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

It is concluded that besides NA, some other hormones (adrenaline, glucagon, growth hormone, ACTH, insulin and adrenal steroids) are also thermogenic. While brown adipose tissue is the most important site of heat during NA thermogenesis, some other organs, namely muscles, also contribute to thermogenesis due to various hormones. Hormones seem to potentiate heat production due to their action in target organs. Humoral thermogenesis not only can compensate the heat loss from the body of cold exposed individuals, but it can also prevent obesity under conditions of an high caloric intake. Some substance, on the other hand, induce a hypometabolic effect (rT3, hibernation trigger, antabolone, bombesin). Additionally, absence of gonadal steroids induce hibernation. Thus, humoral substances contribute both to the control of hyper- and hypometabolic states.
 ...
PMID:Humoral control of hyper- and hypometabolic states. 631 84

The regulation of body weight depends upon the control of food intake and the regulation of energy expenditure. In man, the control system for food intake may be overwhelmed by psychological or social influences and the thermogenic response to a variable energy input may play an important role in the energy regulatory system. Energy expenditure can be divided into 3 components: basal metabolic rate, thermogenesis and physical activity. Of these 3 components, thermogenesis, (i.e. the energy expended above the metabolic rate in the resting state) is the expenditure. The two main factors which contribute to thermogenesis, i.e food intake and cold exposure, elicit diet-induced thermogenesis (DIT) and non-shivering thermogenesis (NST), respectively. It is of interest to study thermogenesis in individuals who present a tendency to gain weight, in order to assess whether the thermogenic responses may be lower in these subjects than in lean controls. It has recently been shown that DIT consists of two separate components which can be described as "obligatory" and "regulatory" thermogenesis. The former is due to the energy costs of digesting, absorbing and converting the nutrients to their respective storage forms. The latter is an energy dissipative mechanism, mainly studied in animals. There is good experimental evidence showing that brown adipose tissue (BAT) is involved in the adaptive thermogenesis observed in rats fed a varied and palatable "cafeteria" diet. In addition, a thermogenic defect in BAT has been demonstrated in adult as well as young genetically obese animals, and this defect is present not only in adult, but also in young (12 day old) ob/ob mice, i.e. before the development of obesity. Thus, a defective thermogenesis seems to be a cause, rather than a consequence, of obesity in these animals. In man, the role of thermogenesis in energy balance regulation is not yet understood. Some conflicting results may have arisen from inadequate techniques to measure energy expenditure. In our laboratory, we have developed three different techniques to measure energy expenditure in man, namely direct calorimetry, indirect calorimetry using an open-circuit ventilated hood system, and a respiratory chamber. Data from recent studies on DIT in man support the concept that a defect in thermogenesis may contribute to energy imbalance and weight gain in obese individuals.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Thermogenic responses induced by nutrients in man: their importance in energy balance regulation. 635 48

Obese (ob/ob) and lean mice at 4 weeks of age were housed at 23 degrees C or 14 degrees C for 4 or 8 weeks to determine effects of acclimation to mild cold on the growth of skeletal muscle, bone, and fat. Body weights at 12 weeks of age averaged 48 +/- 0.6 g and 27 +/- 1.9 g for obese mice housed at 23 degrees C and 14 degrees C and 29 +/- 0.5 g and 26 +/- 0.6 g and 26 +/- 0.6 g for lean mice housed at 23 degrees C and 14 degrees C, respectively. At 23 degrees C, muscle weights of obese mice were approximately 60% of those in lean mice. Muscles of obese mice did not grow during the first 4 weeks at 14 degrees C (4 to 8 weeks of age) but did show a small gain during the second 4 weeks (9 to 12 weeks of age) at 14 degrees C. As a result, by the end of 8 weeks at 14 degrees C, muscles of obese mice weighed only 35% to 45% as much as muscles of lean mice. Growth of the tibia and femur followed the same pattern as the muscles. Obese mice housed at 23 degrees C from 4 to 12 weeks of age contained about six times as much fat as lean mice at this age. Although exposure to 14 degrees C for 8 weeks depressed the accumulation of fat in obese mice, they still contained approximately three times the percentage body fat as lean counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cold acclimation of obese (ob/ob) mice: effects on skeletal muscle and bone. 638 62

