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

The genetically obese mouse, C57 B1/6J ob/ob, has been suggested as an appropriate model for the study of obesity associated with diabetes mellitus. Employing glucose 14C(microliter) as a tracer, the data presented here indicate that obese mice are able to clear glucose from the blood compartment at the same rate as their lean littermates. This was demonstrated with or without an associated cold glucose load. The abnormal glucose tolerance curves observed in the obese animals may be a result of secretion of glucose into the blood. Removal of the adrenal glands from the obese mice and their lean littermate does not impair their ability to clear a glucose load from the vascular compartment. The capacity for endogenous glucose secretion of ob/ob mice is severely curtailed by adrenalectomy, in that the glucose tolerance curves of these adrenalectomized animals become similar to those of sham-operated lean littermates. Thus, it appears that a considerable component of the hyperglycemia in ob/ob mice reflects major adrenal involvement that is activated by stress, ie, ether anesthesia and blood sampling. The hyperglycemia in ob/ob mice may reflect glucocorticoid-dependent gluconeogenesis.
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PMID:Effect of adrenalectomy on the metabolism of glucose in obese (C57 Bl/6J ob/ob) mice. 664 60

The genetically obese adult Zucker rat (fafa) exhibits reduced thermogenesis when stimulated by physiological agents (cold, catecholamines). Recent evidence suggests that this thermogenic defect may be important in the manifestation of the animal's obesity and that it reflects a reduced thermogenic contribution from brown adipose tissue, the major nonshivering thermogenic site in many mammals. The present study describes the effects of the obese genotype on brown (and white) adipocyte size, number, and lipid content and tissue lipoprotein lipase (LPL) activity. In the obese rats, brown fat depots were increased in mass. This increase could be accounted for by brown fat hypertrophy (due primarily to an increase in the amount of triglyceride present in each cell) rather than hyperplasia (there being no increase in the number of brown fat cells). In addition, unlike the situation in white fat, the brown fat from the obese rats did not exhibit higher LPL activity than did the brown fat from their lean littermates. This absence of an increased capacity for triglyceride uptake, coupled with the greater amount of triglyceride per brown adipocyte, is consistent with a reduction of triglyceride oxidation (and, thus, heat production) in the cells from the obese (v the lean) rats.
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PMID:Lipoprotein lipase activity and cellularity in brown and white adipose tissue in Zucker obese rats. 670 19

High-fat diet-feeding increases body weight and adiposity in Syrian hamsters (Mesocricetus auratus), effects due in part to decreased energy expenditure. The effects of voluntary exercise- or cold exposure-induced increases in energy expenditure were examined in fat- or chow-fed, female Syrian hamsters. In Experiment 1, voluntary exercise (10 weeks) caused a moderate hyperphagia and actually increased body weight in both diet groups through increases in lean body mass. Carcass lipid was not affected by by exercise in chow-fed hamsters and only slightly reduced in fat-fed animals. In Experiment 2, chronic (8 weeks) cold exposure (5 degrees C) increased energy intake to the same extent in both dietary groups relative to the warm-exposed (23 degrees C) controls. High-fat diet-induced obesity was largely prevented by cold exposure. Cold exposure reduced lean body mass in chow-fed hamsters, but this carcass component was spared by fat-feeding. These results indicate that the increased metabolic demands of cold exposure were more effective in preventing this form of diet-induced obesity than those of voluntary exercise (80% and 17% reductions in carcass lipid, respectively). These results are discussed in terms of possible beneficial effects of eating a lipid-rich diet prior to winter.
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PMID:Dietary obesity in exercising or cold-exposed Syrian hamsters. 671 40

