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

Many gastrointestinal structural and functional properties are known to be altered in diabetes. In this study, we investigated whether serum and tissue gastrin levels are abnormally altered in a strain of genetically diabetic mice (C57BL/KSJ). Both serum and antral gastrin concentration were found to be significantly increased 3.4- and 2-fold above normal values in diabetic mice fed ad libitum. The increase in tissue gastrin concentration is most probably due to an increase in both cellular gastrin content and G-cell number, since the latter property is increased 130% in diabetic animals. Pair feeding studies demonstrated that diabetes associated hyperphagia is not a major factor in inducing these endocrine changes, since antral and serum gastrin are still significantly elevated above normal in diabetic animals fed a restricted diet. G-cell number, however, is not significantly increased above normal values in pair fed diabetic mice. The peak serum gastrin concentration after a meal and the duration of postprandial hypergastrinemia are also significantly increased above normal in diabetic animals. Gel filtration chromatography studies indicate that the antral nucosae of normal and diabetic mice have identical molecular forms of the hormone. It is therefore concluded that antral and serum gastrin concentration are increased in genetically diabetic mice due to both dietary alterations and other, as yet undefined, factors specific for the disease, and that the resultant hypergastrinemia may contribute to some of the gastrointestinal alterations seen in diabetes.
Gastroenterology 1979 Dec
PMID:Alterations in serum and antral gastrin levels in genetically diabetic mice. 49 15

Obese (ob/ob) and diabetes (db/db) mice are genetic mutants that have been shown to have altered levels of central catecholamines as well as syndromes of obesity, hyperphagia, and hyperglycemia. Because of catecholamines, and particularly norepinephrine (NE), are implicated in the control of feeding, levels of central catecholamines were experimentally reduced in ob/ob and db/db mice to investigate the role of the catecholamines in these cases of spontaneously occurring obesity. Lesions produced by 6-hydroxydopamine (6-OHDA) were used to produce large depletions of NE and dopamine (DA) in both ob/ob and db/db mice and in lean control mice of the same background strains. In the db/db but not the ob/ob, central catecholamine depletion was accompanied by a significant and persistent weight loss and by a reduction in plasma glucose levels when compared with vehicle-infused controls. Treatment with the NE uptake blocker desmethylimipramine (DMI) prior to 6-OHDA infusions attenuated NE but not DA depletion. Diabetes mice that received DMI pretreatment showed a weight loss and decrease in plasma glucose proportional to the amount of NE depletion. Lean mice that received the 6-OHDA treatments showed only a transient weight loss and no significant change in blood glucose. It is concluded that abnormalities in central noradrenergic systems may account for part of the obesity syndrome observed in the diabetes mouse.
J Comp Physiol Psychol 1979 Dec
PMID:Differential effects on body weight of central 6-hydroxydopamine lesions in obese (ob/ob) and diabetes (db/db) mice. 52 20

A young man with severe multiple injuries following a motorcycle accident was admitted with head and mandible fractures, coma, fracture dislocation at C5-C6 resulting in total leg paralysis, partial paralysis of the right arm and intercostal muscles, and closed chest injury with possible pulmonary contusion. On the fourth day he developed fulminating mediastinitis and massive empyema, and was found to have a ruptured esophagus. Recovery became possible with surgical drainage of the pleural cavity and mediastinum, proximal and distal decompression of the esophagus, antimicrobial therapy, irrigation of the pleural cavity, complete intravenous hyperalimentation, and infusions of salt-poor albumin. The patient was discharged after 95 days, and 7 months after injury is neurologically intact except for a partial right wrist drop. This rare esophageal rupture should be suspected in any chest injury patients, especially those characterized by extreme cyanosis, dyspnea, shock, and prostration incompatible with thoracic cage injury.
J Trauma 1977 Dec
PMID:Rupture of the thoracic esophagus from blunt trauma. 59 47

Small doses of the opiate antagonist naloxone selectively abolished overeating in genetically obese mice (ob/ob) and rats (fa/fa). Elevated concentrations of the naturally occurring opiate beta-endorphin were found in the pituitaries of both obese species and in the blood plasma of the obese rats. Brain levels of beta-endorphin and Leu-enkephalin were unchanged. These data suggest that excess pituitary beta-endorphin may play a role in the development of the overeating and obesity syndrome.
Science 1978 Dec 01
PMID:beta-Endorphin is associated with overeating in genetically obese mice (ob/ob) and rats (fa/fa). 71 55

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.
J Clin Invest 1978 Dec
PMID:Hypophosphatemia and rhabdomyolysis. 74 77

Stress ulcers are multiple, superficial erosions which occur mainly in the fundus and body of the stomach. They develop after shock, sepsis, and trauma and are ofter found in patients with peritonitis and other chronic medical illness. Stress ulcers should be differentiated from reactivation of chronic duodenal or gastric ulcers. Cushing's ulcer following head injury, or drug-induced gastritis. Digestive symptoms are usually absent, hemorrhage is the most common manifestation, and perforation and obstruction are rare. The presence of luminal acid and ischemia are necessary for the production of stress ulcer, while disruption of the gastric mucosal barrier by refluxed duodenal content may contribute to the pathogenesis. Endoscopy is the mainstay of the diagnostic procedure, and angiography should be used if endoscopy fails to identify the bleeding lesions. Medical management should include volume replacement, nasogastric aspiration, and the use of antacid. Selective intraarterial infusion of pitressin has shown encouraging preliminary results. Surgical treatment is reserved only for those patients who continue to bleed despite all medical management. The operation of choice is open to question. We prefer vagotomy, pyloroplasty, and oversewing the ulcers as an initial operation. Since the result of all forms of therapy has been poor, it seems resonable to try to prevent ulcer development. The use of vitamin A, hyperalimentation, and growth hormones is still in an experimental stage. Large clinical studies with case control are necessary before recommendations can be made. The use of potent and frequent antacid to buffer the gastric content has shown promising results; however, these observations need to be confirmed in a properly controlled and randomized study.
Surg Clin North Am 1976 Dec
PMID:Stress ulcers: their pathogenesis, diagnosis, and treatment. 79 64