The concept that thermogenesis in brown adipose tissue can play a role as an energy buffer has developed during the last 5 years. The history of this development is reviewed. Control of brown adipose tissue thermogenesis resides in regions of the brain, located primarily but not exclusively in the hypothalamus, that control the activity of the sympathetic nervous system in response to diet and to environmental temperature. Brown adipose tissue mitochondria are uniquely specialized for thermogenesis, possessing a specific proton leakage mechanism that is regulated by the concentration of fatty acids in the cells of the brown adipose tissue. The level of fatty acids is in turn controlled by the lipolytic action of noradrenaline on the tissue. Sympathetic stimulation also exerts a trophic influence on brown adipose tissue. Effective thermogenesis in brown adipose tissue is associated with leanness and decreased metabolic efficiency, as in the rat rendered hyperphagic and hypermetabolic, by either cold acclimation or cafeteria feeding. Conversely, food restriction is associated with suppressed thermogenesis in brown adipose tissue and increased metabolic efficiency. Defective brown adipose tissue thermogenesis is associated with obesity in a number of different types of obese animals. In three of these (the genetically obese fa/fa Zucker rat, the mouse with hypothalamic damage induced by gold thioglucose, the rat with a surgically induced hypothalamic lesion), diet-induced thermogenesis is defective in brown adipose tissue, but cold-induced thermogenesis is normal. In another type of obese animal, the genetically obese (ob/ob) mouse, control of brown adipose tissue is defective. Studies of this control are complicated by the frequency of torpor in the fed state.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Brown adipose tissue thermogenesis, energy balance, and obesity. 638 75

Gold thioglucose (GTG)-obese mice have a larger than normal amount of brown adipose tissue (BAT) with ultrastructurally normal mitochondria. The tissue grows normally when the mice adapt to cafeteria feeding or to cold (8 degrees C). Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. More prolonged cafeteria feeding for 11-13 wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. The capacity of GTG-obese mice to respond to noradrenaline (norepinephrine) by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG.
 ...
PMID:Brown adipose tissue of mice with gold thioglucose-induced obesity: effect of cold and diet. 640 32

Catecholamine turnover in response to fasting, cold exposure, and a high-fat diet has been measured in the Osborne-Mendel rat, which readily develops obesity when fed a high-fat diet, and the S 5B/P1 rat, which does not. We have tested the hypothesis that this difference in response to diet might be associated with altered rates of norepinephrine or epinephrine turnover. The endogenous norepinephrine concentration in interscapular brown adipose tissue was significantly greater in fasted S 5B/P1 rats than in fasted Osborne-Mendel rats. The fractional norepinephrine turnover rate in interscapular brown adipose tissue of fasted animals was also greater in the S 5B/P1 rat than in the Osborne-Mendel rat. Cold exposure increased the fractional norepinephrine turnover rate in interscapular brown adipose tissue for both strains of rats but increased the fractional norepinephrine turnover rate in the pancreas in only the Osborne-Mendel rats. The turnover of epinephrine and the adrenal concentration of this hormone were not different between the two strains. Normal and high-fat diets were fed to both strains; the Osborne-Mendel rats were pair fed the high-fat diet to prevent excess weight gain. Endogenous concentrations of norepinephrine in interscapular brown adipose tissue was increased by the high-fat diet; the increase was greater in S 5B/P1 rats. The high-fat diet resulted in increased norepinephrine turnover in interscapular brown adipose tissue of the S 5B/P1 rat but not the Osborne-Mendel rat.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Catecholamine turnover in S 5B/P1 and Osborne-Mendel rats: response to a high-fat diet. 646 44

