Quercetin Upregulates Uncoupling Protein 1 in White/Brown Adipose Tissues through Sympathetic Stimulation

We attempted to clarify whether leptin and uncoupling protein 1 (UCP1) are involved in the action of nicotine on the energy balance. Male Wistar rats were infused subcutaneously with nicotine (12 mg · kg−1 · day−1) for 4 or 14 days. At the end of the 4-day period, the plasma concentrations of leptin of the nicotine-treated and pair-fed rats were lower than those of the freely fed rats, although the levels of leptin mRNA expression in various white adipose tissues did not differ among the three groups. At the end of the 14-day nicotine infusion period, plasma concentrations of leptin were higher, and leptin mRNA expression in the omentum and epididymal and retroperitoneal adipose tissues was stronger in the nicotine-treated rats than in the pair-fed and freely fed rats. UCP1 mRNA expression in the brown adipose tissue of nicotine-treated was stronger than that of the pair-fed rats. These results suggest that continuous nicotine infusion differentially affects the synthesis and secretion of leptin according to the duration of infusion and stimulates UCP1 mRNA expression, probably in a manner independent of leptin.

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The thermogenic and metabolic responses to photoperiod manipulations in Apodemus chevrieri

Animal Biology ◽

10.1163/15707563-00002408 ◽

2013 ◽

Vol 63 (3) ◽

pp. 241-255 ◽

Cited By ~ 1

Author(s):

Wan-long Zhu ◽

Lin Zhang ◽

Zheng-kun Wang

Keyword(s):

Body Mass ◽

Uncoupling Protein ◽

Resting Metabolic Rate ◽

Mitochondrial Protein ◽

Short Photoperiod ◽

Uncoupling Protein 1 ◽

Mitochondrial Uncoupling ◽

Adipose Tissues ◽

Serum Leptin ◽

Brown Adipose

Environmental cues play important roles in the regulation of an animal’s physiology and behavior. In the present study, we examined the effects of short photoperiod on body weight as well as on several physiological, hormonal, and biochemical measures indicative of thermogenic capacity to test our hypothesis that short photoperiod stimulates increases in thermogenesis without cold stress in Apodemus chevrieri. A. chevrieri were randomly assigned to either a long or short photoperiod for 4 weeks at constant temperature. The short photoperiod group of A. chevrieri showed increases in resting metabolic rate and nonshivering thermogenesis during the 4-week photoperiod acclimation. At the end, A. chevrieri at short photoperiod had lower body weights, higher levels of mitochondrial protein content and cytochrome C oxidase activity in liver and brown adipose tissues, and had higher levels of mitochondrial uncoupling protein-1 contents in brown adipose tissues. No difference in serum leptin levels were found between short and long photoperiod groups, but serum leptin levels were positively correlated with body mass and body fat mass, and negatively correlated with energy intake and uncoupling protein-1 content in brown adipose tissues, respectively. All results suggest that the short photoperiod may induce an increased thermogenesis capacity in A. chevrieri and that leptin is potentially involved in the photoperiod induced body mass regulation and thermogenesis in A. chevrieri.

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Brown adipose tissue lipoprotein and glucose disposal is not determined by thermogenesis in uncoupling protein 1-deficient mice

The Journal of Lipid Research ◽

10.1194/jlr.ra119000455 ◽

2020 ◽

Vol 61 (11) ◽

pp. 1377-1389 ◽

Cited By ~ 2

Author(s):

Alexander W. Fischer ◽

Janina Behrens ◽

Frederike Sass ◽

Christian Schlein ◽

Markus Heine ◽

...

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Cold Exposure ◽

Uncoupling Protein ◽

Surrogate Marker ◽

Glucose Disposal ◽

Uncoupling Protein 1 ◽

Adipose Tissues ◽

Brown Adipose ◽

Deficient Mice

Adaptive thermogenesis is highly dependent on uncoupling protein 1 (UCP1), a protein expressed by thermogenic adipocytes present in brown adipose tissue (BAT) and white adipose tissue (WAT). Thermogenic capacity of human and mouse BAT can be measured by positron emission tomography-computed tomography quantifying the uptake of 18F-fluodeoxyglucose or lipid tracers. BAT activation is typically studied in response to cold exposure or treatment with β-3-adrenergic receptor agonists such as CL316,243 (CL). Currently, it is unknown whether cold-stimulated uptake of glucose or lipid tracers is a good surrogate marker of UCP1-mediated thermogenesis. In metabolic studies using radiolabeled tracers, we found that glucose uptake is increased in mildly cold-activated BAT of Ucp1−/− versus WT mice kept at subthermoneutral temperature. Conversely, lower glucose disposal was detected after full thermogenic activation achieved by sustained cold exposure or CL treatment. In contrast, uptake of lipoprotein-derived fatty acids into chronically activated thermogenic adipose tissues was substantially increased in UCP1-deficient mice. This effect is linked to higher sympathetic tone in adipose tissues of Ucp1−/− mice, as indicated by elevated levels of thermogenic genes in BAT and WAT. Thus, glucose and lipoprotein handling does not necessarily reflect UCP1-dependent thermogenic activity, but especially lipid uptake rather mirrors sympathetic activation of adipose tissues.

