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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of mifepristone (RU 486), a blocker of type II glucocorticoid receptors on the development of obesity that follows the feeding of a high-fat (HF) diet to Osborne-Mendel (OM) rats, has been investigated. OM rats fed a HF diet gained more weight and had larger retroperitoneal and parametrial fat pads than OM rats fed a high-carbohydrate low-fat (LF) diet. RU 486 (30 mg.kg-1.day-1) for 14 days completely reversed the body weight gain and the increase in fat pad size of OM rats fed a HF diet. RU 486 had no effect on body weight of OM rats fed a LF diet, but did reduce fat pad weights. The data suggest that type II glucocorticoid receptor activity modulates body fat deposition and is essential for the development of obesity, although a minor role for progestin receptor activity cannot be ruled out.
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PMID:Mifepristone (RU 486), a blocker of type II glucocorticoid and progestin receptors, reverses a dietary form of obesity. 162 65

Whole brain concentrations of 3-hydroxybutyrate, glutamate and gamma-aminobutyric acid (GABA) have been measured in two strains of rats with differing susceptibility to obesity. S 5B/Pl rats are resistant to developing obesity when eating a high-fat diet, whereas Osborne-Mendel rats readily develop obesity when eating the same diet. We tested the hypotheses that brain 3-hydroxybutyrate, glutamate and GABA differ between S 5B/Pl rats and Osborne-Mendel rats, and that these substrates/neuroregulators are altered when eating a high-fat diet primarily in S 5B/Pl (resistant) rats. Blood and brain 3-hydroxybutyrate concentrations were higher in S 5B/Pl rats than in Osborne-Mendel rats (p less than 0.05) but diet effects were not significant. Brain glutamate concentration, like 3-hydroxybutyrate, was higher in S 5B/Pl rats than in Osborne-Mendel rats (p less than 0.01) and was not affected by adding fat to the diet. Brain GABA differed only slightly between strains but increased after adding fat to the diet (p less than 0.05) in both strains with a greater increase occurring in S 5B/Pl rats. The brains of S 5B/Pl rats are chronically exposed to higher levels of 3-hydroxybutyrate and glutamate than are those of Osborne-Mendel rats. Thus, 3-hydroxybutyrate is a potential signal in the regulation of body weight. Brain GABA increases with fat feeding, especially in S 5B/Pl rats, suggesting that the ability to adjust to an energy dense diet may be through suppression of food intake by elevated brain GABA.
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PMID:Brain 3-hydroxybutyrate, glutamate, and GABA in a rat model of dietary obesity. 266 5

These studies have examined the effect of fasting and nutrient loads on sympathetic firing rate in three groups of rats that develop widely divergent degrees of obesity when eating a high-fat diet. Starvation of Sprague-Dawley rats for 24 or 48 h was associated with a decrease in basal sympathetic activity of nearly 25% in the first 24 h and of slightly greater than 30% in 48 h. This decline in sympathetic activity paralleled the loss of body weight and reduction in adipose tissue mass. After starvation for 48 h, Osborne-Mendel rats, which readily develop obesity when eating a high-fat diet, showed a greater decrease in basal sympathetic activity than did the diet-resistant S 5B/P1 rats. A single liquid 36-kcal intragastric meal was associated with an acute 30% increase in sympathetic firing rate in the overnight-fasted Sprague-Dawley rats. The values 3 h after the meal had returned halfway to normal, and by 6 h they were more than 85% of the way to normal. An intravenous injection of glucose produced a greater rise in sympathetic activity in diet-resistant S 5B/P1 rats than in the diet-sensitive Osborne-Mendel rats. These data are consistent with the hypotheses that sympathetic activity is positively related to nutrient status, that it varies between strains of rats, and that it can be acutely increased by an intragastric meal or by intravenous glucose.
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PMID:Effect of starvation and food intake on sympathetic activity. 304 48

