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

Differential temperature measurement between interscapular brown adipose tissue (BAT, Tbat), rectum (Trect) and a subcutaneous point in the back left of the vertebral column (Tsc) was useful for examination of BAT-thermogenesis in glutamate-induced obese Wistar-rats. Positive temperature gradients Tbat-Tsc pointed to a basal BAT-thermogenesis, whereas negative temperature gradients Tbat-Trect did not indicate that heat production in lean and obese rats. One may conclude from this, that inclusion of subcutaneous points outside the BAT improves sensitivity of differential temperature measurements for BAT-thermogenesis. Basal temperatures Tbat, Trect and Tsc were reduced in obese rats compared to lean rats, although thermoinsulation of obese rats is improved on account of their high fat content. This points to a diminished heat production in obese rats. Cold exposure at 4 degrees C elicited an increase of temperature gradients Tbat-Trect in lean as well as in obese rats, with positive values found only in lean rats. However, positive values Tbat-Tsc were calculated for both groups. Increases were noted only in lean rats. Injection of noradrenaline (0.5 mg/kg i.m.) was followed by positive temperature gradients Tbat-Trect and increased positive values for Tbat-Tsc, pointing to a remarkable activation of BAT-thermogenesis in lean and obese rats. These findings confirm, that glutamate-induced obese rats preserved the ability to activate BAT-thermogenesis. There were, however, hints of reduced heat production in BAT of obese rats, thus contributing to obesity despite normophagia.
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PMID:Examination of brown adipose tissue thermogenesis of glutamate-induced obese rats by differential temperature measurements. 129 79

1. Adipose mass and cellularity were studied in congenic female SHR/N-cp rats fed iosenergetic diets containing 54% carbohydrate as sucrose (SU) or cooked cornstarch (CS), 20% protein, 16% mixed dietary fat plus vitamins, minerals, and non-nutritive fiber ad libitum from 5 weeks until 8.5 months of age. Measures of adipocyte lipid content, cell number per depot, and mass of principal white (WAT) and interscapular brown (IBAT) adipoe tissue depots were determined at the end of the study. 2. Final body weights (BW) of corpulent rats were more than twice those for their lean littermates, and were greater when fed the SU than the CS diet in both phenotypes. Phenotype effects (corpulent greater than lean) were present for fat pad weight, adipocyte number, and adipocyte lipid content in the dorsal (DOR) and retroperitoneal (RP) WAT depots. Diet effects were present for depot weight, adipocyte number, and adipocyte lipid content in both WAT depots, and were of qualitatively similar magnitude in both phenotypes. 3. IBAT weights, IBAT:BW ratios, and IBAT cell number of corpulent greater than lean, and were greater than with SU than CS diet in both phenotypes. 4. These results indicate that obesity in the corpulent phenotype of the SHR/N-cp rat occurs as the result of hypertrophy and hyperplasia of white adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate resulted in greater fat accretion in both phenotypes. The greater diet and phenotype-associated adiposity occurred despite greater mass and cellularity of BAT. The results also indicate that sexual dimorphism occurs regarding effects of diet and phenotype on expression of adipose tissue development in this strain.
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PMID:Effects of dietary carbohydrate and phenotype on adipose cellularity in female SHR/N-cp rats. 167 51

1. Groups of lean and corpulent LA/N-cp rats were fed isoenergetic diets containing, 54% carbohydrate as maize starch (MS) or sucrose (SU), 20% protein, 16% mixed fats, plus other essential nutrients and fiber from 1.5-9 months of age. Final body weights of corpulent rats were 2-3 times those of their lean littermates, and were greater with SU than MS diet in both phenotypes. 2. Interscapular brown adipose tissue (IBAT) mass was greater in corpulent than lean and was greater with SU than MS diet in lean but not corpulent rats. IBAT cell diameters and adipocyte volumes were generally similar in both phenotypes, and were not markedly affected by dietary carbohydrate type. 3. Brown adipocyte locularity profiles were qualitatively similar in both phenotypes, and were morphologically indicative of thermogenic activity in both phenotypes. Locule profiles of corpulent animals contained a greater proportion of thermogenically less active types IV and V brown adipocytes than similarly fed lean animals, however, and locule distribution profiles were not influenced by diet. 4. Serum T3 concentrations were similar in both phenotypes, were greater in SU than MS lean rats and were not influenced by diet in the corpulent phenotype. In contrast, serum thyroxine concentrations and percent thyroxine uptake were not influenced by diet or phenotype. 5. These results are consistent with a partial impairment in BAT-mediated thermogenic activity in the corpulent phenotype and suggest that obesity in this strain may be due to factors other than biochemically defective brown adipose tissue thermogenesis.
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PMID:Effects of dietary carbohydrate and phenotype on thyroid hormones and brown adipose tissue locularity in adult LA/N-cp rats. 257 70