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Modulation of uncoupling protein 2 and uncoupling protein 3: regulation by denervation, leptin and retinoic acid treatment

Journal of Endocrinology ◽

10.1677/joe.0.1640331 ◽

2000 ◽

Vol 164 (3) ◽

pp. 331-337 ◽

Cited By ~ 36

Author(s):

PJ Scarpace ◽

M Matheny ◽

RL Moore ◽

MV Kumar

Keyword(s):

Retinoic Acid ◽

Uncoupling Protein ◽

Sympathetic Innervation ◽

Sympathetic Stimulation ◽

Uncoupling Protein 1 ◽

Adrenergic Agonist ◽

Uncoupling Protein 3 ◽

Brown Adipose ◽

Cgp 12177 ◽

Ucp2 Mrna

We recently reported that the leptin-induced increase in uncoupling protein 1 (UCP1) mRNA in brown adipose tissue (BAT) is prevented by the denervation of BAT. We also reported that retinoic acid (RA) increases UCP1 mRNA in BAT. To extend these finding to UCP2 and UCP3 in BAT, we examined UCP2 and UCP3 mRNA after unilateral denervation of BAT, as well as after leptin, beta(3)-adrenergic agonist, RA, and glucocorticoid administration to rats. UCP3 mRNA was 20% less in the denervated compared with the intact BAT, whereas UCP2 mRNA was unchanged with denervation. The beta(3)-adrenergic agonist, CGP-12177 (0.75 mg/kg), increased UPC3 mRNA by 40% in the innervated and by 85% in the denervated BAT. Leptin (0.9 mg/day for 3 days) increased both UCP2 and UCP3 mRNA by 30% in the innervated and, surprisingly, in the denervated BAT. RA (7.5 mg/kg) increased UCP1 mRNA but decreased UCP2 and UCP3 mRNA by 50%, whereas methylprednisolone (65 mg/kg, two doses 24 h apart) suppressed all three uncoupling proteins by greater than 60%. The present findings indicate that: sympathetic innervation is necessary to maintain basal levels of UCP3 mRNA; beta(3)-adrenergic agonist stimulation induces UCP3 mRNA; leptin induces UCP2 and UCP3 mRNA and this induction is not dependent on sympathetic innervation; RA increases UCP1 but decreases UCP2 and UCP3 mRNA; and methylprednisolone suppresses UCP1, UCP2, and UCP3 mRNA equally. These data suggest that there are distinct patterns of regulation between UCP1, UCP2, and UCP3, and there may be at least two modes by which leptin could modulate thermogenesis in BAT; first, by increasing sympathetic stimulation of BAT and induction of UCP1 mRNA and, secondly, by increasing UCP2 and UCP3 mRNA by a mechanism independent of sympathetic stimulation.

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Limited proteolysis reveals conformational changes in uncoupling protein-1 from brown adipose tissue mitochondria

Archives of Biochemistry and Biophysics ◽

10.1016/j.abb.2003.07.005 ◽

2003 ◽

Vol 420 (1) ◽

pp. 40-45 ◽

Cited By ~ 6

Author(s):

Shu-Gui Huang

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Conformational Changes ◽

Uncoupling Protein ◽

Limited Proteolysis ◽

Uncoupling Protein 1 ◽

Brown Adipose

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The Role of Uncoupling Protein 1 in the Metabolism and Adiposity of RIIβ-Protein Kinase A-Deficient Mice

Molecular Endocrinology ◽

10.1210/me.2004-0194 ◽

2004 ◽

Vol 18 (9) ◽

pp. 2302-2311 ◽

Cited By ~ 21

Author(s):

Michael A. Nolan ◽

Maria A. Sikorski ◽

G. Stanley McKnight

Keyword(s):

Adipose Tissue ◽

Oxygen Consumption ◽

Protein Kinase ◽

Protein Kinase A ◽

Uncoupling Protein ◽

Mrna Level ◽

Regulatory Subunit ◽

Uncoupling Protein 1 ◽

Brown Adipose ◽

Kinase A

Abstract Mice lacking the RIIβ regulatory subunit of protein kinase A exhibit a 50% reduction in white adipose tissue stores compared with wild-type littermates and are resistant to diet-induced obesity. RIIβ−/− mice also have an increase in resting oxygen consumption along with a 4-fold increase in the brown adipose-specific mitochondrial uncoupling protein 1 (UCP1). In this study, we examined the basis for UCP1 induction and tested the hypothesis that the induced levels of UCP1 in RIIβ null mice are essential for the lean phenotype. The induction of UCP1 occurred at the protein but not the mRNA level and correlated with an increase in mitochondria in brown adipose tissue. Mice lacking both RIIβ and UCP1 (RIIβ−/−/Ucp1−/−) were created, and the key parameters of metabolism and body composition were studied. We discovered that RIIβ−/− mice exhibit nocturnal hyperactivity in addition to the increased oxygen consumption at rest. Disruption of UCP1 in RIIβ−/− mice reduced basal oxygen consumption but did not prevent the nocturnal hyperactivity. The double knockout animals also retained the lean phenotype of the RIIβ null mice, demonstrating that induction of UCP1 and increased resting oxygen consumption is not the cause of leanness in the RIIβ mutant mice.

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