We examined the effect of dietary fat on the response to 3-hydroxybutyrate (3-OHB) and insulin infused chronically into the third ventricle in three strains of rats with differing susceptibility to obesity induced by a high-fat diet: Osborne-Mendel rats are most susceptible; Sprague-Dawley-rats are intermediate; and S 5B/Pl rats are most resistant. Ten days after implantation of cannulas into the third ventricle, rats were fed either a low-fat diet or a high-fat diet for 14 days. On day 7, osmotic minipumps were attached to the ventricular cannulas. 3-OHB infusions (3.6 mumol/24 h) reduced food intake and body weight in Sprague-Dawley and Osborne-Mendel rats eating either diet. The dietary fat-resistant S 5B/Pl rats did not respond to the intracerebroventricular infusion of 3-OHB. The infusion of insulin (10 mU/24 h) lowered food intake and body weight in animals eating the low-fat (high-carbohydrate) diet but not in animals eating the high-fat diet. Diet profoundly affects the response to intracerebroventricular infusions of insulin but is without effect on the response to 3-OHB.
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PMID:Intracerebroventricular infusions of 3-OHB and insulin in a rat model of dietary obesity. 305 29

The effects of cold acclimation on cellularity, lipoprotein lipase (LPL) activity and lipolysis were studied in white adipose tissue of rats fed a high fat diet. Male Osborne-Mendel rats (7 weeks old) were exposed at either 28 or 5 degrees C for 10 weeks. The rats were fed a semipurified diet (normal fat (NL): 5% lard, high fat (HL): 54% lard) for the last 9 weeks. Caloric intake with NL and HL diets were comparable and cold exposure led to the same increase with both diets. At 28 degrees C, HL diet initiated both hypertrophy and hyperplasia; however, at 5 degrees C only hyperplasia was observed. Total LPL activity showed high stimulation both in 28 and 5 degrees C HL rats. In vitro lipolytic stimulation by norepinephrine was lowered at 5 degrees C and abolished at 28 degrees C in HL-fed rats. HL diet resulted in enhanced lipid deposition without an increase in caloric intake. Even in cold-adapted Osborne-Mendel rats a relative obesity could be produced by a HL diet.
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PMID:Effect of environmental temperature on dietary obesity in Osborne-Mendel rats. 325 90

The effects of chronic feeding of a high-fat diet or a cafeteria-type diet on weight gain and thermogenesis in brown adipose tissue as measured by the binding of a purine nucleotide (guanosine 5'-diphosphate, GDP) to mitochondria of brown adipose tissue have been studied in two strains of rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats, which are resistant to developing obesity when eating a high-fat diet or drinking sucrose solutions, have greater specific GDP binding in interscapular brown adipose tissue (IBAT) than do Osborne-Mendel rats, which are sensitive to fat-induced obesity. A high-fat diet, fed isoenergetically to the low-fat diet, did not increase the growth of IBAT and decreased specific GDP binding in both strains. Feeding a cafeteria diet resulted in obesity and increased mass and protein content of the IBAT in both strains of rats. However, specific GDP binding increased in response to cafeteria feeding only in the Osborne-Mendel rats. These studies show that thermogenesis, as measured by GDP binding to mitochondria in brown adipose tissue, is suppressed by both isoenergetic and ad libitum feeding of a high-fat diet. The higher basal GDP binding in the brown fat of the S 5B/Pl rats suggests that higher thermogenesis of this tissue contributes to the resistance of this strain to fat-induced obesity. The inability of S 5B/Pl rats to further increase thermogenesis when eating a cafeteria diet may contribute to their becoming obese.
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PMID:Brown fat thermogenesis in a rat model of dietary obesity. 368 76

The effect of a low- and high-fat diet on the transport of 3-hydroxybutyrate and glucose across the blood brain barrier has been measured in two strains of animals that have a marked difference in the degree of obesity that develops when they eat a high fat diet. The S 5B/Pl rats are resistant to dietary obesity whereas the Osborne-Mendel rats readily develop obesity when eating a high-fat diet. The transport of 3-hydroxybutyrate and glucose across the blood-brain barrier was measured as the ratio of radioactive compound (3-hydroxybutyrate or glucose) to radioactively labeled water by the technique of Oldendorf. The uptake of 3-hydroxybutyrate was significantly higher in the S 5B/Pl rats than in the Osborne-Mendel rats when they were eating either the low-fat diet or the high-fat diet. In addition, there was a significant increase in the transport of 3-hydroxybutyrate in the animals of both strains when eating the high-fat diet as compared to the low-fat diet. However, there was no difference in the transport of glucose between the two strains of rats whether they ate a low-fat or high-fat diet. These data are consistent with the hypothesis that resistance to dietary obesity is associated with increased transport of 3-hydroxybutyrate across the blood-brain barrier.
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PMID:Brain uptake of ketones in rats with differing susceptibility to dietary obesity. 379 95