Nonshivering thermogenesis was originally defined as a cold-induced increase in heat production not associated with the muscle activity of shivering. Recent research shows it to be a metabolic process located primarily in brown adipose tissue and controlled by the activity of the sympathetic nervous supply of this tissue. Another stimulus to sympathetic nervous activity, the ingestion of food, promotes diet-induced thermogenesis in brown adipose tissue. Brown adipose tissue grows and regresses in accordance with the extent to which it is stimulated, either by cold or by diet, and the capacity of the animal for cold-induced nonshivering thermogenesis and diet-induced thermogenesis increases or decreases accordingly. In certain hibernators another stimulus, photoperiod, promotes growth or regression of brown adipose tissue. The neural regulation of thermogenesis in brown adipose tissue is thus not only part of the central control mechanisms involved in thermoregulation but also part of those involved in the regulation of energy balance. In hibernators , such as the hamster, the neural regulation of thermogenesis in brown adipose tissue includes, in addition, central components that control the function of brown adipose tissue during entry into and arousal from hibernation and pineal or melatonin-related components that control its growth in response to photoperiod. In animals which become intermittently torpid, such as the mouse, the regulation includes in addition central components that control the function of brown adipose tissue during entry into and arousal from torpor. The central neural components involved in control of thermoregulation are better understood than are those involved in the regulation of energy balance. Studies of animal with hypothalamic obesity indicate that the control of diet-induced thermogenesis in brown adipose tissue requires the participation of the ventromedial region of the hypothalamus whereas the control of cold-induced nonshivering thermogenesis does not. The importance of comparative studies in different species is emphasized since any neural model for the control of brown adipose tissue thermogenesis is likely to apply in detail only to the species for which it was developed.
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PMID:Nonshivering thermogenesis. 672 94

The onset of cold-induced thermogenesis was studied in a strain of mice which produced among their offspring genetically-obese (ob/ob) individuals. A thermogenic response was present in a majority by day 5 after birth. The thermogenic response to cold was measured on days 5, 10 or 15 after birth, and the animals reared and the onset of obesity noted. The correlation between the subsequent development of obesity and a poor thermogenic response in early life was low. A poor thermogenic response at day 15 was associated with the presence in brown adipocytes of mitochondria with disordered internal structures. At day 42 both non-obese and obviously-obese mice showed a similar thermogenic response to moderate cold exposure. It would seem that in this strain of mice disordered internal mitochondrial structure in brown adipose tissue is associated with a poor thermogenic response to cold, but not invariably with the subsequent onset of obesity.
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PMID:The development of cold-induced thermogenesis and the structure of brown adipocyte mitochondria in genetically-obese (ob/ob) mice. 674 39

The past 10-15 years have produced a significant increase in knowledge and theories concerning the regulation of energy balance, but the precision of this regulation is still uncertain. However, the fact that investigators have had to resort to a variety of techniques and ploys (some of them bizarre) to produce marked pertubations in body weight is in itself an indication that the regulatory system can be very robust. Although control of food intake obviously plays a major role in this system, control of energy expenditure (i.e. DIT) also has to be considered as an important factor in the maintenance of energy balance. In this review most of the evidence for DIT and its biochemical origins has been derived from studies on experimental animals. Many of the overfeeding studies carried out on man are consistent with the animal work, but because of differences in interpretation and some equivocal results, the role of DIT in human metabolism is still a contentious issue. This problem may not be fully resolved to everyone's satisfaction until complete, continuous, and very precise energy balance measurements are made on chronically overfed lean subjects. Before this expensive and arduous experiment is undertaken, evidence for thermogenesis in man will continue to depend on acute measurements of the metabolic response to various stimuli. An increasing number of studies (e.g. 35, 80) have demonstrated the existence of NST in man, and the possibility that this could originate from BAT is supported by histological (62, 148) and thermographic data (130). Conversely, reductions in cold tolerance (2, 18) and thermogenic responses to noradrenaline (82) with increasing adiposity are similar to the blunted responses seen in genetically obese animals, which suggests that human obesity may also involve an impairment in thermogenesis. At the present time these ideas concerning the important of DIT in man and its role in obesity remain somewhat speculative, but no doubt this area will now be the subject of further research. Similarly, the impact of early nutritional influences on subsequent energy balance regulation and resistance to obesity will receive more attention following the report (144) that hyperphagia in rats during early life results in a reduced body fat content and leanness in adulthood. The relative contributions and interactions between intake and output in energy balance need clarifying, and in terms of central organization, the mechanisms of appetite control should now be considered for their relevance to the control of thermogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of energy balance. 676 16

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
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PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91