To clarify whether cigarette smoke stimulates the sympathetic nervous system (SNS) and thermogenesis in interscapular brown adipose tissue (IBAT), we measured norepinephrine (NE) turnover, an indicator of SNS activity, guanosine-5'-diphosphate (GDP) binding, a thermogenic indicator, and oxygen consumption in IBAT in monosodium-L-glutamate (MSG)-induced obese and saline control mice following a two-week exposure to cigarette smoke. Cigarette smoke significantly increased NE turnover, GDP binding and oxygen consumption in IBAT, and significantly reduced body weight in MSG obese mice as well as in control mice. However, food intake was unchanged in the MSG group. These results suggest that cigarette smoke stimulates NE turnover and thermogenesis in BAT, which contribute to the mitigation of obesity.
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PMID:Effects of cigarette smoke on norepinephrine turnover and thermogenesis in brown adipose tissue in MSG-induced obese mice. 258 62

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in all organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF]. At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT] balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.
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PMID:Role of thermogenesis in the regulation of energy balance in relation to obesity. 266 32

High levels of dietary fat may contribute to both insulin resistance and obesity in humans but evidence is limited. The euglycemic clamp technique combined with tracer administration was used to study insulin action in vivo in liver and individual peripheral tissues after fat feeding. Basal and nutrient-stimulated metabolic rate was assessed by open-circuit respirometry. Adult male rats were pair-fed isocaloric diets high in either carbohydrate (69% of calories; HiCHO) or fat (59% of calories; HiFAT) for 24 +/- 1 days. Feeding of the HiFAT diet resulted in a greater than 50% reduction in net whole-body glucose utilization at midphysiological insulin levels (90-100 mU/l) due to both reduced glucose disposal and, to a lesser extent, failure to suppress liver glucose output. Major suppressive effects of the HiFAT diet on glucose uptake were found in oxidative skeletal muscles (29-61%) and in brown adipose tissue (BAT; 78-90%), the latter accounting for over 20% of the whole-body effect. There was no difference in basal metabolic rate but thermogenesis in response to glucose ingestion was higher in the HiCHO group. In contrast to their reduced BAT weight, the HiFAT group accumulated more white adipose tissue, consistent with reduced energy expenditure. HiFAT feeding also resulted in major decreases in basal and insulin-stimulated conversion of glucose to lipid in liver (26-60%) and brown adipose tissue (88-90%) with relatively less effect in white adipose (0-43%). We conclude that high-fat feeding results in insulin resistance due mainly to effects in oxidative skeletal muscle and BAT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fat feeding causes widespread in vivo insulin resistance, decreased energy expenditure, and obesity in rats. 353 32

Half of the 3-mo male Sprague-Dawley rats fed a high-fat (DIO) diet for 5 mo became obese and had increased carcass lipid (106%) and plasma insulin levels (61%), despite 8% less total energy intake than chow-fed controls. Their interscapular brown adipose tissue (IBAT) was 52% heavier with 45% more lipid and larger uni- and multilocular cells. Norepinephrine turnover was normal in their hearts, pancreases, and aortas but undetectable in IBAT where in vitro lipolysis, but not O2 consumption (VO2), was enhanced. Half the rats fed the DIO diet ate 17% fewer calories, gained weight equally to controls, but still had 34% more carcass lipid. Their IBAT was heavier, contained 103% more protein, with no detectable norepinephrine turnover, whereas maximal lipolysis was 73% lower and maximal VO2 was the same or even lower than controls. IBAT VO2 was stimulated by switching 8-mo chow-fed controls to the DIO diet for 7 days (which caused a 480% greater weight gain) but not by switching 8-mo obese rats to chow for 3 days. Therefore metabolic efficiency was increased while BAT VO2 and norepinephrine turnover were unchanged or reduced compared with controls by either chronic obesity or a high-fat diet.
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PMID:Brown adipose and metabolic features of chronic diet-induced obesity. 389 May 63

