scholarly journals Sensory denervation of inguinal white fat modifies sympathetic outflow to white and brown fat in Siberian hamsters

2018 ◽  
Vol 190 ◽  
pp. 28-33 ◽  
Author(s):  
Ngoc Ly T. Nguyen ◽  
Bingzhong Xue ◽  
Timothy J. Bartness
Keyword(s):  
Brown Fat ◽  
Sympathetic Outflow ◽  
Siberian Hamsters ◽  
Sensory Denervation ◽  
White Fat

CNS sympathetic outflow neurons to white fat that express MEL receptors may mediate seasonal adiposity

2001 ◽  
Vol 281 (2) ◽  
pp. R666-R672 ◽  
Author(s):  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Body Fat ◽  
Pseudorabies Virus ◽  
Brain Regions ◽  
Sympathetic Outflow ◽  
Receptor Stimulation ◽  
Siberian Hamsters ◽  
The Central Nervous System ◽  
White Fat ◽  
Short Days

Many animals show seasonal changes in adiposity that are triggered by changes in the photoperiod. For example, in short “winterlike” days, the nocturnal duration of pineal melatonin (MEL) secretion increases ultimately resulting in body fat decreases by Siberian hamsters. These decreases in body fat are mediated through increases in the sympathetic drive on white adipose tissue (WAT). The central nervous system (CNS) origins of the sympathetic outflow from brain to WAT include the suprachiasmatic nucleus (SCN), an area necessary for the reception of season-encoded MEL signals in Siberian hamsters. Therefore, we tested whether SCN neurons that are part of the sympathetic outflow to WAT also express MEL receptors (MEL1a). This was accomplished by labeling the sympathetic outflow from brain to WAT using a transsynaptic retrograde tract tracer, the pseudorabies virus (PRV), injected into inguinal WAT combined with labeling of brain MEL1areceptors using in situ hybridization. We found PRV-labeled neurons that also expressed MEL1a-receptor mRNA in several brain regions including the SCN. Thus the increased duration of MEL secretion in short days may increase MEL1a-receptor stimulation that, in turn, increases the sympathetic drive on WAT, thereby increasing lipolysis and decreasing adiposity.

Burn Injury or Cutaneous Wound Injury to Mice Stimulates Brown Fat but not White Fat Uptake of F18-FDG in Vivo

2006 ◽  
Vol 27 (Supplement) ◽  
pp. S166
Author(s):  
Q Zhang ◽  
E A. Carter ◽  
B Y. Ma ◽  
L J. Mcintosh ◽  
E Cyr ◽  
...  
Keyword(s):  
Burn Injury ◽  
Brown Fat ◽  
Cutaneous Wound ◽  
Fat Uptake ◽  
White Fat

Anti-obesity effect of taurine through inhibition of adipogenesis in white fat tissue but not in brown fat tissue in a high-fat diet-induced obese mouse model

Amino Acids ◽  
2018 ◽  
Vol 51 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Kyoung Soo Kim ◽  
Min Ju Jang ◽  
Sungsoon Fang ◽  
Seul Gi Yoon ◽  
Il Yong Kim ◽  
...  
Keyword(s):  
Mouse Model ◽  
High Fat Diet ◽  
Brown Fat ◽  
Obese Mouse ◽  
Fat Tissue ◽  
High Fat ◽  
White Fat

Tissue distribution of immunoreactive mouse extracellular superoxide dismutase

1998 ◽  
Vol 275 (3) ◽  
pp. C840-C847 ◽  
Author(s):  
Tomomi Ookawara ◽  
Nobuo Imazeki ◽  
Osamu Matsubara ◽  
Takako Kizaki ◽  
Shuji Oh-Ishi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Superoxide Dismutase ◽  
Adrenal Gland ◽  
Sandwich Elisa ◽  
Brown Fat ◽  
Extracellular Superoxide Dismutase ◽  
Physiological Importance ◽  
Vascular Walls ◽  
Mouse Tissues ◽  
White Fat

Protein content and mRNA expression of extracellular superoxide dismutase (EC-SOD) were investigated in 16 mouse tissues. We developed a double-antibody sandwich ELISA using the affinity-purified IgG against native mouse EC-SOD. EC-SOD could be detected in all of the tissues examined (lung, kidney, testis, brown fat, liver, adrenal gland, pancreas, colon, white fat, thymus, stomach, spleen, heart, skeletal muscle, ileum, and brain, in decreasing order of content measured as μg/g wet tissue). Lung showed a markedly higher value of EC-SOD than other tissues. Interestingly, white fat had a high content of EC-SOD in terms of micrograms per milligram protein, which corresponded to that of lung. Kidney showed the strongest expression of EC-SOD mRNA. Relatively strong expression of the mRNA was observed in lung, white fat, adrenal gland, brown fat, and testis. Heart and brain showed only weak signals, and no such expression could be detected in either digestive organs or skeletal muscle. Immunohistochemically, EC-SOD was localized mainly to connective tissues and vascular walls in the tissues examined. Deep staining in the cytosol was observed in the cortical tubular cells of kidney. These results suggest that EC-SOD is distributed systemically in mice and that the physiological importance of this enzyme may be a compensatory adaptation to oxidative stress, particularly in lung and kidney.