Rats consuming Coca-Cola and Purina chow ad libitum increased their total energy intake by 50% without excess weight gain. Their resistance to cold was markedly improved. These phenomena were characterized by significant increases in interscapular brown adipose tissue weight (IBAT) (91%), cellularity (59%), triglyceride content (52%), protein content (94%), and cytochrome oxidase activity (167%). In contrast, Coca-Cola consumption did not significantly affect the cellularity or triglyceride content of parametrial white adipose tissue (PWAT), although it slightly augmented PWAT weight. The effects of Coca-Cola on cold resistance, IBAT cellularity, and composition were entirely reproduced by sucrose, but not caffeine, consumption. Although caffeine also increased IBAT cellularity and composition, it significantly decreased the rate of body weight gain, PWAT weight, and adipocyte size. Moreover, it markedly inhibited adipocyte proliferation in PWAT thereby mimicking the effects of exercise training and food restriction (Bukowiecki et al., Am. J. Physiol. 239 (Endocrinol. Metab. 2): E422-E429, 1980). It is concluded a) that sucrose and Coca-Cola consumption improve the resistance of rats to cold, most probably by increasing brown adipose tissue cellularity, and b) that moderate caffeine intake might be useful for inhibiting proliferative activity in white adipose tissue, thereby preventing obesity.
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PMID:Effects of sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity. 683 66

The aim of the investigation was to see whether a defect in energy expenditure could be found in the Zucker rat at the onset of obesity. Obese (fa/fa) and lean (Fa/fa) 7-day-old pups were studied at three ambient temperatures. At 33 degrees C fa/fa pups showed a reduction in oxygen consumption, respiratory CO2 production, in vivo oxidation of injected [1-14C]palmitic acid, as well as in core temperature. When the pups were kept at 28 degrees C, the difference between genotypes was considerably accentuated, thus indicating a subnormal thermogenic response of the fa/fa pups to a mildly cold environment. At 20 degrees C, however, the metabolic rates dropped to the same low level, and the core temperature equilibrated with ambient temperature in both genotypes. The results demonstrate that the 1-wk-old fa/fa pup has a defect in thermoregulatory thermogenesis. The magnitude of the deficit in energy expenditure was more than adequate to account for the 50% greater fat content of 7-day-old fa/fa pups.
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PMID:Evidence of a defect in energy expenditure in 7-day-old Zucker rat (fa/fa). 688 26

Certain aspects of intermediary metabolism of white (epididymal) and brown (interscapular) adipose tissue (BAT) were studied in cold-acclimated weanling rats with hypothalamic obesity. Groups of rats with ventromedial hypothalamic lesions (VMNL rats) and controls were maintained for four weeks at 6 degrees C and 22 degrees C, respectively. Sham-operated rats served as controls. Cold-acclimated VMNL rats showed greater percent BAT but normal percent epididymal fat pad weight, hypophagia, reduced body weight and body weight gains, hyperdipsia, hyperinsulinemia, normoglycemia and normal circulating fatty acid levels, higher carcass lipid and lower carcass protein. They also exhibited a higher rate of epididymal fat pad lipolysis than the controls, but the increment during cold adaptation was less in the VMNL rats compared with the 22 degrees C-maintained VMNL animals. In-vitro metabolism was determined in both the basal and the epinephrine-stimulated state. Basal-state 14C-palmitate oxidation, BAT fatty acid and lipid contents were increased in VMNL rats but protein content, incorporation into phospholipid and triglycerides, BAT lipolysis and glycolysis were normal in cold-acclimated VMNL rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats. Epinephrine-stimulated BAT showed similar fatty acid content and palmitate oxidation and incorporation into triglycerides in VMNL and control rats, but the epinephrine-stimulated increase in lipolysis only in the cold-acclimated VMNL rats. Whereas at 22 degrees C BAT of VMNL rats showed decreased palmitate oxidation and no change of incorporation into phospholipid and triglyceride, during cold acclimation VMNL rats showed normal BAT metabolism and normal response to epinephrine, except for an increase in lipolysis. The data are in agreement with the observation that hypothalamic-obese mature rats have normal cold survival potential and allow us to extend this fact to the normophagic-obese-weanling rat.
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PMID:Brown adipose tissue metabolism in cold-acclimated weanling rats with hypothalamic obesity. 688 32


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