP mRNA level, whereas refeeding increased it. A prolonged starvation (53 h) induced an unexpected rise in UCP mRNA, which was associated with a fall in body temperature. Increasing the ambient temperature to thermoneutrality (28 degrees C) suppressed the fall in body temperature as well as the rise in UCP mRNA, which could then be characterized as a cold-induced response. Under the same environmental conditions (28 degrees C), refeeding still triggered a sharp, though transient, increase in UCP mRNA, showing that DIT was dissociated from NST.
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PMID:Effects of fasting and refeeding on the level of uncoupling protein mRNA in rat brown adipose tissue: evidence for diet-induced and cold-induced responses. 226 17

In rats with perifornical lateral hypothalamic (LH) electrodes that induced feeding, self-stimulation through the same electrodes increased immediately after ventromedial hypothalamic (VMH) lesions and did not return to normal until food intake normalized and the rats had become obese. In a second experiment a unilateral far-LH lesion decreased both feeding and contralateral perifornical LH self-stimulation. In Experiment 3, 6-hydroxydopamine (6-OHDA) injected into the midbrain to destroy the ventral noradrenergic bundle (VNAB) caused hyperphagia and increased LH self-stimulation. In summary, VMH or VNAB damage increased feeding and self-stimulation; contralateral far-LH damage decreased both. These results confirm the earlier suggestion that the VMH region is necessary for normal inhibition of feeding and feeding reward as reflected in self-stimulation rate. Although massive 6-OHDA-induced depletion of the dopamine system that passes through the LH can cause starvation and impair self-stimulation, the results suggest that selective catecholamine depletion of ventral midbrain neurons with sparing of the A9 and A10 dopaminergic cells can disinhibit feeding and self-stimulation. In all three experiments LH self-stimulation and food intake covaried, which suggests that they are functionally related.
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PMID:Food intake and lateral hypothalamic self-stimulation covary after medial hypothalamic lesions or ventral midbrain 6-hydroxydopamine injections that cause obesity. 249 4

1. The effects of starvation post partum (24 h) and tumour growth pre partum on the initiation of lactation in the rat were studied. 2. Tumour growth decreased food intake at 24 h, but not at 2 days post partum. 3. Pup growth rate increased with hyperphagia; starvation and tumour burden decreased pup growth, and starvation decreased maternal body weight. 4. Starvation decreased gastrointestinal-tract mass; tumour growth decreased gastrointestinal-tract and mammary-gland mass. 5. Mammary-gland DNA-synthesis rate was high immediately post partum, but decreased by day 3 of lactation; starvation and tumour burden decreased this rate, and also decreased gastrointestinal-tract DNA-synthesis rate. 6. Arteriovenous differences for glucose and lactate across the mammary gland did not change with time, nor were they affected by the tumour. Starvation decreased arterial glucose and lactate, and the gland extracted less glucose but produced lactate. 7. Mammary-gland lipogenesis was sensitive to starvation and to tumour growth. 8. In contrast with the gradual development of mammary-gland lipogenic enzyme activities, lipoprotein lipase activity was high in the gland by 2 days post partum; starvation or tumour burden decreased the activity. 9. The mammary gland is sensitive post partum to decreased food intake, and to tumour presence. The effects of the latter are apparently independent of hypophagia.
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PMID:Lipid metabolism during the initiation of lactation in the rat. The effects of starvation and tumour growth. 259 Jan 73

Anorexia nervosa is a common psychiatric disorder predominantly affecting young women, associated with significant morbidity and mortality, much involving the cardiovascular system. In contrast, protein-calorie malnutrition, while not strictly analogous to the protein-sparing characteristics often noted in anorexia nervosa, is a problem of global stature. Physiologic consequences of anorexia nervosa include rhythm disturbances, mitral valve prolapse, plus both systolic and diastolic ventricular dysfunction. Diminished exercise capacity occurs in both states, with marked blunting of the heart rate and blood pressure response. Congestive heart failure may appear, especially during refeeding. In addition to the myofibrillar destruction associated with protein-calorie malnutrition, hypophosphatemia, particularly when exacerbated by unrestricted glucose-rich refeedings or hyperalimentation, may be one additional cause of ventricular dysfunction. A high level of suspicion for cardiovascular complications is, therefore, warranted in the evaluation and therapy of weight loss conditions such as starvation and anorexia nervosa.
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PMID:Weight loss and the heart. Effects of anorexia nervosa and starvation. 265 Jun 47

Based on laboratory results, restrained eating has been linked to the development of binge eating and eating disorder syndromes such as bulimia nervosa. This study was designed to extend the scope of investigation of the concept of restrained eating beyond the laboratory. Eating behavior and biochemical indices of nutritional state were investigated in 60 young women, who were divided in restrained and unrestrained eaters by questionnaire. Seven-day records of food intake showed that the high-restraint group ate around 400 kcal a day fewer than the low-restraint group. Group differences in actual macronutrient intake and long-term food preferences pointed to a qualitatively altered eating pattern in restrained eaters. Actual protein portion was higher in restrained eaters. They tried to avoid calorie dense food items of high carbohydrate and fat content. Instead, they preferred food regarded as low-caloric and healthy. Plasma levels of triiodothyronine and glucose, which could be taken as indices of long-term adaptation to starvation, were not decreased in the high-restraint group. However, significantly higher levels of triglycerides in restrained eaters may reflect a biological state due to short-term starvation. The results indicate that the concept of dietary restraint predicts eating behavior not only under experimental conditions, but also in normal life. As a consequence of altered eating patterns, psychological and physiological deprivation can be hypothesized in restrained eaters, making them prone to the occurrence of overeating.
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PMID:Behavioral and biological correlates of dietary restraint in normal life. 276 57


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