Defective BAT thermogenesis is associated with obesity in all the different types of obese animal so far studied. The deficit in normal energy expenditure may be presumed to contribute to the high metabolic efficiency and, together with the hyperphagia, to the obesity of these animals. In two types of obese animal (the ob/ob mouse, the db/db mouse) an increased propensity to become torpid provides an additional energy conserving mechanism that contributes to the high metabolic efficiency. In all these animals an abnormality of hypothalamic function appears likely. Obviously animals with induced hypothalamic lesions (the VMH-lesioned rat, the GTG-obese mouse) have an interruption in the normal pathway that links diet and the sympathetic innervation of BAT. The fa/fa rat resembles these animals in failing to activate BAT thermogenesis in response to diet: the lesion may lie in the hypothalamus itself or elsewhere in the food-intestine-hypothalamus-BAT axis, for example in intestinal peptide hormones. The ob/ob mouse has a peculiar hypothalamic defect that interferes with control of thermogenesis in BAT as well as impairing or exaggerating some aspects of thermoregulation. The db/db mouse resembles the ob/ob mouse but, since the defect is genetically distinct, presumably has a different lesion at the molecular level.
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PMID:Defective brown adipose tissue thermogenesis in obese mice. 406 36

Adult female rats that underwent sympathectomy induced by guanethidine treatment (10, 20 or 40 mg/kg) exhibited markedly increased water intake, but did not display significant alterations of either food intake, body weight, or the Lee Index of obesity. Guanethidine treatment did not attenuate amphetamine anorexia as evidenced by comparable dose-dependent reductions in food intake to d-amphetamine sulfate (0.25, 0.50, 1.0, and 2.0 mg/kg) in sympathectomized and control rats. These data are not consistent with the hypothesis that amphetamine anorexia is partially mediated via enhanced BAT thermogenesis.
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PMID:Effects of guanethidine sympathectomy on feeding, drinking, weight gain and amphetamine anorexia in the rat. 407 Apr 17

There are a number of animals in which obesity is genetically determined. In some the inheritance is polygenic while in others it is by a single-gene mutation. In the most widely studied single-gene mutants--the obese (ob/ob) mouse, the diabetic-obese (db/db) mouse and the Zucker (fa/fa) rat-obesity is very substantial and is initiated before the animals are weaned. Although hyperphagia is a feature of all the major obese mutants, it is not a prerequisite for the development of obesity. The initiation of the disorder during the suckling period takes place on a normal energy intake, and excess rates of energy deposition will still continue after weaning if the obese mutants are pair-fed to the ad libitum energy intake of lean siblings. The ability to become obese without hyperphagia indicates that one or more components of energy expenditure must be reduced in the obese mutants. Studies on the ob/ob mouse have demonstrated that a reduction in thermogenesis in BAT is the main way by which this is achieved. The reduction in energy expenditure in BAT is due primarily to a low activity of the sympathetic innervation to the tissue. Once hyperphagia is established, apparently as a secondary feature of the obese syndrome, the development of obesity is accelerated, the obese mutants having an impairment in the dietary stimulation of BAT thermogenesis. Studies on different types of obese animal suggest that an inability to respond to dietary stimuli is a general feature of obesity. The final syndrome presented by genetically obese animals is of considerable metabolic and endocrinological complexity. However, it is now possible to begin to integrate some of the endocrinological abnormalities within the energy balance framework, centred on BAT, that has been developed over the past few years. This is particularly evident in the case of adrenal function in the Zucker rat; adrenalectomy of this mutant has important effects on energy balance and in the normalization of the thermogenic activity of BAT. The sensitivity of BAT to insulin is also emerging as a possible factor of importance in the modulation of thermogenesis in obese animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The development of obesity in animals: the role of genetic susceptibility. 639 50


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