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

Metabolism of perfused livers from control and ventromedial hypothalamus (VMH)-lesioned rats has been studied. To eliminate the possibility that observed metabolic abnormalities could be realted to hyperphagia, VMH-lesioned rats were placed on restricted diet matching that of controls. Ten days postoperatively, VMH-lesioned rats had hyperinsulinemia, hypertriglyceridemia, increased blood urea nitrogen levels, together with decreased plasma free fatty acid (FFA) and glucose levels. Insulin release produced in vivo by a glucose load was much higher in VMH-lesioned than in control rats. Perfused livers from VMH-lesioned rats secreted more triglycerides and produced more urea than controls, whereas production of glucose and ketone bodies was reduced. Lipogenesis, newly synthesized triglyceride secretion, and the activity of acetyl-CoA carboxylase and fatty acid synthetase were greatest in livers from VMH-lesioned rats. Fasting abolished hyperinsulinemia and most of these observed metabolic alterations. After treatment with anti-insulin serum, the high rate of lipogenesis observed in livers from VMH-lesioned rats was restored toward normal. It is suggested that hyperinsulinemia may be partly responsible for the metabolic disorders observed in livers from nonhyperphagic VMH-lesioned rats.
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PMID:Consequences of ventromedial hypothalamic lesions on metabolism of perfused rat liver. 1 11

The present experiments have tested the hypothesis that ventromedial hypothalamic (VMH) lesions enhance insulin secretion by neural mechanisms. Rats were made diabetic by injecting streptozotocin to destroy their own pancreatic beta-cells. Subsequently, transplants of fetal pancreatic tissue were placed under the renal capsule. VMH lesions were placed in rats whose diabetes was cured with transplants as well as sham-transplanted animals. The animals were followed for 4 wk. The lesioned rats with pancreatic transplants gained no more weight than the sham-operated controls. There was no significant rise in insulin in the transplanted rats after VMH lesioning, but the VMH lesioned rats with intact pancreatic tissue showed the expected rise in insulin. Food intake rose 71% in the VMH lesioned rats with intact beta-cells, but only 23% in the VMH lesioned rats with transplants. Hypertrophy of the pancreatic islets was also observed in the VMH lesioned rats with an intact pancreas, but was not found in the VMH lesioned rats with a transplanted pancreas. Thus, transplantation of pancreatic tissue beneath the renal capsule of diabetic rats prevented the characteristic hyperphagia, hyperinsulinemia, and obesity in VMH lesioned rats whose pancreas was free from intact innervation. The results support the hypothesis that neural mediation of the rise in insulin is the primary factor in the development of hypothalamic obesity.
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PMID:Transplantation of pancreatic beta-cells prevents development of hypothalamic obesity in rats. 10 13

Metabolic studies were performed on 19 patients with acute renal failure. Therapy included intravenous hyperalimentation using 15 to 20 g of essential amino acids or 20 to 40 g of essential plus nonessential amino acids and hypertonic glucose (37 to 50%). The effect of this parenteral feeding appears to be primarily pharmacological. Hypertonic glucose promotes the hyperinsulinemia important to be membrane function, the operation of the sodium pump, and cell metabolism. Administration of high biological value crystalline amino acdis potentiates the effect of insulin by inhibiting protein breakdown and promoting protein synthesis, particularly in muscle. This reduces tissue catabolism and urea formation, and promotes potassium, magnesium, and phosphate homeostasis. The branched-chain ketogenic amino acids valine, leucine, and isoleucine may be of particular importance. When indicated, administration of renal failure hyperalimentation and peritoneal or hemodialysis can be expected to complement each other and accelerate recovery. This intravenous fluid therapy, in turn, must be coordinated with proper hemodynamics, usually requiring a colloidal solution to maintain intravascular volume, and cardiotrophic agents such as digitalis and dopamine. Early use of renal failure can be expected to demonstrate the most striking response in terms of survival, early recovery from acute renal failure, and the preservation of physiological homeostasis.
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PMID:Criteria for choosing amino acid therapy in acute renal failure. 10 Oct 72

Human obesity is a manifestation of a positive energy balance. A variety of different factors influence this balance. The varieties of human obesity may be classified as follows: 1. Childhood onset with or without an increased number of adipocytes; 2. The syndromes of neuroendocrine dysfunction including hypothalamic obesity, Cushing's disease, and hyperinsulinism; 3. Dietary obesity; 4. Obesity due to physical inactivity; and 5. Genetic forms of obesity. Among the genetic form of obesity are the Laurence-Moon-Bardet-Biedl syndrome. Alstrom's syndrome, and possibly the Prader-Willi syndrome. Studies in experimental animals have increased our understanding of two of these forms of human obesity. These are: 1. Hypothalamic obesity associated with decreased sympathetic activity, hyperphagia and an increased secretion of insulin. Subdiaphragmatic vagotomy can reverse this syndrome; 2. Genetic forms of obesity inherited as recessive or dominant traits.
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PMID:Human obesity and some of its experimental counterparts. 11 2

