UNIPROT:P56851 - FACTA Search

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Query: UNIPROT:P56851 (epididymal)
11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous studies showed atrophy of brown adipose tissue (BAT) in capsaicin-desensitized rats during the period 11-28 days after injections [Cui et al., Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R324-R332, 1990]. The objective of the present studies was to assess the rapidity with which the atrophy occurred and the extent to which recovery had occurred by 8 wk. Rats, either vehicle-injected controls or capsaicin injected, were studied 1, 3, 14, 28, and 52 days after the last injection. BAT was markedly atrophied at 1 day, having less total protein, fewer mitochondria (less total cytochrome oxidase and total uncoupling protein), and fewer cells (less DNA). Atrophy persisted for up to 14 days but had largely disappeared by 28-52 days. A transient reduction in body weight gain and white epididymal adipose tissue weight had also reversed by 28-52 days. We suggest that the rapid atrophy of BAT after capsaicin desensitization is secondary to the loss of sensory neuropeptides in its sensory nerves, neuropeptides that either exert a trophic effect on synthesis of mitochondria or an inhibitory influence on processes that promote degradation of mitochondria. The retardation of the normal age-associated increase in DNA content of BAT in the capsaicin-desensitized rat suggests that sensory neuropeptides might also modulate cell proliferation.
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PMID:Rapid but transient atrophy of brown adipose tissue in capsaicin-desensitized rats. 131 14

Ability to express uncoupling protein (UCP) and establish UCP-dependent thermogenesis was analyzed in anatomical areas of mice that are generally considered to be white adipose tissue: mesenterial, perimetral, epididymal, inguinal, and superficial layer of interscapular white adipose tissue. The mice were acclimatized for 1 week to 4 degrees C; the following week they were exposed to cold stress (1 h at -20 degrees C, 2-3 times daily). In such conditions in inguinal adipose tissue, slot-blot analysis detected significant amount of UCP mRNA and lipoprotein lipase mRNA. Immuno-electron-microscopic localization of UCP showed that developed mitochondria of cold-stressed inguinal adipocytes contained UCP in the same amount as uncoupled (UC)-mitochondria of brown adipocytes. Morphological and morphometrical analysis showed that such inguinal adipose tissue appeared as brown adipose tissue. Since in control mice, inguinal adipose tissue was UCP-negative and tissue appeared as white adipose tissue, the duration of this white-to-brown adipose tissue conversion was analyzed. Mice, cold stressed for 1 week, were rewarmed at 28 degrees C and their inguinal adipose tissue was analyzed in comparison with interscapular brown adipose tissue and epididymal white adipose tissue for another 37 days. During that time inguinal adipocytes ceased expressing UCP mRNA; UC-mitochondria in inguinal adipocytes were destroyed and replaced with common, C-mitochondria; and UCP was undetectable immunohistochemically. Adipocytes accumulated lipids, and the tissue morphologically once again resembled white adipose tissue. Described changes showed that besides typical brown and white adipose tissue in mice, there existed a third type of adipose tissue described as convertible adipose tissue.
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PMID:Convertible adipose tissue in mice. 174 9

The role of insulin in the regulation of the thermogenic activity and capacity (uncoupling protein content) of brown adipose tissue (BAT) has been investigated using mice made diabetic with streptozotocin and then subsequently infused with different doses of insulin. After 12 days of diabetes, the animals received either 0, 8, 16, or 32 units of insulin.kg body wt-1.day-1 delivered by osmotic minipumps implanted subcutaneously for 12 days. After 12 days of diabetes, body weight, interscapular BAT, and epididymal white adipose tissue weights were each reduced. In BAT, significant decreases (P less than 0.05) in the mitochondrial protein content (63%), cytochrome oxidase activity (79%), mitochondrial GDP binding (51%), and the specific mitochondrial concentration and total tissue content of uncoupling protein (71 and 89%, respectively) were obtained, indicating that the thermogenic activity and capacity of the tissue were reduced in diabetes. The infusion of insulin at a dose of 8 units.kg-1.day-1 normalized mitochondrial GDP binding and doubled the concentration of uncoupling protein. Body weight, epididymal white adipose tissue weight, and the mitochondrial protein content of BAT were restored with 16 units of insulin.kg-1.day-1. Higher doses of insulin did not further increase the specific mitochondrial concentration of uncoupling protein, but the mitochondrial content (and thereby the total uncoupling protein content) of BAT was increased and blood glucose normalized. There was a significant correlation between the dose of insulin replacement and several of the parameters measured in BAT: mitochondrial protein content (r = 0.68, P less than 0.001), cytochrome oxidase activity (r = 0.54, P less than 0.001), and total uncoupling protein content (r = 0.68, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the level of uncoupling protein in brown adipose tissue by insulin. 213 90