The effects of dietary fat content, lighting cycle, and feeding time on norepinephrine turnover in interscapular brown adipose tissue, heart, and pancreas, and on blood 3-hydroxybutyrate, serum glucose, insulin, and corticosterone have been studied in two strains of rats that differ in their susceptibility to dietary obesity. S 5B/Pl rats, which are resistant to dietary obesity, have a more rapid turnover of norepinephrine in interscapular brown adipose tissue and heart and a greater increase in the concentration of norepinephrine in brown fat when eating a high-fat diet than do Osborne-Mendel rats, which are sensitive to fat-induced obesity. Light cycle and feeding schedule are important modulators of sympathetic activity in heart and pancreas but not in brown fat. Rats of the resistant strain also have higher blood 3-hydroxybutyrate concentrations and lower insulin and corticosterone levels than do rats of the susceptible strain. A high-fat diet increases 3-hydroxybutyrate concentrations and reduces insulin levels in both strains. These studies show, in rats eating a high-fat diet, that differences in norepinephrine turnover, particularly in brown adipose tissue, may play an important role in whether dietary obesity develops and in the manifestations of resistance to this phenomenon observed in the S 5B/Pl rat.
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PMID:Diet, lighting, and food intake affect norepinephrine turnover in dietary obesity. 381 77

The effect of several drugs on food intake has been examined in two strains of rats, one (S 5B/P1) which is resistant to developing obesity when eating a high fat diet, and one (Osborne-Mendel) which readily develops obesity when eating the same diet. Insulin and 2-deoxy-D-glucose increased food intake in a dose dependent manner in both S 5B/P1 and Osborne-Mendel rats. However, the S 5B/P1 rats showed a greater response, with a shorter latency period, to both agents than did the Osborne-Mendel rats. Conversely, d-amphetamine at the higher doses produced a dose dependent suppression of food intake with maximal suppression being similar for both strains. At a lower dose, however, d-amphetamine significantly increased food intake in the Osborne-Mendel rats, but not in the S 5B/P1 rats. The S 5B/P1 rats were also slightly more sensitive to the anorexic effects of lower dose adenosine than were the Osborne-Mendel rats whereas the reverse was true following higher dose adenosine. Naloxone suppressed food intake equally in both strains and D-glucose did not alter food intake in either strain. These studies identify three drugs, all stimulatory, to which the two strains of rat respond differently.
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PMID:Dietary obesity: effects of drugs on food intake in S 5B/P1 and Osborne-Mendel rats. 388 47

The role of brown fat thermogenesis in the development of obesity is considered from a number of perspectives. In adult rats, the impact of scapular brown fat lipectomy on carcass fat accretion was examined in three different rodent models: the Zucker lean (Fa/-) rat which is relatively resistant to obesity, the Zucker obese (fa/fa) rat which is characterized by a particularly severe form of hyperplastic obesity and the Osborne Mendel rat which remains lean on a standard pelleted diet but readily becomes obese on a palatable high fat diet. The consequences of brown fat lipectomy varied from no effect on carcass white fat accretion in Zucker Fa/- lean rats to a significant increase in adiposity in the Zucker fatty fa/fa relative to their respective sham-operated controls. The effect of the Osborne Mendel rat was intermediate between the Fa/- and the fa/fa. The results point to the importance of genetic background with respect to the impact of brown fat lipectomy on the development of white fat adiposity. In the developing Zucker rat at 2 and 8 days of age, in vivo evidence is presented to support the concept that brown fat thermogenesis is attenuated in the fatty fa/fa preobese pup. In animals of the fatty fa/fa genotype, maximum oxygen consumption in response to acute cold exposure was lower than in lean pups of the Fa/Fa genotype. Moreover, at 8 days of age, the rectal temperature of the cold-exposed fa/fa pups fell more precipitously than did that of the lean during the period of cold exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brown fat thermogenesis and its role in the development of obesity. 402 97


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