Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenalectomy has been shown to reduce the development of obesity in adult Zucker fatty rat. In this study, we examined whether adrenalectomy could prevent the emergence of obesity and correct any of the first abnormalities to develop in fa/fa pups. Four-day-old Zucker pups were adrenalectomized and fed by adrenalectomized wet nurses until 11 days of age. The frequency distribution curves of fat cell volume clustered in two groups as they do in control litters, providing evidence that two phenotypes were present. Oxygen consumption measured at 8 days of age was significantly lower in fa/fa than in Fa/fa. Adrenalectomy did not restore the decreased oxygen consumption of fa/fa. In control litters, the GDP binding to brown adipose tissue mitochondria was twofold lower, whereas fatty acid synthase activity of this tissue was significantly increased in fa/fa pups. In inguinal adipose tissue of fa/fa pups, fatty acid synthase, and lipoprotein lipase activities were twice as active as in the tissue of lean pups. In adrenalectomized fa/fa pups, none of these metabolic abnormalities was corrected. The results demonstrate that adrenalectomy early in life did not prevent the emergence of obesity in suckling fa/fa rats.
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PMID:Deprivation of corticosterone does not prevent onset of obesity in Zucker fa/fa pups. 355 27

Rats with obesity-producing, hypothalamic knife cuts (KC) were fed a purified high fat diet for 9 wk. KC rats consumed more energy (+70-100%) and retained energy with a much higher efficiency than control rats. Adrenalectomy of KC rats 1 wk (before gross obesity was evident) or 5 wk (when KC rats were 70% overweight) after KC surgery caused a reduction in energy intake to levels approximating those of control rats. Furthermore, energy retention in adrenalectomized KC rats was depressed more than could be explained on the basis of the reduction in energy intake. Two factors associated with the reduction in energy retention, urinary excretion of norepinephrine, an indicator of sympathetic nervous system activity, and GDP binding to brown adipose tissue mitochondria, an indicator of the thermogenic capacity of the tissue, were higher in vadrenalectomized KC rats than in pair-fed KC rats. Removal of the adrenals not only suppressed hyperphagia in KC rats fed a high fat diet, but also increased energy expenditure per kilocalorie consumed.
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PMID:Energy balance in rats with obesity-producing hypothalamic knife cuts: effects of adrenalectomy. 359 23

Adult male Sprague-Dawley rats were divided into three groups and fed diets containing either 10, 20, or 40% protein for 56 days. Half of the rats in each dietary condition were given a 32% sucrose solution plus the standard diet and water. Sucrose intake varied directly as a function of dietary protein levels. Rats fed either the 10 or 20% protein diet and sucrose had higher caloric intakes, gained more weight, were more efficient at using calories for weight gain, and had more adipose tissue than rats given the same diet without sucrose. Rats fed the 40% protein diet and sucrose did not exhibit overeating, excess weight gain, or increased feed efficiency relative to animals fed the 40% diet alone. Animals given sucrose had more interscapular brown adipose tissue (IBAT) and a greater metabolic potential for thermogenesis in IBAT as determined by GDP binding in mitochondria than rats not fed sucrose. These results demonstrate that dietary protein is important in the development of sucrose-induced obesity and that increases in IBAT mass and activity can occur concomitant with increased feed efficiency.
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PMID:Sucrose-induced obesity: effect of diet on obesity and brown adipose tissue. 360 81

Adrenalectomy prevents development of obesity in ob/ob mice fed high-carbohydrate stock diets partly by stimulating the low thermogenic capacity of their brown adipose tissue (BAT). Adrenalectomy, however, fails to prevent development of obesity in ob/ob mice fed a high-fat diet. Effects of adrenalectomy on BAT metabolism in ob/ob mice fed a high-fat diet were thus examined. ob/ob mice fed the high-fat diet developed gross obesity despite normal BAT metabolism, as assessed by rates of norepinephrine turnover in BAT, GDP binding to BAT mitochondria, and GDP-inhibitable, chloride-induced mitochondrial swelling. Adrenalectomy failed to arrest the development of obesity or to influence BAT metabolism in ob/ob mice fed the high-fat diet. Development of obesity in ob/ob mice fed a high-fat diet is not associated with low thermogenic capacity of BAT or with adrenal secretions, as it is in ob/ob mice fed high-carbohydrate stock diets.
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PMID:Brown adipose tissue metabolism in ob/ob mice: effects of a high-fat diet and adrenalectomy. 361 69