We have previously shown that after severe cold stress of rats the epididymal white adipose tissue (WAT) acquires many of the morphological characteristics (innervation, vascularization, appearance of adipocytes) of brown adipose tissue (BAT). In the present study, the mitochondrial characteristics have been analyzed. Mitochondria from the epididymal fat pad of cold-stressed rats became enlarged and had a volume 1.7 times greater than that in the control group (0.5 microns 3 in the experimental versus 0.3 microns 3 in the control group). The mitochondria occupied about 60% of the cytoplasm (14% in the control group), thus approaching the highest value reported for any cell. The straight or slightly wavy cristae completely traversed the width of the mitochondria and occupied an area of 26 microns 2/1 microns 3 of mitochondrion in the experimental adipose tissue (7 microns 2 in the control group) and 15 microns 2/1 microns 3 of cytoplasm (1.4 microns 2 in the control). The mitochondrial matrix became electron lucid and could contain lamellar whorls, as could the surface of the mitochondria. These mitochondria of epididymal WAT resembled, both morphologically and morphometrically, mitochondria in the BAT of cold-exposed rodents. In the epididymal mitochondria, immunoelectron microscopy did not reveal the presence of the BAT-specific uncoupling protein thermogenin, nor could the slot-blot technique detect thermogenin mRNA. We conclude that even under these extreme conditions of cold stress, WAT cannot adopt the thermogenin-dependent thermogenesis of BAT. The dramatic mitochondriogenesis can be interpreted only as being indicative of an extremely high metabolism in the tissue, thus placing unprecedented pressure on the energy turnover capacity of the cell.
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PMID:Epididymal white adipose tissue after cold stress in rats. II. Mitochondrial changes. 315 5

The objective was to assess the effect of a new, highly selective beta 3-adrenergic agonist, CL-316,243 (CL) (J. D. Bloom, M. D. Dutia, B. D. Johnson, A. Wissner, M. G. Burns, E. E. Largis, J. A. Dolan, and T. H. Claus., J. Med. Chem. 35: 3081, 1992), on energy balance and brown and white adipose tissues (BAT and WAT, respectively) in young rats eating a high-fat diet to induce obesity. Chronic treatment with CL increased body temperature and 24-h energy expenditure, mainly by increasing resting metabolic rate. Food intake was not altered but carcass fat was reduced. Interscapular BAT was markedly hypertrophied, with three- to fourfold increases in the content of uncoupling protein (UCP) and cytochrome oxidase. Quantitative immunoelectron microscopy of interscapular BAT of CL-treated rats showed smaller mitochondria with an unchanged total amount of UCP per mitochondrion. The relative frequency of the four major cell types in BAT (mature brown adipocytes, preadipocytes, interstitial cells, endothelial cells) was not altered. The CL-induced hypertrophy differed from that induced by chronic stimulation by endogenous norepinephrine (as in cold-adaptation) in absence of hyperplasia (there was a slightly reduced DNA content), absence of an increase in the thyroxine (T4) 5'-deiodinase activity, and absence of a selective increase in UCP concentration. WAT depots weighed less and had fewer cells (lower DNA content) in the CL-treated rats. Some multilocular adipocytes appeared in these normally almost exclusively unilocular WAT depots (mesenteric, inguinal, epididymal, retroperitoneal). We conclude that CL not only promotes BAT mitochondrial proliferation and thermogenesis and overall energy expenditure and leanness, but also retards the development of WAT hyperplasia during the early stage of diet-induced obesity.
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PMID:Effect of CL-316,243, a thermogenic beta 3-agonist, on energy balance and brown and white adipose tissues in rats. 791 Apr 36

C57BL6/J mice with the expression of the mitochondrial uncoupling protein (UCP) gene from the fat-specific aP2 gene promoter were used to study the mechanism by which the aP2-Ucp transgene affects adiposity and reduces high-fat diet induced obesity. In the transgenic mice, UCP synthesized in white fat was inserted into mitochondria, and oxygen uptake by epididymal fat fragments indicated UCP-induced thermogenesis. The respirometry data, UCP content, cytochrome oxidase activity, and tissue morphology suggested functional involution of brown fat. Despite 25- to 50-fold lower mitochondrial cytochrome oxidase activity in white than in brown fat cells, total oxidative capacity in white and brown adipose tissue is comparable. Appearance of novel small cells in the gonadal fat of the transgenic mice was associated with a higher DNA content than that of the nontransgenic mice. The results prove a potential of transgenically altered mitochondria in white fat to modulate adiposity and energy expenditure and suggest the existence of a yet unidentified site-specific link between energy metabolism in adipocytes and cellularity.
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PMID:Reduction of dietary obesity in aP2-Ucp transgenic mice: mechanism and adipose tissue morphology. 896 65