Obese (ob/ob) and lean mice at 4 weeks of age were housed at 23 degrees C or 14 degrees C for 4 to 8 weeks to examine effects of acclimation to mild cold on energy balance. Energy intake of young lean mice increased by about 50% when housed at 14 degrees C, but energy intake of cold-acclimated obese mice increased by only 8%. Efficiency of energy retention (ratio of energy gain to energy intake) in obese mice declined from 22% +/- 1.2% at 23 degrees C to 10% +/- 1.8% after 4 weeks at 14 degrees C. Lean mice exhibited a less pronounced response to temperature; their efficiency of energy retention declined from 7% +/- 1.3% at 23 degrees C to 4% +/- 2.2% after 4 weeks at 14 degrees C. After 8 weeks of cold exposure, body weights and efficiency of energy retention became equal in obese and lean mice. Calculated heat production of cold-acclimated obese and lean mice was 40% higher than that of respective controls. Obese mice reacclimated to 23 degrees C after being kept for 4 weeks at 14 degrees C consumed the same amount of energy and were 16% more efficient than obese maintained at 23 degrees C; reacclimated lean mice consumed 12% more energy but were 53% less efficient than lean mice maintained at 23 degrees C. The results indicate that obese mice are able to increase heat production and markedly reduce their efficiency of energy retention when acclimated to mild cold but that they, unlike lean mice, rapidly revert to a high efficiency of energy retention after 4 weeks of reacclimation to 23 degrees C.
 ...
PMID:Cold acclimation of obese (ob/ob) mice: effects of energy balance. 647 17

Previous studies have suggested the presence, in hypothalamic obesity, of an impairment of the energy-dissipating capacity of brown adipose tissue ascribed to a functional disconnection of the sympathetic innervation of this tissue. The following observations demonstrate, with electrophysiological techniques, the presence of a functional link between the ventromedial hypothalamic (VMH) area and the interscapular brown adipose tissue (IBAT) in the rat: the spontaneous activity of the efferent sympathetic nerves reaching the IBAT of normal rats was increased in response to an acute cold stimulus, whereas this increase failed to occur in nerves of VMH-lesioned rats studied 4-7 days after the lesions; and the spontaneous activity of the efferent sympathetic nerves of IBAT decreased rapidly (by greater than or equal to 80% within 30 min) after acute lesions of the VMH area. It is suggested that the VMH area plays a role in increasing the activity of the efferent sympathetic nerves of IBAT during an acute cold stimulus and that alone or in relationship with other, as yet undetermined, central nervous system sites, it has a tonic stimulatory effect on the final common pathways that innervate the IBAT via the efferent sympathetic nerves.
 ...
PMID:Role of ventromedial hypothalamus on sympathetic efferents of brown adipose tissue. 649 14

To investigate the contribution of brown fat (BAT) to the development of obesity in genetically obese Zucker rats (fa/fa), scapular brown fat (SBAT) was removed from obese and lean 4-wk-old females. Eight weeks after surgery there was no regrowth of SBAT. Lipectomy had no effect on body weight gain, food intake, and body composition when rats were housed at 25 degrees C. Lean rats completely compensated for the lipectomy by increasing BAT mass, protein, cellularity, and activity of citrate synthase (CS) in axillary, perirenal, and thoracic depots. beta-Hydroxyacyl-coenzyme A dehydrogenase (HOAD) activity was increased, but compensation was incomplete. In lipectomized obese rats, only BAT protein and cell number were increased sufficiently for complete compensation. In a second experiment SBAT was removed from obese and lean rats, but rats were housed in the cold (10 degrees C) for 8 wk. In lean rats, although compensation was incomplete, it was sufficient to maintain a weight gain and body composition comparable with sham-operated lean rats. In obese rats, where there was little or no compensation for lipectomy, weight gain and fat deposition were greater than observed in sham-operated obese controls. These data support the hypothesis that reducing the amount of functional BAT contributes to the development of increased adiposity.
 ...
PMID:Scapular brown fat removal enhances development of adiposity in cold-exposed obese Zucker rats. 649 75

A diurnal hyperphagia is certainly the main factor of adiposity in the genetically obese Zucker fa/fa rat. In a previous experiment it was observed that cold-acclimatization suppressed hyperphagia and stopped the increase in obesity. In this work, the chronology of modification in the feeding pattern is studied during the first month of cold exposure (10 degrees C). The main cold-induced modifications are observed after 2 weeks of cold exposure. Possibly the decrease in metabolic efficiency of food could parallel the cold-induced enhancement of energetic capacity of brown adipose tissue which has been described elsewhere. This tissue could play a role in the obesity of the Zucker rat.
 ...
PMID:[Effect of cold adaptation on the feeding behavior of genetically obese Zucker rats]. 652 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>