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

The plasma-lipoprotein response to intravenous hyperalimentation was studied in three patients with severe familial hypercholesterolaemia. Hyperalimentation substantially lowered plasma concentrations of cholesterol, low-density lipoproteins (L.D.L.P.), and high-density lipoproteins. The chemical composition of L.D.L.P. did not change. Triglyceride levels increased slightly in two patients and decreased in the third. Turnover of radiolabelled L.D.L.P. was disturbed as L.D.L.P. concentration fell but then returned to normal. The mechanism by which intravenous hyperalimentation rapidly lowers plasma-cholesterol in severe hypercholesterolaemia is unknown.
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PMID:Effects of intravenous hyperalimentation of plasma-lipoproteins in severe familial hypercholesterolaemia. 4 47

Four patients with homozygous hyperbetalipoproteinaemia who had proved resistant to intensive medical therapy have undergone portacaval shunt. During 3 weeks of total parenteral alimentation before the operation, the serum-cholesterol decreased significantly in each of the four patients. During the fat-emulsion phase of hyperalimentation, one patient experienced a rise in cholesterol. Postoperatively, the size of xanthomas decreased in all cases; serum-cholesterol levels rose above those achieved during hyperalimentation, and this rise continued for as long as 3 months before a further reduction was recorded. In patients with angina, this improved considerably; and in most cases bruits decreased in itensity. The results at this stage do not, however, suggest portacaval shunt for all patients with homozygous hypercholesterolaemia.
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PMID:Portacaval shunt in four patients with homozygous hypercholesterolaemia. 4 58

The serum lipid values (total lipids, cholesterol) and the amounts of fat components (total fat, cholesterol, saturated and multiply unsaturated fatty acids) in food were determined for 1000 subjects of primary obesity and 200 subjects having normal weight. The age of the subjects included in this study was between 18 and 60. From the second to sixth decades of life, obese subjects showed increases in hypercholesterolemia and hyperlipidemia from 2.3% to 22% and from 4.6% to 26%, respectively. Lower percentages were determined for the controls. The consumption of total fat, cholesterol, saturated and multiply unsaturated fatty acids in food was lower in subjects of obesity than in normal-weight subjects. Problems of the dynamic and static phases of obesity, hyperphagia, hypophagia, and longitudinal behavior are discussed with particular reference to the causes thereof. With males, the intake of all fatty substances contained in food decreased with increasing age. Possible causes of this include changes in environmental and working conditions as well as nutritional consciousness.
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PMID:[Fat consumption, blood lipids and age (author's transl)]. 54 19

There exist certain pathological eating behaviors (they deviate from the usual eating pattern in a given environment; ex.: hyperphagia, alcoholism, bulimia, nibbling sweets, etc.): there also exist certain pathogenic, though not pathological, eating behaviors (a "normal" behavior may induce an affection in given subjects; ex.: obesity in subjects with a normal caloric intake, hypercholesterolemia in subjects with a normal lipid intake, etc.). In the perspective of Public Health, the field of pathological behavior calls for specialized individual interventions, which can sometimes serve as research models; but the field of pathogenic behavior is now such a widespread social phenomenon (50% of the female population wishes to reduce, 50% of the male population dies from alimentary-linked cardiovascular diseases) that it must be systematically investigated. Such investigations would require: 1. A typology assessing the effectiveness of all the techniques aimed at a modification of eating behavior, whether preventive or therapeutic (through information, pressure, learning); 2. A typology of the resistance to change, whether physiological, psychological or psychosocial. A study of both typologies is necessary since until now all the attempts to induce a population as a whole to renounce food plethora have been unsuccessful, except when imposed by economic or political motivations. Moreover, in a society oriented toward consuming, a change in eating behaviors must be "consumable", that is, at once adequate and gratifying, in order to be accepted.
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PMID:[Resistance to modification of dietary behavior]. 80 Jul 13

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

Japan has been experiencing ever more rapid socioeconomic development and changes in eating habit, especially in children, since the end of the Second World War. These occurrences (westernized life style) have greatly affected the growth of Japanese. Nutrition is the most important factor in promoting the physical growth in childhood during food supply shortage, and for a relatively short term the secular trend in linear growth will reach a plateau if the food supply is adequate, but the secular trend is also limited. Since the condition for this limitation should be comprised by genetic factors, we are most interested in investigating and analyzing these genetic factors in the near future. Overeating adversely affects growth in childhood, with most common representatives of these ill effects being atherogenic risk factors such as obesity, hypertension and hypercholesterolaemia.
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PMID:Nutrition and the secular trend of growth. 129 20