In the guinea pig, cold acclimation induced a conversion of unilocular to multilocular adipocytes in interscapular (IS) and retroperitoneal (RP) fat depots but not in the epididymal (EP) fat pad. The conversion was associated with an increase in mitochondriogenesis and the appearance of the uncoupling protein. The maximal lipolytic responses to norepinephrine and dibutyryl adenosine 3',5'-cyclic monophosphate were decreased in IS cells, unchanged in RP cells, and increased in EP cells, suggesting a site-specific regulation of lipolysis at the postreceptor level. beta 3-Adrenergic agonists were not lipolytic regardless of the depot and the thermal environment of the animal. These agents did not inhibit glucose transport and lipogenesis, as was previously reported for rodents. Cloning and sequencing of the guinea pig beta 3-adrenoceptor gene revealed a slightly higher amino acid sequence similarity with the human than with the rodent beta 3-adrenoceptors. beta 3-Adrenoceptor transcripts were present at a very low level in guinea pig adipocytes, and mRNA levels did not increase to a significant extent after cold acclimation. The guinea pig thus differs from rodents by an absence of beta 3-adrenergic effects and by low beta 3-adrenoceptor expression in brown and white adipose tissues.
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PMID:Beta 3-adrenoceptor in guinea pig brown and white adipocytes: low expression and lack of function. 899 76

To investigate the role of beta 3-adrenergic receptors in the suppression of leptin gene expression, we fasted F-344 rats to decrease leptin mRNA levels, refed the rats to stimulate leptin mRNA production, and examined the ability of the beta 3-adrenergic agonist CGP-12177 to prevent the rise in leptin mRNA levels. In the initial 2 h after CGP-12177 (0.75 mg/kg), there were significant reductions in both food consumption and leptin mRNA levels in epididymal, perirenal, and interscapular white adipose tissue. We were unable to detect leptin mRNA in interscapular brown adipose tissue (IBAT), whereas there was a significant increase in uncoupling protein mRNA levels in IBAT after CGP-12177. The suppression of leptin mRNA and food intake by CGP-12177 was confirmed in a second experiment using another rat strain, the F-344 x BN. Furthermore, refeeding after a period of fasting increased leptin mRNA, which was prevented by CGP-12177. These data indicate a role for beta 3-adrenergic-mediated regulation of leptin gene expression in nonmutant rodents and are consistent with other reports suggesting that beta 3-adrenergic agonists suppress food intake.
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PMID:beta 3-Adrenergic-mediated suppression of leptin gene expression in rats. 922 48

Three experiments were conducted to investigate the effect of restraint stress applied at different times of the light-dark cycle on feeding behavior and body weight of rats. Sprague-Dawley rats were restrained for 3 h in restraining tubes either at the start or the end of the light cycle. There was a significant reduction in food intake on the day of restraint and no change in food intake during a 10-day recovery period in either experiment. Reductions of food intake on the day of restraint were about the same for both restrained groups compared with their controls. When stress was applied in the evening, eating was inhibited during the first 2 h after restraint, whereas in rats restrained in the morning, feeding was suppressed twice: during the 4 h after restraint and during the first 2 h of the dark cycle. Restraint induced a significant weight loss that was greater in the rats stressed in the morning. Neuropeptide Y (NPY) levels determined at the time of food suppression for both experiments (beginning of the dark cycle) revealed an elevation of NPY in the paraventricular nucleus of rats stressed in the morning compared with other groups, but no difference in hypothalamic NPY mRNA expression. Expression of uncoupling protein mRNA in brown adipose tissue and leptin mRNA in epididymal fat, measured at the start of the dark period, was not altered by stress. There was an elevation of dopamine turnover in the hypothalami of rats restrained at the end of light cycle, but not those restrained in the morning. These results show that restraint stress has a greater effect on metabolism and energy balance when it is applied in the morning. Additional studies are needed to elucidate mechanisms involved in the suppression of food intake 9 h after restraint.
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PMID:Effect of restraint stress on food intake and body weight is determined by time of day. 937 1

Humans and rats tend to gain weight as they age. Leptin is one regulator of food intake and energy expenditure. To determine if the increase in adiposity with age is related to altered leptin gene expression, we assessed adiposity levels, leptin mRNA levels in epididymal and inguinal white adipose tissue (EWAT and IWAT), and uncoupling protein (UCP1) mRNA levels in interscapular brown adipose tissue (IBAT) from F344 x BN rats ages 3, 12, 18, 24, and 30 months (n = 8/age). Levels of adiposity determined by the adiposity index and the Lee index increased between ages 3 and 24 months, with a decrease at age 30 months. There were parallel increases with age in body weight, EWAT, and IWAT depot size up to age 24 months, followed by a nonsignificant decrease at age 30 months. Daily food intake was unchanged with age. In EWAT, leptin mRNA per microgram of RNA was unchanged with age, whereas in IWAT, it increased up to 24 months, then declined at 30 months. Total leptin mRNA levels in both IWAT and EWAT depots increased with age, peaking at age 24 months, and were correlated with adiposity. Serum leptin levels increased with age, also peaking at age 24 months, and were correlated with total leptin mRNA in WAT pads and adiposity. The rate of increase in serum leptin was greater than the increase in adiposity with age, suggesting contributions from both the increase in leptin expression per unit of WAT and the increase in WAT depot size. In addition, UCP1 mRNA levels in IBAT did not change with age. These data suggest that adiposity increases with age and cannot be attributed to increased food intake, impaired leptin gene expression, or decreased UCP1 mRNA level in IBAT. Furthermore, leptin gene expression in IWAT increases with age independent of increasing adiposity.
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PMID:Leptin gene expression increases with age independent of increasing adiposity in rats. 939 92

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