The effects of ventromedial hypothalamic (VMH) lesions were studied in female rats made diabetic with streptozotocin that were given twice daily injections of protamine zinc insulin (0.75 mu/100g/day) and in non-diabetic animals of the same sex. Hyperphagia resulted from VMH lesions in both diabetic animals whose insulin levels were controlled and in non-diabetic animals. All animals with lesions exhibited persistent increases in feeding during the light protion of the light-dark cycle. Significant increases in body weight gain were observed in both diabetic and non-diabetic lesioned animals, but the magnitude of wegith gain was greater after VMH lesions in non-diabetic rats. VMH lesions also reduced wood-gnawing and increased emotionality, aversion to quinine and reactivity to electric shock. None of the behavioral changes were dependent on hyperinsulinemia, although hyperinsulinemia may contribute to the magnitude of certain of these effects.
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PMID:Behavioral changes following VMH lesions in rats with controlled insulin levels. 12 24

A new strain of obese mouse, the PBB/Ld, has been studied in terms of fat pad cellularity, serum insulin and blood glucose levels, and response to gold thioglucose injections. Age-matched C57B1/6J mice were used as controls. Adipocyte size and number in the major fat depots were determined at various ages from weanling to maturity in the PBB/Ld and C57B1/6J strains. Results indicated that obesity in the PBB/Ld was due to hypertrophy of adipocytes in retroperitoneal and subcutaneous fat depots and to hypertrophy and hyperplasia in the epididymal fat pad. PBB/Ld mice also developed hyperinsulinemia and hyperglycemia and these findings have been discussed in terms of the developmental changes in fat pad cellularity. The injection of gold thioglucose led to increased food intake in both PBB/Ld and C57B1/6J mice. Hyperphagia was also present in the PBB/LD control group, but increased efficiency of converting calories to body weight was not observed in this group when compared to control C57B1/6J mice. The characteristics of obesity seen in the PBB/Ld mouse are discussed and comparisons are made to similar studies in other rodent models of obesity.
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PMID:Description of obesity in the PBB/Ld mouse. 34 7

At the present time, two major factors limit further clinical application of islet cell transplantation in treatment of the insulin-deficient diabetic patient. First, the yield of islet tissue obtainable from a single donor pancreas is insufficient for adequate reconstitution of normal beta cell mass. The purification procedures required to eliminate acinar contamination and allow safe portal vein infusion cause large islet cell losses. Other procedures designed to minimize islet loss result in crude preparations containing substantial acinar tissue. In dogs and rats, crude preparations have been inoculated with safety into the spleen and function well in this location, but such a procedure might not be feasible in the human. Preliminary trials of these techniques in the monkey have not been successful. Second, dispersed and isolated islets inoculated into any site are exceptionally vulnerable to rejection and cease to function within a few days. Successful human islet allografting must await development of improved techniques of histocompatibility matching and/or immunosuppression. An additional question, unanswered in experiments to date, relates to the probable requirement for accuracy in replacement of alpha cells and beta cells for cure of the insulin-deficient juvenile diabetic patient. In rats, transplantation of large volumes of islet cells has resulted in hyperglucagonemia, hyperinsulinemia, and polyphagia, although the rats remain normoglycemic and have normal glucose tolerance tests. Bewick has elicited hyperinsulinemia in dogs by denervation and shunting the pancreatic venous drainage from portal to systemic. The metabolic effects of this abnormal state have not been adequately studied. These unresolved issues mandate that pancreatic transplantation remain an experimental procedure in humans. Whole or segmental pancreatic implants are technically feasible and are capable of function for extended periods of time. Islet implantation is reserved for carefully controlled experiments and in patients immunosuppressed for other organ transplants.
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PMID:Replacement of pancreatic beta cells as treatment for diabetes mellitus: a review. 41 7

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

The acute effect of bilateral electrolytic ventromedial hypothalamic lesions (20-25-m Coulomb stainless steel electrodes) on plasma levels of insulin and glucose was studied in anesthetized rats to determine early effects that would occur before hyperphagia and obesity. In rats fed ad libitum, lesions in the ventromedial hypothalamus (VMH) but not in the cortex produced a marked increase in circulating insulin levels (starting at 20 min postlesion) and a small increase in glycemia which, however, was not significant and could therefore not be the cause of increased insulin secretion. Hyperinsulinemia after VMH lesions was more pronounced when glucose was infused iv at a rate of 7-8 mg/kg . min. Bilateral subdiaphragmatic vagotomy, performed 50 min after VMH lesions, immediately and completely reversed the observed hyperinsulinemia. With the exception of a tendency of lesions producing the highest degree of hyperinsulinemia to be slightly larger than the lesions not producing any hyperinsulinemia, no statement about the critical involvement of a specific hypothalamic locus can be made. It is concluded that electrolytic VMH destruction causes immediate hypersecretion of the pancreatic B cell, an effect that requires the integrity of the vagus nerves. Further localization of the central circuitry responsible for this mechanism, however, will require more specific methods than electrolytic lesions.
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PMID:Acute hyperinsulinemia and its reversal by vagotomy after lesions of the ventromedial hypothalamus in anesthetized rats. 44 4

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48


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