Albumin synthesis was measured, in vivo, in rats 16 hours after partial hepatectomy or after sham operation. When albumin synthesis was expressed in terms of whole body weight, partially hepatectomized rats synthesized significantly less than sham-operated rats. However, when albumin synthesis was expressed as a function of dry liver weight, the two groups synthesized similar amounts. Intragastric hyperalimentation with amino acids significantly increased albumin synthesis in partially hepatectomized rats.
Am J Clin Nutr 1975 Dec
PMID:Stimulation of albumin synthesis by amino acids following partial hepatectomy in the rat. 80 3

Phosphate depletion occurring during total parenteral nutrition has been frequently reported during the part 4 years. Hypophosphatemia may be associated with confusion, hyperventilation, and neuromuscular irritability, suggesting a total body phosphate deficiency. If inorganic phosphate levels fall below 1.0 mg %, diminished red cell glycolysis occurs with low erythrocyte levels of 2,3 diphosphoglycerate and adenosine triphosphate. Lowered red cell organic phosphates are associated with increased hemoglobin oxygen affinity. If severe hypophosphatemia occurs, hemolytic anemia, which is correctible by phosphate infusion, may result. In addition, leucocyte function is impaired by low levels of serum inorganic phosphate. While recognized as a needed additive, recommended phosphate supplements vary. Different infusion regimens have been suggested over the past 4 years, based primarily on assumed daily requirements. In the 19 trauma patients described who received hyperalimentation as part of their treatment, phosphate administration was calculated retrospectively and prospectively as a function of non-protein calories infused. Four different groups were studied. Group A received no phosphate additive and quickly became severely hypophosphatemic. Group B received from one to 15 meg of potassium acid phosphate per 1,000 K cal and developed a more gradual lowering of serum inorganic phosphate levels. Group C received 15 to 25 meg of potassium acid phosphate per 1,000 K cal and maintained normal phosphate levels throughout the course of treatment. Group D received greater than 25 meq of potassium acid phosphate per 1,000 K cal and gradually increased their serum inorganic phosphate levels. A significant positive correlation was found between serum inorganic phosphate levels, 2,3 diphosphoglycerate levels, adenosine triphosphate levels, and P50 of the oxy-hemoglobin dissociation curve. No patients developed hemolytic or neuromuscular syndromes which were attributable to hypophosphatemia. This study describes a simple method for the maintenance of adequate phosphate levels in patients whose dextrose-protein solutions may vary from day to day, by relating it to non-protein calories. Provision of 20 to 25 meq of potassium dihydrogen phosphate per 1,000 K cal will maintain normal serum levels of inorganic phosphate during total parenteral nutrition.
Ann Surg 1975 Dec
PMID:Phosphate depletion and repletion: relation to parenteral nutrition and oxygen transport. 81 Nov 82

The effects of parenteral hyperalimentation on postoperative gastric function were studied in eleven patients undergoing abdominal aortic surgery. Positive nitrogen balance was achieved in hyperalimented patients. Hyperalimentation was found to augment gastric mucosal regeneration, allowing for more physiologic secretory patterns and the maintenance of the protective gastric mucosal mechanism.
Am J Surg 1975 Dec
PMID:Effects of parenteral alimentation on postoperative gastric function. 81 76

Streptozotocin-induced diabetes in the rat alters intestinal function, causes hyperphagia and arrests body growth, but stimulates intestinal growth, particularly in the mucosa. Therefore we measured several indices of epithelial cell proliferation to gain insight on possible factors responsible for the increased mucosal cell mass in the small intestine. We examined epithelial cell proliferation in upper jejunum and terminal ileum of weight-matched control and diabetic rats pair fed or eating ad libitum. Cell proliferation was measured two ways: (1) isolating whole crypts 1 hr after injection of [3H]thymidine ([3H]TdR) and calculating disintegrations per minute per crypt (dpm per crypt), and (2) autoradiography of mucosal sections to obtain labeled cells per crypt, total cells per crypt-villus column, and cell migration rates. Autoradiography showed diabetes: (1) increased cell number of crypt-villus columns and increased labeled cells per crypt section, primarily jejunum, and (2) did not alter cell migration except for an increase in the ileum of diabetics eating ad libitum. Cell proliferation measured as dpm per crypt virtually doubled in diabetics in both segments regarless of dietary regimen. Dpm per crypt is a three-dimensional measurement based on the whole crypt. The increase in cell number and labeled cells per crypt in jejunal sections is also consistent with increased cell division, but shows a much smaller effect. The nature of the histological technique (two-dimensional) limits its usefulness for measuring morphological changes, and this may explain the discrepancy. Hence, the primary effect of diabetes is increased DNA synthesis (dpm per crypt) and this appears to be the main explanation for stimulated mucosal growth.
Gastroenterology 1977 Dec
PMID:Proliferation rate and transit time of mucosal cells in small intestine of the diabetic rat. 91 75


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