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

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

The lipogenic capacity and thermogenic activity (assessed by GDP binding to mitochondrial) of brown adipose tissue was studied in lean (Fa/fa) and obese (fa/fa) suckling Zucker rat pups 2 and 10 days old. By 10 days of age, fat deposition, lipogenesis in vivo and fatty acid synthetase activity were 1.5 to 2-fold higher, whereas GDP binding to mitochondria was 40% lower in pre obese than in lean pups. Compared with lean pups, 2-day old fa/fa pups showed a 60% increase in triglyceride accumulation in interscapular brown adipose tissue and a 30% decrease in GDP binding to mitochondria, while no change occurred in fatty acid synthetase activity. These results strongly suggest that an impaired thermogenic activity in the brown adipose tissue of fa/fa pups could play a key role in the development of obesity. However, the concomitant increase in fat content in the brown adipose tissue of 2-day old pre-obese pups raises the question of the causal relationship between these two disorders.
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PMID:[Role of brown adipose tissue in the development of genetic obesity in the obese Zucker rat (fa/fa)]. 399 87

Restricting the food intake of the genetically obese (ob/ob) mouse is known to ameliorate its cold intolerance. Cold intolerance of the ob/ob mouse is associated with defective thermogenesis in its brown adipose tissue. The objective of the experiments was to find out whether food restriction could increase the thermogenic function of brown adipose tissue of the ob/ob mouse. Obese and lean mice were fed a restricted amount of chow in one meal per day for 3-7 mo. Both lean and ob/ob mice were torpid (rectal temperature of approximately 32 degrees C) in the early morning and aroused spontaneously to a normal body temperature before the anticipated meal time. Obese mice were also torpid during the dark phase, whereas lean mice were active and had a normal body temperature at this time. Brown adipose tissue was in a thermogenically inactive state (low level of mitochondrial GDP binding) in torpid lean and ob/ob mice but became thermogenically active (increase in mitochondrial GDP binding) during stimulated arousal when body temperature increased by 6-7 degrees C in 15-30 min. Ad libitum-fed ob/ob mice had a normal diurnal rhythm in a rectal temperature that was at a lower level than in lean ad libitum-fed mice. They did not raise their rectal temperatures when stimulated and no activation of brown adipose tissue thermogenesis occurred under these conditions. Food restriction increased the capacity of both lean and ob/ob mice to raise their metabolic rate in response to injection of noradrenaline, indicating an increased capacity for thermogenesis in their brown adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Food restriction increases torpor and improves brown adipose tissue thermogenesis in ob/ob mice. 403 35

Studies on BRL 26830A in rodents have shown that thermogenic beta-adrenoceptor agonists have potential for the therapy of obesity. BRL 26830A reduced body weight gain in ob/ob mice and fa/fa rats by reducing lipid accumulation. It had no effect on lean body mass. BRL 26830A did not reduce food intake, its anti-obesity effect being due to stimulation of energy expenditure. This thermic effect was enhanced in the obese animals by repeat dosing. BRL 26830A did not affect body weight gain in the lean counterparts of the obese animals because its thermic effect in lean animals was reduced by repeat dosing. Brown adipose tissue is an important site of BRL 26830A-induced thermogenesis. A single dose of BRL 26830A raised brown adipose tissue temperature, depleted brown adipose tissue lipid and unmasked GDP-binding sites in brown adipose tissue mitochondria. Repeat dosing caused hypertrophy of brown adipose tissue and improved cold tolerance in mice. In-vitro studies showed that the rat brown adipocyte beta-adrenoceptor does not fall into the beta 1/beta 2 classification and BRL 28410, which mediates the biological effects of BRL 26830A in vivo, selectively stimulated the brown adipocyte receptor. It is concluded that BRL 26830A achieves its anti-obesity effect by mimicking natural mechanisms involved in thermogenesis and the control of body weight.
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PMID:Treatment of obesity with thermogenic beta-adrenoceptor agonists: studies on BRL 26830A in rodents. 615 55

The properties and activity of brown adipose tissue have been investigated in suckling, pre-obese, ob/ob mice in order to determine whether decreased thermogenesis in the tissue precedes the development of obesity in this mutant. At 14 days of age there was no difference between the ob/ob and normal animals in the total amount of interscapular brown adipose tissue, and the DNA content, protein content, and cytochrome oxidase activity of the tissue were similar in the two groups of mice. Respiration rates of brown adipose tissue mitochondria in the presence of albumin were, however, greater in the normal than the ob/ob animals, although after the addition of GDP to recouple the mitochondria there was no difference between the two groups. The mitochondrial membrane potential, measured with [3H]methyltriphenylphosphonium, was less affected by exogenous GDP in ob/ob mice than in normal animals. GDP binding to brown adipose tissue mitochondria, an index of the proton conductance pathway, was much greater in normal than in ob/ob mice at both 10 and 14 days of age; the decreased GDP binding in the mutant animals was found to result from a reduction in the number of binding sites. It is concluded that brown adipose tissue mitochondria of pre-obese ob/ob mice are more tightly coupled than those of normal siblings, and that the activity of the 'thermogenic' proton conductance pathway is lower in the mutant animals. A decrease in thermogenesis in brown adipose tissue is therefore an early event in the development of the ob/ob mouse and precedes the appearance of obesity.
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PMID:Studies on the activity of brown adipose tissue in suckling, pre-obese, ob/ob mice. 709 44


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