Contrary to normal rats, diabetic rats are known to develop marked hypercholesterolemia when fed a cholesterol-enriched diet. The triggering factor involved in this hyperresponse has not been identified. With the aim of clarifying the role of the intestinal acyl-CoA:cholesterol acyltransferase (ACAT), we studied the effects of a high fat diet and the changes of intestinal ACAT activity during the early development of streptozotocin-diabetes in rats. Feeding diabetic rats with a diet enriched in cholesterol and saturated fat produced an increase in plasma and in tissue cholesterol as early as 3 days after streptozotocin injection in the absence of hyperphagia. Under these experimental conditions, treatment with insulin or with the ACAT inhibitor CL-277082 significantly reduced the plasma cholesterol to levels measured in nondiabetic rats fed the same high fat diet. An increase in [14C]cholesterol in plasma very low density lipoprotein was observed after oral administration of labeled cholesterol to 3-day diabetic rats. In parallel experiments, the direct measurement of small intestine microsomal ACAT activity revealed an increase, averaging 288% in diabetic rats 3 days after diabetes induction. This change in ACAT activity occurred simultaneously with an increase in plasma glucagon and was normalized by insulin treatment. The induction of intestinal ACAT activity in diabetic rats, its modulation by insulin, and the hypocholesterolemic effects of insulin or CL-277082 treatment clearly indicate that ACAT activity plays a major role in the initiation of diabetes-associated hypercholesterolemia.
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PMID:Role of the intestinal acyl-CoA:cholesterol acyltransferase activity in the hyperresponse of diabetic rats to dietary cholesterol. 143 72

We previously reported that dog diabetes results in hypercholesterolemia and the accumulation of a high-density lipoprotein (HDL) subclass, HDL1. Hypercholesterolemic diabetic rodents exhibit hyperphagia, intestinal hypertrophy, and increased intestinal cholesterol synthesis and absorption; intestinal 3-hydroxy-3-methylglutaryl (HMG) CoA reductase activity is increased, whereas hepatic activity is unchanged or reduced. To determine whether similar mechanisms operate in the hypercholesterolemic diabetic dog, we measured hepatic and intestinal cholesterologenesis. Streptozocin-alloxan-induced diabetic dogs allowed access to food ad libitum were hyperphagic and hypercholesterolemic (10.1 vs. 4.47 mM) but normotriglyceridemic. Plasma HDL1 concentrations were markedly increased. Differences in renal and hepatic function were not statistically significant, except serum alkaline phosphatase, which was elevated 4-fold (P = 0.0003). Urinary mevalonate, an index of whole-body cholesterol synthesis, was increased 6-fold. Intestinal and hepatic weights were both increased, and direct measurements showed crypt and villus thickening. The activity of HMG CoA reductase per gram organ weight was increased 1.7-fold in liver and 2.1-fold in intestine. Calculated whole-organ activity in intestine was nearly twice that in liver. These observations provide strong evidence that intestinal cholesterogenesis is involved in the pathogenesis of hypercholesterolemia in dog diabetes and support the conclusion that increased cholesterol synthesis plays a role in the hypercholesterolemia of diabetes.
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PMID:Intestinal and hepatic cholesterogenesis in hypercholesterolemic dyslipidemia of experimental diabetes in dogs. 175 3

To determine how insulin deficiency leads to hypercholesterolemia, we examined cholesterol absorption, synthesis, and utilization in streptozocin-induced diabetic rats fed a grain-based diet ad libitum. Absorbed dietary cholesterol was determined from measurement of dietary cholesterol intake and previous data for cholesterol fractional absorption. Daily rates of cholesterol synthesis in the small intestine, liver, and periphery were calculated from recovery of labeled sterols after injection of 3H2O at six times during 24 h. Utilization of cholesterol for growth, fecal excretion, and bile acid synthesis were also determined. Absorbed dietary cholesterol in diabetic rats was double that in control rats. The contribution of absorbed cholesterol to total cholesterol production (sum of absorbed dietary cholesterol) and endogenous cholesterol synthesis) in control rats was 24% compared to 48% in diabetic rats. The increase in diabetic rats was due to overeating and, to a lesser extent, to increased fractional absorption. Overeating also induced intestinal hypertrophy and a twofold increase in cholesterol synthesis by the small intestine to 24% of whole-body production in diabetic rats. Consequently, the small intestine accounted for 72% of daily cholesterol input in diabetic rats compared to 37% in control rats, with diet accounting for two-thirds of the cholesterol input via the small intestine in both groups. In response to this increased input from the intestine, cholesterol synthesis in the periphery was 39% of whole-body production in control rats compared to 22% in diabetic rats, and synthesis in the liver was 26 and 6% of total cholesterol production in control and diabetic rats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contributions of absorbed dietary cholesterol and cholesterol synthesized in small intestine to hypercholesterolemia in diabetic rats. 339 47

A new strain of genetically obese mouse, the dbPas mouse, has been studied in terms of fat pad cellularity, serum parameters and thermogenesis. This obesity was observed in the inbred DW strain of mice at the Institut Pasteur-France, and is due to a recessive mutation on chromosome 4 at the diabetes locus. The mice became grossly obese, gaining weight until at least 16 mo of age. By 6 mo of age they exhibited hyperphagia, hypercholesterolemia, severe hyperinsulinemia, hypertrophy and hyperplasia of adipocytes, and impaired fertility. In contrast with other diabetic strains of mice, glycemia was normal in females and slightly elevated in males. This result indicates that the mutation of the db locus does not necessarily lead to a frank diabetes. Body temperature was normal either at 22 degrees C or after a cold exposure at 4 degrees C. GDP (guanosine diphosphate) binding to brown adipose tissue mitochondria was normal in obese mice as compared to lean. These data differentiate this model from other genetic obesities in mice and rats. This new model of genetic obesity offers interesting characteristics for the study of obesity.
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PMID:Description of a new model of genetic obesity: the dbPas mouse. 388 10


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