Regional blood flow in rats after a single low-protein, high-carbohydrate test meal

1984 ◽  
Vol 247 (1) ◽  
pp. R160-R166 ◽  
Author(s):  
Z. Glick ◽  
S. J. Wickler ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Blood Flow ◽  
Test Meal ◽  
Resting State ◽  
Brown Fat ◽  
Blood Flows ◽  
High Carbohydrate ◽  
Low Protein ◽  
Brown Adipose ◽  
White Fat

It was previously observed that a single low-protein, high-carbohydrate test meal results in increased in vitro thermic activity of brown adipose tissue. In the present study, we have examined whether such a meal increases the in vivo thermic activity, estimated from measurement of the rate of blood flow. With radioactively labeled microspheres, blood flows into brown fat and several other tissues were determined in meal-deprived (n = 11) and meal-fed (n = 11) rats. The microspheres were injected into the heart of anesthetized animals about 2-2.5 h after the test meal, one injection in the resting state and one during maximal norepinephrine stimulation. In the resting state, blood flow per gram tissue more than doubled in the brown fat (P less than 0.05) and was increased more than 50% in the heart (P less than 0.01) of the fed group. Blood flows into liver and retroperitoneal white fat were reduced by 40 (P less than 0.01) and 30%, respectively, in the fed group. During norepinephrine infusion, significant meal-associated increases in blood flow were evident only in brown fat (P less than 0.05) and the soleus muscle (P less than 0.05), whereas a significant decrease was observed in the liver (P less than 0.05). No statistically significant meal-associated changes in norepinephrine-stimulated blood flow were found in the other tissues examined (i.e., heart, gastrocnemius, and diaphragm muscles, kidneys, white fat, spleen, and adrenals). Our in vivo data thus support the view that brown fat plays a role in the thermic effect of a meal.

scholarly journals Emergence during development of the white-adipocyte cell phenotype is independent of the brown-adipocyte cell phenotype

2001 ◽  
Vol 356 (2) ◽  
pp. 659-664 ◽  
Author(s):  
Karine MOULIN ◽  
Nathalie TRUEL ◽  
Mireille ANDRÉ ◽  
Emmanuelle ARNAULD ◽  
Maryse NIBBELINK ◽  
...  
Keyword(s):  
Brown Fat ◽  
Late Gestation ◽  
Brown Adipocyte ◽  
Cell Phenotype ◽  
Lacz Gene ◽  
Experimental Proof ◽  
Brown Adipocytes ◽  
White Adipocytes ◽  
Adipocyte Cell ◽  
White Fat

In mammals, two types of adipose tissue are present, brown and white. They develop sequentially, as brown fat occurs during late gestation whereas white fat grows mainly after birth. However, both tissues have been shown to have great plasticity. Thus an apparent transformation of brown fat into white fat takes place during post-natal development. This observation raises questions about a possible conversion of brown into white adipocytes during development, although indirect data argue against this hypothesis. To investigate such questions in vivo, we generated two types of transgenic line. The first carried a transgene expressing Cre recombinase specifically in brown adipocytes under the control of the rat UCP1 promoter. The second corresponded to an inactive lacZ gene under the control of the human cytomegalovirus promoter. This dormant gene is inducible by Cre because it contains a Stop sequence between two loxP sequences, separating the promoter from the coding sequence. Adipose tissues of progeny derived by crossing independent lines established from both constructs were investigated. LacZ mRNA corresponding to the activated reporter gene was easily detected in brown fat and not typically in white fat, even by reverse transcriptase PCR experiments. These data represent the first direct experimental proof that, during normal development, most white adipocytes do not derive from brown adipocytes.

scholarly journals β3-Adrenergic agonist induces a functionally active uncoupling protein in fat and slow-twitch muscle fibers

1998 ◽  
Vol 274 (3) ◽  
pp. E469-E475 ◽  
Author(s):  
Toshihide Yoshida ◽  
Tsunekazu Umekawa ◽  
Kenzo Kumamoto ◽  
Naoki Sakane ◽  
Akinori Kogure ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Muscle Fibers ◽  
Ectopic Expression ◽  
Brown Fat ◽  
Obese Mice ◽  
Adrenergic Agonist ◽  
Brown Adipose ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
White Fat

The mitochondrial uncoupling protein (UCP) has usually been found only in brown adipose tissue. We recently observed that a chronic administration of the β3-adrenergic agonist CL-316,243 (CL) induced the ectopic expression of UCP in white fat and skeletal muscle in genetic obese yellow KK mice. The aim of the present study was to examine whether UCP could be induced in nongenetic obese animals produced by neonatal injections of monosodiuml-glutamate (MSG). The daily subcutaneous injection of CL (0.1 mg/kg) to MSG-induced obese mice for 2 wk caused significant reductions of body weight (15%) and white fat pad weight (58%). Northern and Western blot analyses showed that CL induced significant expressions of UCP in the white fat and muscle, as well as in brown fat. Immunohistochemical observations revealed that the UCP stains in white fat were localized on multilocular cells and that those in muscle were localized on slow-twitch fibers rich in mitochondria. Immunoelectron microscopy confirmed the mitochondrial localization of UCP in the myocytes. The guanosine 5′-diphosphate (GDP) binding to mitochondria in brown fat doubled after the CL treatment. Moreover, significant GDP binding was detected in the white fat and muscle of the CL-treated mice, at about one-fourth and one-thirteenth the activity of brown fat, respectively, suggesting that ectopically expressed UCP is functionally active. We concluded that the β3-adrenergic agonist CL can induce functionally active UCP in white fat and slow-twitch muscle fibers of obese mice.

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